नोट्स ओं senescence

Cell death and organ development in plants

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Author(s): Rogers HJ
Source: CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY, VOL 71 Book Series: CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY Volume: 71 Pages: 225-+ Published: 2005
Times Cited: 19 References: 167 Citation MapCitation Map
Abstract: Programmed cell death (PCD) is an important feature of plant development; however, the mechanisms responsible for its regulation in plants are far less well understood than those operating in animals. In this review data from a wide variety of plant PCD systems is analyzed to compare what is known about the underlying mechanisms. Although senescence is clearly an important part of plant development, only what is known about PCD during senescence is dealt with here. In each PCD system the extracellular and intracellular signals triggering PCD are considered and both cytological and molecular data are discussed to determine whether a unique model for plant PCD can be derived. In the majority of cases reviewed, PCD is accompanied by the formation of a large vacuole, which ruptures to release hydrolytic enzymes that degrade the cell contents, although this model is clearly not universal. DNA degradation and the activation of proteases is also common to most plant PCD systems, where they have been studied; however, breakdown of DNA into nucleosomal units (DNA laddering) is not observed in all systems. Caspase-like activity has also been reported in several systems, but the extent to which it is a necessary feature of all plant PCD has not yet been established. The trigger for tonoplast rupture is not fully understood, although active oxygen species (AOS) have been implicated in several systems. In. two systems, self incompatibility and tapetal breakdown as a result of cytoplasmic male sterility, there is convincing evidence for the involvement of mitochondria including release of cytochrome c. However, in other systems, the role of the mitochondrion is not clear-cut. How cells surrounding the cell undergoing PCD protect themselves against death is also discussed as well as whether there is a link between the eventual fate of the cell corpse and the mechanism of its death. (c) 2005, Elsevier Inc.
Document Type: Review
Language: English
KeyWords Plus: TRACHEARY-ELEMENT DIFFERENTIATION; CASTOR BEAN ENDOSPERM; SENESCENCE-ASSOCIATED GENES; CYTOPLASMIC MALE-STERILITY; CYSTEINE PROTEASE GENE; WHEAT ALEURONE CELLS; ZEA-MAYS L.; LEAF SENESCENCE; AERENCHYMA FORMATION; BARLEY ALEURONE
Reprint Address: Rogers, HJ (reprint author), Cardiff Univ, Sch Biosci, Cardiff CF10 3TL, Wales
Addresses:
1. Cardiff Univ, Sch Biosci, Cardiff CF10 3TL, Wales
Publisher: ELSEVIER ACADEMIC PRESS INC, 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
Subject Category: Developmental Biology
IDS Number: BDI97
ISSN: 0070-2153
DOI: 10.1016/S0070-2153(05)71007-3

The molecular and genetic control of leaf senescence and longevity in Arabidopsis

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Author(s): Lim PO, Nam HG
Source: CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY, VOL 67 Book Series: CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY Volume: 67 Pages: 49-83 Published: 2005
Times Cited: 18 References: 111 Citation MapCitation Map
Abstract: The life of a leaf initiated from a leaf primordium ends with senescence, the final step of leaf development. Leaf senescence is a developmentally programmed degeneration process that is controlled by multiple developmental and environmental signals. It is a highly regulated and complex process that involves orderly, sequential changes in cellular physiology, biochemistry, and gene expression. Elucidating molecular mechanisms underlying such a complex, yet delicate process of leaf senescence is a challenging and important biological task. For the past decade, impressive progress has been achieved on the molecular processes of leaf senescence through identification of genes that show enhanced expression during senescence. In addition, Arabidopsis has been established as a model plant for genetic analysis of leaf senescence. The progress on the characterization of genetic mutants of leaf senescence in Arabidopsis has firmly shown that leaf senescence is a genetically controlled developmental phenomenon involving numerous regulatory elements. Especially, employment of global expression analysis as well as genomic resources in Arabidopsis has been very fruitful in revealing the molecular genetic nature and mechanisms underlying leaf senescence. This progress, including molecular characterization of some of the genetic regulatory elements, are revealing that senescence is composed of a complex regulatory network. In this review, we will present current understanding of the molecular genetic mechanisms by which leaf senescence is regulated and processed, focusing mostly on the regulatory factors of senescence in Arabidopsis. We also present a potential biotechnological implication of leaf senescence studies on the improvement of important agronomic traits such as crop yield and post-harvest shelf life. We further provide future research prospects to better understand the complex regulatory network of senescence. (c) 2005, Elsevier Inc.
Document Type: Review
Language: English
KeyWords Plus: END RULE PATHWAY; CAENORHABDITIS-ELEGANS; PROTEIN-DEGRADATION; PLANT SENESCENCE; PATHOGEN-DEFENSE; PHOSPHOLIPASE-D; MESSENGER-RNAS; TOMATO PLANTS; JASMONIC ACID; LARGE SUBUNIT
Reprint Address: Lim, PO (reprint author), Cheju Natl Univ, Dept Sci Educ, Cheju 690756, South Korea
Addresses:
1. Pohang Univ Sci & Technol, Natl Res Lab Plant Mol Genet, Div Mol & Life Sci, Pohang 790784, Kyungbuk South Korea
Publisher: ELSEVIER ACADEMIC PRESS INC, 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
Subject Category: Developmental Biology
IDS Number: BCM26
ISSN: 0070-2153
DOI: 10.1016/S0070-2153(04)67002-5

The molecular analysis of leaf senescence - a genomics approach

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Author(s): Buchanan-Wollaston V, Earl S, Harrison E, Mathas E, Navabpour S, Page T, Pink D
Source: PLANT BIOTECHNOLOGY JOURNAL Volume: 1 Issue: 1 Pages: 3-22 Published: JAN 2003
Times Cited: 155 References: 140 Citation MapCitation Map
Abstract: Senescence in green plants is a complex and highly regulated process that occurs as part of plant development or can be prematurely induced by stress. In the last decade, the main focus of research has been on the identification of senescence mutants, as well as on genes that show enhanced expression during senescence. Analysis of these is beginning to expand our understanding of the processes by which senescence functions. Recent rapid advances in genomics resources, especially for the model plant species Arabidopsis, are providing scientists with a dazzling array of tools for the identification and functional analysis of the genes and pathways involved in senescence. In this review, we present the current understanding of the mechanisms by which plants control senescence and the processes that are involved.
Document Type: Review
Language: English
Author Keywords: Arabidopsis; cell death; post-harvest; senescence; signalling pathways; stress
KeyWords Plus: PROGRAMMED CELL-DEATH; CYTOSOLIC GLUTAMINE-SYNTHETASE; PATHOGENESIS-RELATED PROTEINS; SENESCING ARABIDOPSIS LEAVES; ATP-DEPENDENT PROTEASE; DEFENSE-RELATED GENES; STAY-GREEN; DIFFERENTIAL EXPRESSION; FESTUCA-PRATENSIS; PLANT SENESCENCE
Reprint Address: Buchanan-Wollaston, V (reprint author), Hort Res Int, Prod Qual Team, Wellesbourne CV35 9EF, Warwick England
Addresses:
1. Hort Res Int, Prod Qual Team, Wellesbourne CV35 9EF, Warwick England
E-mail Addresses: vicky.b-wollaston@hri.ac.uk
Publisher: BLACKWELL PUBLISHING LTD, 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
Subject Category: Biotechnology & Applied Microbiology; Plant Sciences
IDS Number: 774QE
ISSN: 1467-7644

F-box proteins in flowering plants


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Author(s): Wang HY, Huang J, Lai Z, Xue YB
Source: CHINESE SCIENCE BULLETIN Volume: 47 Issue: 18 Pages: 1497-1501 Published: SEP 2002
Times Cited: 1 References: 45 Citation MapCitation Map
Abstract: In eukaryotes, the ubiquitin-mediated protein degradation pathway has been shown to control several key biological processes such as cell division, development, metabolism and immune response. F-box proteins, as a part of SCF (Skp1-Cullin (or Cdc53)-F-box) complex, functioned by interacting with substrate proteins, leading to their subsequent degradation by the 26S proteasome. To date, several F-box proteins identified in Arabidopsis and Antirrhinum have been shown to play important roles in auxin signal transduction, floral organ formation, flowering and leaf senescence. Arabidopsis genome sequence analysis revealed that it encodes over 1000 predicted F-box proteins accounting for about 5% of total predicted proteins. These results indicate that the ubiquitin-mediated protein degradation involving the F-box proteins is an important mechanism controlling plant gene expression. Here, we review the known F-box proteins and their functions in flowering plants.
Document Type: Review
Language: English
Author Keywords: SCF complex; F-box protein; proteolysis; auxin signal transduction
KeyWords Plus: UBIQUITIN-DEPENDENT PROTEOLYSIS; AUXIN RESPONSE; CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; ARABIDOPSIS-THALIANA; AUX/IAA PROTEINS; COP9 SIGNALOSOME; LIGASE COMPLEX; GENE; DEGRADATION
Reprint Address: Xue, YB (reprint author), Chinese Acad Sci, Inst Genet & Dev Biol, Beijing 100080, Peoples R China
Addresses:
1. Chinese Acad Sci, Inst Genet & Dev Biol, Beijing 100080, Peoples R China
E-mail Addresses: ybxue@genetics.ac.cn
Publisher: SCIENCE CHINA PRESS, 16 DONGHUANGCHENGGEN NORTH ST, BEIJING 100717, PEOPLES R CHINA
Subject Category: Multidisciplinary Sciences
IDS Number: 595TD
ISSN: 1001-6538

Current molecular understanding of the genetically programmed process of leaf senescence

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Author(s): Chandlee JM
Source: PHYSIOLOGIA PLANTARUM Volume: 113 Issue: 1 Pages: 1-8 Published: SEP 2001
Times Cited: 33 References: 47 Citation MapCitation Map
Abstract: Natural leaf senescence proceeds through an orderly program of events referred to, generally, as the 'senescence syndrome'. Leaf senescence consists of primarily, but not exclusively, a set of degradative and remobilization activities that salvage valuable nutrients by reallocation to the seeds or other viable parts of the plant. The program requires changes in gene expression and eventually culminates in death of the leaf or whole plant. Leaf/whole plant senescence has now been scrutinized extensively using molecular genetic approaches and a clearer picture of the events that comprise the developmental program is beginning to emerge. However, while understandings of the phenomenological aspects of the program have become apparent, the mechanistic aspects, particularly with regard to the processes required for induction and regulation of the program, are still far from clear. Molecular evidence suggests the process is complex in terms of the wide array of genes and activities expressed, and in terms of the overall regulation of progression of the events of the syndrome. This article attempts to review our current understanding of leaf senescence and includes a brief discussion of aspects of the process that require clarification if we are to more fully understand this complex developmental program.
Document Type: Review
Language: English
KeyWords Plus: GLUTAMINE-SYNTHETASE GENES; ARABIDOPSIS-THALIANA; BRASSICA-NAPUS; DIFFERENTIAL EXPRESSION; STAY-GREEN; TRANSGENIC PLANTS; TOMATO PLANTS; IDENTIFICATION; ETHYLENE; PROTEINS
Reprint Address: Chandlee, JM (reprint author), Univ Rhode Isl, Dept BIochem Microbiol & Mol Genet, Morrill Hall, Kingston, RI 02881 USA
Addresses:
1. Univ Rhode Isl, Dept BIochem Microbiol & Mol Genet, Kingston, RI 02881 USA
Publisher: MUNKSGAARD INT PUBL LTD, 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
Subject Category: Plant Sciences
IDS Number: 467TZ
ISSN: 0031-9317

Plant programmed cell death: A common way to die

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Author(s): Danon A, Delorme V, Mailhac N, Gallois P
Source: PLANT PHYSIOLOGY AND BIOCHEMISTRY Volume: 38 Issue: 9 Pages: 647-655 Published: SEP 2000
Times Cited: 91 References: 62 Citation MapCitation Map
Abstract: In the last few years programmed cell death in plants inspired many studies in development and environmental stresses. Some of these studies showed that hallmarks of animal programmed cell death were found at cellular or molecular level in plant cells in different experimental systems. Additionally the effect of over-expression in plants of animal genes implicated in programmed cell death has been tested, and some plant homologues of these genes have been found. This suggests that, despite some differences, plants and animals could share at least some common components of a core mechanism used to carry out programmed cell death in eukaryotes. In this review, we will concentrate on the last findings that suggest similarity between plant programmed cell death and its better known counterpart in animals. (C) 2000 Editions scientifiques et medicales Elsevier SAS.
Document Type: Review
Language: English
Author Keywords: apoptosis; caspases; DNA ladder; necrosis; plants; programmed cell death; TUNEL
KeyWords Plus: POLY(ADP-RIBOSE) POLYMERASE; HYPERSENSITIVE RESPONSE; ARABIDOPSIS-THALIANA; BARLEY ALEURONE; CYTOCHROME-C; APOPTOSIS; DNA; SENESCENCE; CASPASES; TOBACCO
Reprint Address: Gallois, P (reprint author), Univ Perpignan, Lab Genome & Dev Plantes, CNRS, UMR 5096, 52 Ave Villeneuve, F-66860 Perpignan, France
Addresses:
1. Univ Perpignan, Lab Genome & Dev Plantes, CNRS, UMR 5096, F-66860 Perpignan, France
Publisher: GAUTHIER-VILLARS/EDITIONS ELSEVIER, 23 RUE LINOIS, 75015 PARIS, FRANCE
Subject Category: Plant Sciences
IDS Number: 364CY
ISSN: 0981-9428

Programmed cell death during plant growth and development

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Author(s): Beers EP
Source: CELL DEATH AND DIFFERENTIATION Volume: 4 Issue: 8 Pages: 649-661 Published: DEC 1997
Times Cited: 79 References: 158 Citation MapCitation Map
Abstract: This review describes programmed cell death as it signifies the terminal differentiation of cells in anthers, xylem, the suspensor and senescing leaves and petals. Also described are cell suicide programs initiated by stress (e.g., hypoxia-induced aerenchyma formation) and those that depend on communication between neighboring cells, as observed for incompatible pollen tubes, the suspensor and synergids in some species. Although certain elements of apoptosis are detectable during some plant programmed cell death processes, the participation of autolytic and perhaps autophagic mechanisms of cell killing during aerenchyma formation, tracheary element differentiation, suspensor degeneration and senescence support the conclusion that nonapoptotic programmed cell death pathways are essential to normal plant growth and development. Heterophagic elimination of dead cells, a prominent feature of animal apoptosis, is not evident in plants. Rather autolysis and autophagy appear to govern the elimination of cells during plant cell suicide.
Document Type: Review
Language: English
Author Keywords: programmed cell death; plants; apoptosis; protease
KeyWords Plus: POLLEN-TUBE DEVELOPMENT; LEAF SENESCENCE; ARABIDOPSIS-THALIANA; SEX DETERMINATION; PEA-CHLOROPLASTS; PITH AUTOLYSIS; ZINNIA-ELEGANS; RIBULOSE-1,5-BISPHOSPHATE CARBOXYLASE; POLY(ADP-RIBOSE) POLYMERASE; CAENORHABDITIS-ELEGANS
Reprint Address: Beers, EP (reprint author), VIRGINIA POLYTECH INST & STATE UNIV, DEPT HORT, BLACKSBURG, VA 24061 USA
Publisher: STOCKTON PRESS, HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
Subject Category: Biochemistry & Molecular Biology; Cell Biology
IDS Number: YJ306
ISSN: 1350-9047

Programmed senescence of plant organs

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Author(s): Hadfield KA, Bennett AB
Source: CELL DEATH AND DIFFERENTIATION Volume: 4 Issue: 8 Pages: 662-670 Published: DEC 1997
Times Cited: 36 References: 139 Citation MapCitation Map
Abstract: The senescence of plant organs associated with reproductive development has been studied extensively during the past century, and it has long been recognized that th is type of death is internally programmed. The regulation of organ senescence as well as its biochemical and genetic determinants has been an historically rich area of research. Certain plant hormones have been implicated as regulators or modulators of organ senescence and many of the biochemical pathways associated with the senescence syndrome have been elucidated. The genetic basis of organ senescence has also been well established by the identification of mutations that impair the senescence program and recently, transgenic plants have been used to critically determine the role of specific enzymes and hormonal signals in mediating programmed senescence of plant organs, Here, we review the current understanding of the processes that regulate leaf, flower and fruit senescence, emphasizing the rate that programmed organ senescence plays in the adaptive fitness of plants.
Document Type: Review
Language: English
Author Keywords: survivorship; fruit ripening; organ senescence
KeyWords Plus: ENCODING 1-AMINOCYCLOPROPANE-1-CARBOXYLATE SYNTHASE; TOMATO FRUIT POLYGALACTURONASE; ETHYLENE-INDUCIBLE EXPRESSION; DELAYED LEAF SENESCENCE; CARNATION FLOWER PETALS; MESSENGER-RNA LEVELS; GENE-EXPRESSION; MOLECULAR-CLONING; PROTEIN-SYNTHESIS; AVOCADO FRUIT
Addresses:
1. UNIV CALIF DAVIS, DEPT VEGETABLE CROPS, MANN LAB, DAVIS, CA 95616 USA
Publisher: STOCKTON PRESS, HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
Subject Category: Biochemistry & Molecular Biology; Cell Biology
IDS Number: YJ306
ISSN: 1350-9047

GENE-EXPRESSION DURING LEAF SENESCENCE

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Author(s): SMART CM
Source: NEW PHYTOLOGIST Volume: 126 Issue: 3 Pages: 419-448 Published: MAR 1994
Times Cited: 366 References: 297 Citation MapCitation Map
Abstract: Leaf senescence is a highly-controlled sequence of events comprising the final stage of development. Cells remain viable during the process and new gene expression is required. There is some similarity between senescence in plants and programmed cell death in animals. In this review, different classes of senescence-related genes are defined and progress towards isolating such genes is reported. A range of internal and external factors which appear to cause leaf senescence is considered and various models for the mechanism of senescence initiation are described. The current understanding of senescence at the organelle and molecular levels is presented. Finally, some ideas are mooted as to why senescence occurs and why it should be studied further.
Document Type: Review
Language: English
Author Keywords: LEAF SENESCENCE; PROGRAMMED CELL DEATH; GENES; PLANT GROWTH REGULATORS; ORGANELLES; MOLECULES
KeyWords Plus: NON-YELLOWING MUTANT; SENESCING BARLEY LEAVES; TRITICUM-AESTIVUM L; CYTOSOLIC GLUTAMINE-SYNTHETASE; REJUVENATED SOYBEAN COTYLEDONS; TRANSLATABLE MESSENGER-RNAS; PEPTIDE-HYDROLASE ACTIVITY; DARK-INDUCED SENESCENCE; FESTUCA-PRATENSIS HUDS; PROGRAMMED CELL-DEATH
Reprint Address: SMART, CM (reprint author), AFRC, INST GRASSLAND & ENVIRONM RES, DEPT CELL BIOL, PLAS GOGERDDAN, ABERYSTWYTH SY23 3EB, DYFED WALES
Publisher: CAMBRIDGE UNIV PRESS, 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
Subject Category: Plant Sciences
IDS Number: NG798
ISSN: 0028-646X

Seborrhoeic dermatitis

Collection of words for searching:
Seborrhoeic dermatitis
biotin, pyridoxine (vitamin B6) and riboflavin (vitamin B2)
yeast, Malassezia furfur

salinity tolerance in cereals

Rajendran, K., Tester, M. & Roy, S.J. (2009) Quantifying the three main components of salinity tolerance in cereals. Plant, Cell & Environment 32, 237-249

from Naked Scientist:
http://www.thenakedscientists.com/HTML/content/interviews/interview/1239/

Chris - So how did you do that rather clever trick of making that gene only get turned on in those cells around these xylem vessels because that’s the breakthrough step, isn’t it really?

Mark - Yes, it is. There’s different ways you can do this. One is to try to discover little bits of DNA which will activate genes in specific parts of the plant. So that’s one way you can do it a very direct way. In the meantime, we’re using a model plant. It’s called Arabidopsis. It’s a silly little weed, but you can do lots of really nice molecular genetics with it. And what we did was throw into the genome of this little plant, this little weed, a little bit of DNA which allows us to turn on genes. But we threw it on in random in the genome, made thousands of these plants and then looked at the plants to find ones which had the right pattern of expression. So the initial generation of the plants was random and then we looked to find plants which had by fluke, this bit of DNA landing in a part of the genome that would activate that gene only in the inner half of the root.

Chris - Big question though, Mark must be a course, it’s one thing to do this in thale cress, the plant sciences fruit fly. But we don’t eat that. So what about things that we do eat? Could you put this same genetic combination into rice, into barley, wheat, and so on? The kinds of things we do rely on for food staples.

Mark - Absolutely, Chris. We have done this in rice and the results are looking very promising. We look like we’ve worked out how to reduce the sodium concentration. Well we have reduced the sodium concentration in the shoots of rice and we’re in the process of testing the effect of that on yield. The first experiments did improve yield, but we just want to again be fairly conservative rather than just shooting off the results rapidly. But it’s looking very promising. To turn the genes on in wheat and barley, maze, it’s actually quite difficult because these molecular genetic tricks that we’re able to use on Arabidopsis, we just simply can’t do it. We’re technically not able to do it in wheat and barley. So what we’re doing now is we’re having a program to discover the promoters that would help us turn this on, so going back to a very direct but slower way of manipulating an expression in wheat and barley. We actually have transgenic plants in the glasshouse at the moment for wheat and barley and we’re limited by bulking up the seed, and we’re just at that stage at the moment. So keep your fingers crossed for us and hopefully in the year’s time, we’ll be able to say if we’ve done it in the other crops as well.

salinity tolerance in cereals

Rajendran, K., Tester, M. & Roy, S.J. (2009) Quantifying the three main components of salinity tolerance in cereals. Plant, Cell & Environment 32, 237-249

Fusarium ओक्स्य्स्पोरुम genome

Genome information:
Name GenBank
Master WGS AAXH00000000
Chromosome 1 CM000589
Chromosome 2 CM000590
Chromosome 3 CM000591
Chromosome 4 CM000592
Chromosome 5 CM000593
Chromosome 6 CM000594
Chromosome 7 CM000595
Chromosome 8 CM000596
Chromosome 9 CM000597
Chromosome 10 CM000598
Chromosome 11 CM000599
Chromosome 12 CM000600
Chromosome 13 CM000601
Chromosome 14 CM000602
Chromosome 15 CM000603

Whole genome sequence fungi list

Aspergillus clavatus
Aspergillus fumigatus
Aspergillus niger
Candida glabrata
Cryptococcus neoformans
Debaryomyces hansenii
Encephalitozoon cuniculi
Eremothecium gossypii
Gibberella zeae
Kluyveromyces lactis
Magnaporthe grisea
Neurospora crassa
Pichia stipitis
Saccharomyces cerevisiae
Schizosaccharomyces pombe
Ustilago maydis
Yarrowia lipolytica

A MicroRNA Imparts Robustness against Environmental Fluctuation during Development

Article
A MicroRNA Imparts Robustness against Environmental Fluctuation during Development

Xin Li1, 2, 3, Justin J. Cassidy1, 2, Catherine A. Reinke1, Stephen Fischboeck1 and Richard W. Carthew1, ,

1Department of Biochemistry, Molecular Biology and Cell Biology, 2205 Tech Drive, Northwestern University, Evanston, Illinois 60208, USA


Received 16 May 2008; revised 25 November 2008; accepted 29 January 2009. Published: April 16, 2009. Available online 16 April 2009.

Summary
The microRNA miR-7 is perfectly conserved from annelids to humans, and yet some of the genes that it regulates in Drosophila are not regulated in mammals. We have explored the role of lineage restricted targets, using Drosophila, in order to better understand the evolutionary significance of microRNA-target relationships. From studies of two well characterized developmental regulatory networks, we find that miR-7 functions in several interlocking feedback and feedforward loops, and propose that its role in these networks is to buffer them against perturbation. To directly demonstrate this function for miR-7, we subjected the networks to temperature fluctuation and found that miR-7 is essential for the maintenance of regulatory stability under conditions of environmental flux. We suggest that some conserved microRNAs like miR-7 may enter into novel genetic relationships to buffer developmental programs against variation and impart robustness to diverse regulatory networks.

Fusarium oxysporum

Eukaryota;
Fungi;
Dikarya;
Ascomycota;
Pezizomycotina;
Sordariomycetes;
Hypocreomycetidae;
Hypocreales;
mitosporic Hypocreales;
Fusarium;
Fusarium oxysporum species complex;
Fusarium oxysporum

Structure creates Function: Network analysis of genes determining vascular wilt disease

Structure creates Function: Network analysis of genes determining vascular wilt disease: "Lead Supervisor: Dr Louise Thatcher
Associates: Dr Kemal Kazan, Dr Donald Gardiner

Vascular wilt disease caused by the root infecting fungus Fusarium oxysporum affects over 100 plant species, including many economically important crops. This pathogen survives in soil for long periods and can be extremely difficult to eradicate once soils become infested.

High-throughput screening for altered Fusarium resistance on the model host Arabidopsis thaliana has identified many host mutants with increased susceptibility or resistance. This project aims to confirm the Fusarium disease phenotypes of a selected subset of mutants and develop hypotheses on the involvement of mutated genes in resistance or susceptibility mechanisms to Fusarium. This will involve screening second independent mutant lines in the genes of interest, confirming the mutations through PCR analysis, and the use of other pathogen assays, gene expression analysis and/or bioinformatic approaches to develop a network map of genes determining vascular wilt disease outcomes"

http://www.csiro.au/science/Summer-Studentships-Projects--ci_pageNo-2.html#6

Network analysis of genes determining vascular wilt disease

Network analysis of genes determining vascular wilt disease.

Lead Supervisor: Dr Louise Thatcher
Associates: Dr Kemal Kazan, Dr Donald Gardiner

Vascular wilt disease caused by the root infecting fungus Fusarium oxysporum affects over 100 plant species, including many economically important crops. This pathogen survives in soil for long periods and can be extremely difficult to eradicate once soils become infested.

High-throughput screening for altered Fusarium resistance on the model host Arabidopsis thaliana has identified many host mutants with increased susceptibility or resistance. This project aims to confirm the Fusarium disease phenotypes of a selected subset of mutants and develop hypotheses on the involvement of mutated genes in resistance or susceptibility mechanisms to Fusarium. This will involve screening second independent mutant lines in the genes of interest, confirming the mutations through PCR analysis, and the use of other pathogen assays, gene expression analysis and/or bioinformatic approaches to develop a network map of genes determining vascular wilt disease outcomes

DNA repair proteins

Redox signaling between DNA repair proteins for efficient lesion detection

Published online before print August 31, 2009, doi: 10.1073/pnas.0908059106
PNAS September 8, 2009 vol. 106 no. 36

1. Amie K. Boala,
2. Joseph C. Genereuxa,
3. Pamela A. Sontza,
4. Jeffrey A. Gralnickb,
5. Dianne K. Newmanc,1 and
6. Jacqueline K. Bartona,1

+ Author Affiliations

1.
aDivision of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125;
2.
bDepartment of Microbiology, BioTechnology Institute, University of Minnesota, St. Paul, MN 55108; and
3.
cDepartments of Biology and Earth, Atomospheric and Planetary Science, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139

1.

Contributed by Jacqueline K. Barton, July 21, 2009 (received for review June 25, 2009)

Abstract

Base excision repair (BER) enzymes maintain the integrity of the genome, and in humans, BER mutations are associated with cancer. Given the remarkable sensitivity of DNA-mediated charge transport (CT) to mismatched and damaged base pairs, we have proposed that DNA repair glycosylases (EndoIII and MutY) containing a redox-active [4Fe4S] cluster could use DNA CT in signaling one another to search cooperatively for damage in the genome. Here, we examine this model, where we estimate that electron transfers over a few hundred base pairs are sufficient for rapid interrogation of the full genome. Using atomic force microscopy, we found a redistribution of repair proteins onto DNA strands containing a single base mismatch, consistent with our model for CT scanning. We also demonstrated in Escherichia coli a cooperativity between EndoIII and MutY that is predicted by the CT scanning model. This relationship does not require the enzymatic activity of the glycosylase. Y82A EndoIII, a mutation that renders the protein deficient in DNA-mediated CT, however, inhibits cooperativity between MutY and EndoIII. These results illustrate how repair proteins might efficiently locate DNA lesions and point to a biological role for DNA-mediated CT within the cell.

sexual activity on cycle ergometer stress test parameters

Effect of sexual activity on cycle ergometer stress test parameters, on plasmatic testosterone levels and on concentration capacity - A study in high-level male athletes performed in the laboratory

Author(s): Sztajzel J, Periat M, Marti V, Krall P, Rutishauser W
Source: JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS
Volume: 40
Issue: 3
Pages: 233-239
Published: SEP 2000

Abstract: Background. The purpose of this study was to investigate the effect of sexual activity on cycle ergometer stress test parameters, on plasmatic testosterone levels and on concentration capacity in high-level mate athletes.

Methods. Experimental design. Analysis of two days of testing accomplished in a laboratory setting, comparing a day with to a day without sexual activity (control day). Participants. Fifteen high-level male athletes, consisting of 8 team players, 5 endurance athletes and 2 weight-lifters, participated in the study. Measures. Each subject completed the following on each test day: two maximal graded stress tests on a cycle ergometer and a one-hour exercise stress test coupled to an arithmetic mental concentration test. Blood samples of testosterone were obtained and cardiac activity of each athlete was monitored with a 24-hour ECG tape recording over the two test days.

Results, Significantly higher differences were achieved for posteffort heart rate (HR) values at 5 minutes (p<0.01) and at 10 minutes (p<0.01) during the recovery phase of the morning stress test 2 hours after sexual activity. These differences disappeared during the recovery phase of the afternoon stress test performed approximately 10 hours after sexual intercourse took place.

Conclusions, Our findings show that sexual activity had no detrimental influence on the maximal workload achieved and on the athletes' mental concentration. However, the higher posteffort HR values after the maximal stress test on the morning of sexual intercourse suggest that the recovery capacity of an athlete could be affected if he had sexual intercourse approximately 2 hours before a competition event.

Does Sex the Night Before Competition Decrease Performance?

Does Sex the Night Before Competition Decrease Performance?

McGlone, Samantha; Shrier, Ian MD, PhD*†
Author Information
*Department of Physiology, McGill University, and †Centre for Clinical Epidemiology and Community Studies, Montreal, Quebec, Canada
Received June 7, 1999; accepted August 9, 2000.
Address correspondence and reprint requests to Ian Shrier, MD, Centre for Clinical Epidemiology and Community Studies, 3755 Cote Sainte Catherine Road, Montreal, Quebec H3T 1E2, Canada.

For many years, football coaches, Olympic athletes, and even Muhammad Ali have advocated sexual abstinence the night before an athletic event. 1 Marty Liquori, one the world's number one-ranked 5,000-meter runner believes that “Sex makes you happy, and happy people don't run a 3:47 mile.”2 Marv Levy, head coach of the Buffalo Bills, insisted that the team be separated from their wives before their appearance in four Super Bowls; a policy that apparently was not successful (four losses out of four Super Bowls). On the other hand, there are also plenty of anecdotal stories of athletes who claim to have benefited from sex the night before an event. Both U.S. track star David Wottle and Canadian downhill skier Karin Lee Gardner attribute their Olympic gold medals in part to their “pre-race preparation.”2 As legendary New York Yankees manager Casey Stengel put it, “It's not the sex that wrecks these guys, it's staying up all night looking for it.” Considering the controversy surrounding the topic, the objective of this editorial is to summarize the literature on whether sex the night before competition affects performance, and to suggest possible future areas for research.


The long-standing myth that athletes should practice abstinence before important competitions may stem from the theory that sexual frustration leads to increased aggression, and that the act of ejaculation draws testosterone from the body. 1 In actual fact, sex could alter performance through either physiological or psychological factors. To answer this question, we searched SportDiscus (1975–1988/1989, key words: Coitus and Sexual Intercourse) and MEDLINE for relevant articles. Of the 31 articles we retrieved, only 3 were scientific studies (all physiological). All of these studies suggested that sex the night before competition does not alter physiological testing results. For instance, 14 married male former athletes were given a maximum-effort grip strength test the morning after coitus, and the same test following at least 6 days of abstinence. 3 The results suggested that strength and endurance of the palmar flexing muscles are not adversely affected by sex the previous night. An unpublished follow-up to this study was conducted by researchers at Colorado State University on 10 fit, married men, ages 18–45 years (cited in ref. 4). In their tests for grip strength, balance, lateral movement, reaction time, aerobic power (stair-climbing exercise), and VO2max (treadmill test), the results did not change with sexual activity. Finally, the results from a 1995 randomized cross-over study suggested that sexual intercourse 12 hours prior to the test had no significant effects on maximal aerobic power, oxygen pulse, or double product. 5


Based on the results of these studies, one might conclude that sexual activity the night before competition would not affect performance. However, each of the above-mentioned studies focused on the physiological effects of precompetition sex, which would only be expected to decrease performance if the activity led to exhaustion. Considering that normal sexual intercourse between married partners expends only 25–50 calories (the energy equivalent of walking up two flights of stairs), 6 it is doubtful that sex the previous night would affect laboratory physiological performance tests.


Remembering that the original hypothesis suggested that performance would only be affected through a change in aggression, researchers really should have measured variables that are affected by aggression (e.g., motivation, alertness, and attitude toward competition). According to the current “inverted U” sport psychology hypothesis, 4 there is an optimal level of alertness/anxiety before a competition, and a poor performance will result from either being too anxious or not alert enough. If athletes are too anxious and restless the night before an event, then sex may be a relaxing distraction. If they are already relaxed or, like some athletes, have little interest in sex the night before a big competition, then a good night's sleep is all they need. This theory predicts that the results will be dependent on individual preferences and routines. The night before an important race is not a good time for drastic changes in routine. Consistency is the key.


Clearly there is a need for more research on the topic of sexual activity and athletic performance. However, any research will have difficulty controlling factors related to such sexual behavior such as the time of day, frequency and duration of sexual activity, behavior of subjects between data collection, diet, fatigue, stress, and individual response to sexual activity. Anshel also poses a question worth considering: “How valid are test results when a natural activity such as coitus becomes a required act occurring within a specific time period?”7 In addition, results may be dependent on the sexual partner. For instance, heart rate and blood pressure responses are different if sex is with a spouse of 10 years, compared to a new partner or in strange surroundings. 8 Therefore, any future research will have to control for interindividual variation of the above-mentioned variables with a randomized design, or at least control for differences at the analysis stage.


Finally, the inverted U hypothesis for alertness/anxiety suggests that the performance of some people will improve with sex the night before competition (i.e., responders) and the performance of others will be hindered (i.e., nonresponders). If true, a randomized controlled trial may not be able to detect any differences. For instance, if the “truth” is that 50% of the population improves with sex the night before a competition and 50% is hindered by sex the night before competition, a randomized controlled trial will show that on average there is no effect. Therefore, the best way to test the hypothesis is with a repeated-measures, cross-over design in which the same athletes are tested several times following abstinence, and several times following sex the night before competition. This would allow one to determine not only if sex the night before competition affects performance in certain individuals, but also if there are indeed “responders” and “nonresponders.”

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REFERENCES


1. Krieger L. Scoring before a big event. Winning 1997; 1:88–89. [Context Link]


2. Bloom M. The sex factor. Runner's World 1994; 11:71–74. [Context Link]


3. Johnson W. Muscular performance following coitus. J Sex Res 1968; 4:247–248. Library Holdings [Context Link]


4. Thornton J. Sexual activity and athletic performance: is there a relationship? Phys Sport Med 1990; 18:148–153. [Context Link]


5. Boone T, Gilmore S. Effects of sexual intercourse on maximal aerobic power, oxygen pulse, and double product in male sedentary subjects. J Sports Med Phys Fitness 1995; 35:214–217. Library Holdings [Context Link]


6. Mirkin G. Sex before competition. Report #6750. Mar. 10, 1996. http://drmirkin.com/archive/6750.html [Context Link]


7. Anshel M. Effects of sexual activity on athletic performance. Phys Sports Med 1981; 9:65–68. Library Holdings [Context Link]


8. Bohlen J, Held J, Sanderson M, et al. Heart rate, rate pressure point, and oxygen uptake during four sexual activities. Arch Intern Med 1984; 144:1745–1748. Bibliographic Links Library Holdings [Context Link]

The effect of losing virginity on academic performance

Reading, writing, and sex: The effect of losing virginity on academic performance

View full text from the publisher Blackwell Science
Author(s): Sabia JJ (Sabia, Joseph J.)
Source: ECONOMIC INQUIRY
Volume: 45
Issue: 4
Pages: 647-670
Published: OCT 2007

Abstract: Controlling for a wide set of individual- and family-level observables available in the National Longitudinal Study of Adolescent Health, ordinary least squares (OLS) estimates show that sexually active adolescents have grade point averages that are approximately 0.2 points lower than virgins. However, when information on the timing of intercourse decisions is exploited and individual fixed effects are included, the negative effect of sexual intercourse disappears for females, but persists for males. Taken together, the results of this study suggest that while there may be adverse academic spillovers from engaging in intercourse for some adolescents, previous studies' estimates are overstated due to unmeasured heterogeneity.

DNA methylation analysis by प्य्रोसेक़ुएन्किन्ग

Figure 1 - Enzymatic cascade of the pyrosequencing reaction in the example of a bisulfite-treated template sequence, including a CpG position that is methylated on approximately 50% of all molecules.
From the following article

DNA methylation analysis by pyrosequencing

Jörg Tost & Ivo G Gut

Nature Protocols 2, 2265 - 2275 (2007) Published online: 6 September 2007

doi:10.1038/nprot.2007.314

Importing Mitochondrial Proteins: Machineries and Mechanisms

Review
Importing Mitochondrial Proteins: Machineries and Mechanisms

Agnieszka Chacinska1,2, Carla M. Koehler3, Dusanka Milenkovic1, 2, Trevor Lithgow4 and Nikolaus Pfanner1, 2,

1Institut für Biochemie und Molekularbiologie, ZBMZ, Universität Freiburg, 79104 Freiburg, Germany

2Centre for Biological Signalling Studies, Universität Freiburg, 79104 Freiburg, Germany

3Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA

4Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia

Most mitochondrial proteins are synthesized on cytosolic ribosomes and must be imported across one or both mitochondrial membranes. There is an amazingly versatile set of machineries and mechanisms, and at least four different pathways, for the importing and sorting of mitochondrial precursor proteins. The translocases that catalyze these processes are highly dynamic machines driven by the membrane potential, ATP, or redox reactions, and they cooperate with molecular chaperones and assembly complexes to direct mitochondrial proteins to their correct destinations. Here, we discuss recent insights into the importing and sorting of mitochondrial proteins and their contributions to mitochondrial biogenesis.

sliding β clamp subunit

Preview
Clamping Down on Transposon Targeting

Mick Chandler

1Laboratoire de Microbiologie et Génétique Moléculaire UMR 5100, CNRS, 31062 Toulouse CEDEX, France

Cell, Volume 138, Issue 4, 21 August 2009, Pages 685-695,
Adam R. Parks, Zaoping Li, Qiaojuan Shi, Roisin M. Owens, Moonsoo M. Jin, Joseph E. Peters

The sliding β clamp subunit of the DNA replication machinery in the bacterium Escherichia coli coordinates multiple functions in the cell beyond genome duplication. In this issue, Parks et al. (2009) find that the β clamp interacts with the transposition protein TnsE to target the Tn7 transposon to discontinuously replicating DNA at the replication fork.

सेल Volume 138, Issue 2, 23 July 2009, Pages 271-285

Article
CD47 Is Upregulated on Circulating Hematopoietic Stem Cells and Leukemia Cells to Avoid Phagocytosis

Cell, Volume 138, Issue 2, 23 July 2009, Pages 271-285


References and further reading may be available for this article. To view references and further reading you must purchase this article.

Siddhartha Jaiswal1, Corresponding Author Contact Information, E-mail The Corresponding Author, Catriona H.M. Jamieson2, Wendy W. Pang1, Christopher Y. Park1, Mark P. Chao1, Ravindra Majeti1, David Traver3, Nico van Rooijen4 and Irving L. Weissman1

Summary

Macrophages clear pathogens and damaged or aged cells from the blood stream via phagocytosis. Cell-surface CD47 interacts with its receptor on macrophages, SIRPα, to inhibit phagocytosis of normal, healthy cells. We find that mobilizing cytokines and inflammatory stimuli cause CD47 to be transiently upregulated on mouse hematopoietic stem cells (HSCs) and progenitors just prior to and during their migratory phase, and that the level of CD47 on these cells determines the probability that they are engulfed in vivo. CD47 is also constitutively upregulated on mouse and human myeloid leukemias, and overexpression of CD47 on a myeloid leukemia line increases its pathogenicity by allowing it to evade phagocytosis. We conclude that CD47 upregulation is an important mechanism that provides protection to normal HSCs during inflammation-mediated mobilization, and that leukemic progenitors co-opt this ability in order to evade macrophage killing.

Ergot alkaloid biosynthesis in Aspergillus fumigatus

Ergot alkaloid biosynthesis in Aspergillus fumigatus - Overproduction and biochemical characterization of a 4-dimethylallyltryptophan N-methyltransferase

Author(s): Rigbers O (Rigbers, Ole), Li SM (Li, Shu-Ming)1
Source: JOURNAL OF BIOLOGICAL CHEMISTRY
Volume: 283 Issue: 40 Pages: 26859-26868 Published: OCT 3 2008

Abstract: The putative gene fgaMT was identified in the biosynthetic gene cluster of fumigaclavines in Aspergillus fumigatus. The coding region of fgaMT was amplified by PCR from a cDNA library, cloned into pQE60, and overexpressed in Escherichia coli. FgaMT comprises 339 amino acids with a molecular mass of about 38.1 kDa. The soluble dimeric His(6)-FgaMT was purified to near homogeneity and characterized biochemically. FgaMT was found to catalyze the N-methylation of 4-dimethylallyltryptophan in the presence of S-adenosylmethionine, resulting in the formation of 4-dimethylallyl-L-abrine, which was identified by NMR and mass spectrometry analysis. Therefore, FgaMT represents the second pathway-specific enzyme in the biosynthesis of ergot alkaloids. The enzyme did not require metal ions for its enzymatic reaction and showed a relatively high specificity toward the prenyl moiety at position C-4 of the indole ring. 4-Dimethylallyltryptophan derivatives with modification at the indole ring were also accepted by FgaMT as substrates. Km values for 4-dimethylallyltryptophan and S-adenosylmethionine were determined at 0.12 and 2.4 mM, respectively. The turnover number was 2.0 s(-1).

Determination of Ergot Alkaloids

Determination of Ergot Alkaloids: Purity and Stability Assessment of Standards and Optimization of Extraction Conditions for Cereal Samples


Author(s): Krska R (Krska, Rudolf)1,2, Berthiller F (Berthiller, Franz)1, Schuhmacher R (Schuhmacher, Rainer)1, Nielsen KF (Nielsen, Kristian F.)3, Crews C (Crews, Colin)2

Source: JOURNAL OF AOAC INTERNATIONAL Volume: 91 Issue: 6 Pages: 1363-1371 Published: NOV-DEC 2008

Abstract: Results obtained from a purity study on standards of the 6 major ergot alkaloids ergometrine, ergotamine, ergosine, ergocristine, ergocryptine, and ergocornine and their corresponding epimers are discussed. The 6 ergot alkaloids studied have been defined by the European Food Safety Authority as those that are the most common and physiologically active. The purity of the standards was investigated by means of liquid chromatography with diode array detection, electrospray ionization, and time-of-flight mass spectrometry (LC-DAD-ESI-TOF-MS). All of the standards assessed showed purity levels considerably above 98% apart from ergocristinine (94%), ergosine (96%), and ergosinine (95%). Also discussed is the optimization of extraction conditions presented in a recently published method for the quantitation of ergot alkaloids in food samples using solid-phase extraction with primary secondary amine (PSA) before LC/MS/MS. Based on the results obtained from these optimization studies, a mixture of acetonitrile with ammonium carbonate buffer was used as extraction solvent, as recoveries for all analyzed ergot alkaloids were significantly higher than those with the other solvents. Different sample-solvent ratios and extraction times showed just minor influences in extraction efficacy. Finally, the stability of the ergot alkaloids in both raw cereals and cereal-based processed food extracts was studied. According to these studies, extracts should be prepared and analyzed the same day or stored below ambient temperatures. Barley and rye extracts, which were stored at 4 and 15 degrees C after PSA cleanup, proved to be stable overnight. However, storage over a period of 14 days at 4 degrees C resulted in significant epimerization, which was most pronounced in rye and particularly for ergocornine, ergocryptine, and ergocristine.

The Venus of Hohle Fels.

The Venus of Hohle Fels. (Credit: Photo by H. Jensen; Copyright: Universität Tübingen)

Good News for Night Owls

Good News for Night Owls
By Elsa Youngsteadt
ScienceNOW Daily News
23 April 2009

Night owls seem to have a cognitive edge over early risers--at least when they're on their natural sleep schedule. That's one upshot of a new brain-imaging study that also gives surprising new insights into how the brain manages the urge to sleep and wake. The results, sleep researchers say, may improve predictions of when people are most at risk for drowsy accidents.
Two factors control our bedtime. The first is hardwired: A master clock in the brain regulates a so-called circadian rhythm, which synchronizes activity patterns to the 24-hour day. Some people's clocks tell them to go to bed at 9 p.m., others' at 3 a.m., (ScienceNOW, 24 June 2003). The second factor--called sleep pressure--depends not on time of day but simply on how long someone has been awake already.

Because sleep pressure accumulates during waking hours, logic suggests that we should be most alert--and hence sharpest--shortly after we get up versus right before we go to bed, regardless of whether we're night owls or larks.

But that's not what Christina Schmidt found. The doctoral student at the University of Liège in Belgium and her collaborators, led by sleep researcher Philippe Peigneux, recruited 16 morning people and 15 night people to take alertness tests in a brain scanner. Subjects had to pay attention to numbers on a computer screen and hit a button whenever the numbers began to change. To control for the effect of the circadian clock, the subjects were allowed to sleep on their own natural schedules and take the test 1.5 hours and 10.5 hours after waking, regardless of the actual time of day.

Both groups performed equally well on the test when they took it 1.5 hours after waking. But after 10.5 hours without sleep, the night owls pulled ahead. Their reaction times improved by about 6% relative to the morning people and to their own earlier performance, the researchers report in tomorrow's issue of Science. This suggests that once they wake up, sleep pressure builds up faster in early birds, says Peigneux, and that this hurts their cognition over time.

It's a result with "real-world consequences," says sleep researcher David Dinges of the University of Pennsylvania School of Medicine in Philadelphia. Current risk analyses use the time of day and hours worked to predict when people are in greatest danger of accidents--such as aviation errors. But now, Dinges says, they may need to take into account that morning people tend to lose their concentration faster. At the very least, according to sleep researcher Amita Sehgal, also at the University of Pennsylvania School of Medicine, this is a new and "intriguing" explanation for larks' and owls' different habits.

But the really provocative result, adds Dinges, came from the brain imaging. The night owls showed greater activity in the master-clock region of their brains--a cluster of cells known as the suprachiasmatic nucleus--than the larks when taking the later test. That suggests that sleep pressure and the circadian clock can influence each other directly--bringing together two systems that, for decades, had been thought to operate separately.

Homeostatic Sleep Pressure and Responses to Sustained Attention in the Suprachiasmatic Area

Science 24 April 2009:
Vol. 324. no. 5926, pp. 516 - 519
DOI: 10.1126/science.1167337
Prev | Table of Contents | Next
Reports
Homeostatic Sleep Pressure and Responses to Sustained Attention in the Suprachiasmatic Area
Christina Schmidt,1,2,* Fabienne Collette,1,2 Yves Leclercq,1 Virginie Sterpenich,1 Gilles Vandewalle,1 Pierre Berthomier,3 Christian Berthomier,3 Christophe Phillips,1 Gilberte Tinguely,1 Annabelle Darsaud,1 Steffen Gais,1 Manuel Schabus,1 Martin Desseilles,1 Thien Thanh Dang-Vu,1 Eric Salmon,1 Evelyne Balteau,1 Christian Degueldre,1 André Luxen,1 Pierre Maquet,1 Christian Cajochen,4 Philippe Peigneux1,5,*

Throughout the day, cognitive performance is under the combined influence of circadian processes and homeostatic sleep pressure. Some people perform best in the morning, whereas others are more alert in the evening. These chronotypes provide a unique way to study the effects of sleep-wake regulation on the cerebral mechanisms supporting cognition. Using functional magnetic resonance imaging in extreme chronotypes, we found that maintaining attention in the evening was associated with higher activity in evening than morning chronotypes in a region of the locus coeruleus and in a suprachiasmatic area (SCA) including the circadian master clock. Activity in the SCA decreased with increasing homeostatic sleep pressure. This result shows the direct influence of the homeostatic and circadian interaction on the neural activity underpinning human behavior.

2 micron plasmid hitchhikes on mitotic mechanism of Saccharomyces cerevisiae to maintain equal distribution in host

Published online April 13, 2009
doi:10.1083/jcb.200810130
The Journal of Cell Biology, Vol. 185, No. 2, 251-264
The Rockefeller University Press, 0021-9525 $30.00
© 2009 Cui et al.

The selfish yeast plasmid uses the nuclear motor Kip1p but not Cin8p for its localization and equal segregation

Hong Cui, Santanu K. Ghosh, and Makkuni Jayaram
Section of Molecular Genetics and Microbiology, University of Texas at Austin, Austin, TX 78712

Correspondence to Makkuni Jayaram: jayaram@icmb.utexas.edu


The 2 micron plasmid of Saccharomyces cerevisiae uses the Kip1 motor, but not the functionally redundant Cin8 motor, for its precise nuclear localization and equal segregation. The timing and lifetime of Kip1p association with the plasmid partitioning locus STB are consistent with Kip1p being an authentic component of the plasmid partitioning complex. Kip1–STB association is not blocked by disassembling the mitotic spindle. Lack of Kip1p disrupts recruitment of the cohesin complex at STB and cohesion of replicated plasmid molecules. Colocalization of a 2 micron reporter plasmid with Kip1p in close proximity to the spindle pole body is reminiscent of that of a CEN reporter plasmid. Absence of Kip1p displaces the plasmid from this nuclear address, where it has the potential to tether to a chromosome or poach chromosome segregation factors. Exploiting Kip1p, which is subsidiary to Cin8p for chromosome segregation, to direct itself to a "partitioning center" represents yet another facet of the benign parasitism of the yeast plasmid.

Biogeochemistry: Less nickel for more oxygen

News and Views
Nature 458, 714-715 (9 April 2009) | doi:10.1038/458714a; Published online 8 April 2009


Biogeochemistry: Less nickel for more oxygen
Mak A. Saito1

Top of pageAbstractThe availability (or lack) of oceanic trace elements is providing fresh lines of explanation for turning points in Earth's history — the Great Oxidation Event being one such momentous occasion.

About 2.4 billion years ago, the oxygen content of Earth's atmosphere increased in what is called the Great Oxidation Event (GOE). This marked the beginning of the most significant series of chemical changes Earth has ever experienced, setting the stage for oxidative weathering of the continents, successive changes in ocean chemistry, and the eventual rise of multicellular life.

Yet the sequence of events leading up to the GOE is not well understood. Most researchers agree that the evolution of oxygenic photosynthesis within a group called the cyanobacteria was the source of the molecular oxygen that caused the GOE1. But the timing of the rise of these bacteria is uncertain2, 3, and there may have been a period of inertia — due, for example, to chemical reactions with methane that consumed oxygen4 — that prevented a swift increase in atmospheric oxygen. It remains a matter of debate how these two phenomena might have induced the GOE: an early rise of cyanobacteria and slow crumbling of chemical resistance3, 4; or a late rise of cyanobacteria leading to rapid initiation of the GOE5.

On page 750 of this issue6, Konhauser et al. report evidence for an alternative driving mechanism of the GOE, one that would have decreased microbial methane production in the oceans and paved the way for increased oxygen abundances. The authors find significant decreases in the nickel-to-iron ratios in ancient rocks, known as banded iron formations, that provide records of element concentrations in the oceans (Fig. 1). They estimate that a major decrease in the oceanic inventory of nickel must have occurred around 2.7 billion years ago. This, they conclude, led to a cascade of events in which methanogens, with their gluttonous appetite for nickel to feed three nickel-containing metalloenzymes, would have become starved of the element and so have produced much less methane. With the decrease in chemical inertia associated with methane4, the stage was set for cyanobacterial oxygen to accumulate, leading to the GOE. Moreover, although Konhauser et al. don't go into detail, the decline in atmospheric methane, a powerful greenhouse gas, is believed to help account for the initiation of a planetary-scale glaciation known as Snowball Earth that is thought to have begun between 2.3 billion and 2.2 billion years ago4, 5.

Figure 1: Record site.
This is a view of Dales Gorge, northwest Australia, one of the banded iron formations sampled by Konhauser et al.6.

High resolution image and legend (151K)



The idea that significant changes in seawater trace-metal abundance have occurred during Earth's history is becoming popular7, 8. For example, it is thought that iron and cobalt were abundant in ancient oceans, whereas zinc and copper were probably extremely scarce owing to precipitation with sulphides8. When the oceans became oxygenated, it is likely that this scheme was reversed, with iron and cobalt becoming scarce through oxidation and precipitation as oxyhydroxides, and zinc and copper becoming much more abundant upon the oxidation of sulphide to sulphate in sea water. These predictions of broad changes in ocean chemistry are mirrored by the physiological and genomic traits of archaea and bacteria, relative to those of the later-evolving eukaryotes8, 9.

Nickel has largely been left out of this intriguing story. On the evidence of chemical modelling8, it seems that nickel was not as strongly affected by the variations in sulphide and oxygen during Earth's history. But such a conclusion does not take into account the possible involvement of external factors. Konhauser et al. show how such a factor might have come into play, with the cooling of Earth's mantle resulting in decreased eruption of nickel-rich rocks and causing an estimated 50% fall in the oceanic nickel inventory.

Konhauser and colleagues' thinking6 may come as a surprise to those familiar with the chemistry of the modern oceans. Trace metals — as their name suggests — are extraordinarily scarce in sea water. In vast regions of the modern oceans, photosynthesis is limited by low iron availability, with iron concentrations often being less than 0.05 nanomoles per litre10. Yet, of the trace metals required by life, nickel is one of the more abundant in sea water, with surface water concentrations of 1–2 nanomoles per litre11. In this modern context, the idea of a nickel famine seems odd. But the nickel requirements of methanogens are reported6 to be in the hundreds of nanomoles per litre, suggesting that methanogens cannot live in the modern oceans and are perhaps relegated to sedimentary, coastal and freshwater environments, where nickel is more abundant.

By connecting changes in mantle temperature to nickel fluxes and methanogens, Konhauser and colleagues' study is particularly satisfying. Instead of relying on the uncertain timing of the rise of cyanobacteria to explain the GOE, that event can instead be tied to a specific mechanism recorded in the banded iron formations. In addition, this 'nickel famine' mechanism is consistent with evidence12 of 'whiffs of oxygen' that occurred more than 50 million years before the GOE. But I cannot help but wonder whether there is a reason — such as the slow chemical kinetics of nickel ions — why methanogens could not evolve a high-affinity nickel-uptake mechanism similar to those that exist for the uptake of iron, zinc and cobalt13, 14, 15.

Finally, there is another context in which the research of Konhauser et al. is set — the exciting endeavour of trying to understand how the elemental cycles (of nickel, carbon, iron, nitrogen and so on) have 'co-evolved' with microbial life. Many of the changes in element cycling were probably caused by the rise and fall of specific microbial metabolisms, while also strongly affecting the trajectory and composition of life on Earth. Life and the cycling of elements have both been changing throughout Earth's history, often influencing each other profoundly along the way. One of the sobering realizations of studies such as this is that, although natural selection provides a clear, single positive-feedback mechanism for the continuation of life, elemental cycles are instead influenced by an aggregate of mechanisms, including biological evolution, chemical reactions, changes in ocean circulation and geological events. If, as Konhauser et al. suggest, a single geological change can starve a major oceanic microbial community, and thereby change the trajectory of life on Earth, it suggests that there is a fragility to Earth's elemental cycles that we are only beginning to uncover.

Kinetochore geometry defined by cohesion within the centromere

Article
Nature 458, 852-858 (16 April 2009) | doi:10.1038/nature07876; Received 9 September 2008; Accepted 12 February 2009


Kinetochore geometry defined by cohesion within the centromere
Takeshi Sakuno1,2, Kenji Tada1,3 & Yoshinori Watanabe1,3

Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences,
Promotion of Independence for Young Investigators,
Graduate Program in Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan
Correspondence to: Yoshinori Watanabe1,3 Correspondence and requests for materials should be addressed to Y.W. (Email: ywatanab@iam.u-tokyo.ac.jp).


Top of pageAbstractDuring cell division microtubules capture chromosomes by binding to the kinetochore assembled in the centromeric region of chromosomes. In mitosis sister chromatids are captured by microtubules emanating from both spindle poles, a process called bipolar attachment, whereas in meiosis I sisters are attached to microtubules originating from one spindle pole, called monopolar attachment. For determining chromosome orientation, kinetochore geometry or structure might be an important target of regulation. However, the molecular basis of this regulation has remained elusive. Here we show the link between kinetochore orientation and cohesion within the centromere in fission yeast Schizosaccharomyces pombe by strategies developed to visualize the concealed cohesion within the centromere, and to introduce artificial tethers that can influence kinetochore geometry. Our data imply that cohesion at the core centromere induces the mono-orientation of kinetochores whereas cohesion at the peri-centromeric region promotes bi-orientation. Our study may reveal a general mechanism for the geometric regulation of kinetochores, which collaborates with previously defined tension-dependent reorientation machinery.

The dark side of light at night: physiological, epidemiological, and ecological consequences

The dark side of light at night: physiological, epidemiological, and ecological consequences


Author(s): Navara KJ (Navara, Kristen J.), Nelson RJ (Nelson, Randy J.)
Source: JOURNAL OF PINEAL RESEARCH Volume: 43 Issue: 3 Pages: 215-224 Published: OCT 2007

Abstract: Organisms must adapt to the temporal characteristics of their surroundings to successfully survive and reproduce. Variation in the daily light cycle, for example, acts through endocrine and neurobiological mechanisms to control several downstream physiological and behavioral processes. Interruptions in normal circadian light cycles and the resulting disruption of normal melatonin rhythms cause widespread disruptive effects involving multiple body systems, the results of which can have serious medical consequences for individuals, as well as large-scale ecological implications for populations. With the invention of electrical lights about a century ago, the temporal organization of the environment has been drastically altered for many species, including humans. In addition to the incidental exposure to light at night through light pollution, humans also engage in increasing amounts of shift-work, resulting in repeated and often long-term circadian disruption. The increasing prevalence of exposure to light at night has significant social, ecological, behavioral, and health consequences that are only now becoming apparent. This review addresses the complicated web of potential behavioral and physiological consequences resulting from exposure to light at night, as well as the large-scale medical and ecological implications that may result.

Light pollution, reproductive function and cancer risk

Light pollution, reproductive function and cancer risk

Author(s): Anisimov VN
Source: NEUROENDOCRINOLOGY LETTERS Volume: 27 Issue: 1-2 Pages: 35-52 Published: FEB-APR 2006


Abstract: At present, light pollution (exposure to light-at-night) both in the form of occupational exposure during night work and as a personal choice and life style, is experienced by numerous night-active members of our society. Disruption of the circadian rhythms induced by light pollution has been associated with cancer in humans. There are epidemiological evidences of increased breast and colon cancer risk in shift workers. An inhibition of the pineal gland function with exposure to the constant light (LL) regimen promoted carcinogenesis whereas the light deprivation inhibits the carcinogenesis. Treatment with pineal indole hormone melatonin inhibits carcinogenesis in pinealectomized rats or animals kept at the standard light/dark regimen (LD) or at the LL regimen. These observations might lead to use melatonin for cancer prevention in groups of humans at risk of light pollution.

Exposure to light-at-night increases the growth of DMBA-induced mammary adenocarcinomas in rats

Exposure to light-at-night increases the growth of DMBA-induced mammary adenocarcinomas in rats

Author(s): Cos S, Mediavilla D, Martinez-Campa C, Gonzalez A, Alonso-Gonzalez C, Sanchez-Barcelo EJ
Source: CANCER LETTERS Volume: 235 Issue: 2 Pages: 266-271 Published: APR 28 2006


Abstract: In order to assess whether light exposure at night influences the growth of mammary tumors, as well as the role of melatonin in this process, female rats bearing DMBA-induced mammary adenocarcinomas were exposed to different lighting environments. Animals exposed to light-at-night, especially those under a constant dim light during the darkness phase, showed: (a) significantly higher rates of tumor growth as well as lower survival than controls, (b) higher concentration of serum estradiol, and (c) lower nocturnal excretion of 6-sulfatoxymelatonin, without there being differences between nocturnal and diurnal levels. These results suggest that circadian and endocrine disruption induced by light pollution, could induce the growth of mammary tumors. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

Light pollution, melatonin suppression and cancer growth

Light pollution, melatonin suppression and cancer growth

Author(s): Reiter RJ, Gultekin F, Manchester LC, Tan DX
Source: JOURNAL OF PINEAL RESEARCH Volume: 40 Issue: 4 Pages: 357-358 Published: MAY 2006

Article Text
The naturally occurring daily periods of light and darkness are an important source of internal order as manifested by the circadian rhythmicity exhibited by numerous organismal functions. Alterations of these daily fluctuations, referred to as chronodisruption [1], may be consequential in a number disorders, e.g. 'jet lag' [2], and diseases, e.g. cancer [3–5]. Given that the light:dark cycle is a central factor in circadian regulation, light during the normal dark period (light pollution), is becoming an increasing greater problem as societies become progressively more electrofied. Interruption of the daily dark period may have both subtle and not-so-subtle consequences in terms of human health.

One cycle that is quickly disturbed by light pollution is the pineal and blood melatonin rhythms. The repeated suppression of melatonin by light at night is a condition in which the health consequences may not be at all subtle. This is emphasized by the recent observations of Blask et al. [6] who, after a series of clever experiments, provided a highly plausible mechanism to explain how light suppression of melatonin at night accelerates the metabolic activity and growth of rat hepatoma and human MCF-7 cancer cells. The significance of these findings is reinforced by the earlier epidemiological studies in which the authors claimed that the repeated exposure of women to light at night, e.g. individuals who worked the night shift, had an increased incidence of breast [3,5,7] and colorectal cancer [8].

After transplantation of human MCF-7 cancer cells into nude rats, Blask et al. [6] showed that flooding the tumors with melatonin-deficient blood collected from premenopausal women during the day was inconsequential in terms of inhibiting cancer metabolism and growth. Conversely, melatonin-rich blood collected from the same women at night shut down the uptake and metabolism of the tumor growth promoter, linoleic acid, as well as the proliferation of the cancer cells. The most interesting aspect of the study, however, was that when the female blood donors were exposed to bright light at night to reduce endogenous melatonin levels, their blood was then incapable of inhibiting the cancer cells. Thus, light suppression of physiological melatonin levels negated the ability of the blood to limit tumor linoleic acid metabolism and cellular proliferation.

In the words of Blask, 'physiological nighttime levels of melatonin put tumors to sleep at night' while during the day when melatonin concentrations are normally low there are no limitations on their growth. Blask also is quoted as drawing the analogy that during light exposure at night tumors become 'insomniacs' [9].

There may be factors in addition to reducing linoleic acid uptake and metabolism that may be operative when melatonin, at physiological levels, limits growth of MCF-7 human cancer cells [10]. Leon-Blanco et al. [11] showed that melatonin also inhibits telomerase activity in MCF-7 cells. The activity of this enzyme is typically highly elevated in cancer cells [12] where it maintains the integrity and length of the telomeres of eukaryotic chromosomes. In noncancer cells, the telomeres gradually shorten over time making the chromosomes less stable and vulnerable to damage; this increases the propensity of normal cells to die. In cancer cells, the chromosomes remain durable because of the elevated telomerase activity so the cells are also more sturdy and resistant to death. When nude mice bearing MCF-7 tumors were treated with melatonin in their drinking water, not only was the growth of these tumors reduced but also telomerase activity as well as the levels of the mRNA of its catalytic submit, TERT, were also suppressed in the tumors. Moreover, like Blask et al. [6], Leon-Blanco et al. [11] reported that physiological concentrations of nighttime blood melatonin levels (about 1 nM) shut down telomerase activity of MCF-7 cancer cells. Thus, the ability of physiological levels of melatonin to 'put cancers to sleep at night' [9] extends not only to linoleic acid uptake and metabolism but to telomerase activity as well. Telomerase activity has been targeted as a site for cancer inhibition by the pharmaceutical industry [13].

These findings have additional important implications. Blask et al [6] noted that a 15–25% reduction in nocturnal melatonin levels is sufficient to promote tumor growth. This being the case, the age-related reduction in endogenous melatonin levels (which often exceeds 25%) [14] would be expected to increase the vulnerability of humans to cancer growth. As cancer is an age-related disease, the reduction of melatonin may be significant in mediating accelerated tumor growth in the elderly.

Finally, the amplitude of the nocturnal melatonin rhythm is determined by a variety of factors [15] and there are individuals who have a genetically attenuated nighttime melatonin rise. Given the high fidelity of the melatonin cycle over time, it is possible that these relatively melatonin-depressed humans are more susceptible to aggressive tumor metabolism and growth. These are considerations to ponder for future studies.

Lighting for the human circadian clock: recent research indicates that lighting has become a public health issue

Author(s): Pauley SM
Source: MEDICAL HYPOTHESES Volume: 63 Issue: 4 Pages: 588-596 Published: 2004

Abstract: The hypothesis that the suppression of melatonin (MLT) by exposure to light at night (LAN) may be one reason for the higher rates of breast and colorectal cancers in the developed world deserves more attention. The literature supports raising this subject for awareness as a growing public health issue. Evidence now exists that indirectly links exposures to LAN to human breast and colorectal cancers in shift workers. The hypothesis begs an even larger question: has medical science overlooked the suppression of MLT by LAN as a contributor to the overall incidence of cancer?
The indirect linkage of breast cancer to LAN is further supported by laboratory rat experiments by David E. Blask and colleagues. Experiments involved the implanting of human MCF-7 breast cancer cell xenografts into the groins of rats and measurements were made of cancer cell growth rates, the uptake of linoleic acid (LA), and MLT levels. One group of implanted rats were placed in light-dark (12L:12D) and a second group in tight-light (12L:12L) environments. Constant light suppressed MLT, increased cancer cell growth rates, and increased LA uptake into cancer cells. The opposite was seen in the light-dark group. The proposed mechanism is the suppression of nocturnal MLT by exposure to LAN and subsequent tack of protection by MLT on cancer cell receptor sites which allows the uptake of LA which in turn enhances the growth of cancer cells.

MLT is a protective, oncostatic hormone and strong antioxidant having evolved in all plants and animals over the millennia. In vertebrates, MLT is normally produced by the pineal gland during the early morning hours of darkness, even in nocturnal animals, and is suppressed by exposure to LAN.

Daily entrainment of the human circadian clock is important for good human health. These studies suggest that the proper use and color of indoor and outdoor Lighting is important to the health of both humans and ecosystems. Lighting fixtures should be designed to minimize interference with normal circadian rhythms in plants and animals.

New discoveries on blue-light-sensitive retinal ganglion cell light receptors that control the circadian clock and how those receptors relate to today's modern high intensity discharge (HID) lamps are discussed. There is a brief discussion of circadian rhythms and light pollution. With the precautionary principle in mind, practical suggestions are offered for better indoor and outdoor lighting practices designed to safeguard human health. (C) 2004 Elsevier Ltd. All rights reserved.

hairpin-dependent pausing

Possible effects of antisense oligonucleotides on hairpin-dependent pausing. (Top) The mechanism of hairpin-dependent transcriptional pausing. The four components of thehis pause signal are labeled on the paused TC, which is formed in competition with bypass of the site and then slowly escapes back into the elongation pathway. How the pause hairpin inhibits nucleotide addition is unknown, but it presumably disrupts reactive alignment of the RNA 3′OH and incoming NTP (depicted here by separation of the 3′ OH and NTP-binding subsites, i and i + 1; see Fig. 7). (Bottom) In the direct model of hairpin-dependent pausing, a specific interaction between the RNA hairpin and its binding site on RNAP disrupts nucleotide addition in the active site of RNAP (Chan et al. 1997; Wang and Landick 1997). In the indirect model, the hairpin merely defines a particular length of 3′-proximal, single-stranded RNA transcript and thus could both disrupt RNA–RNAP interactions required for elongation or TC stability and prevent backtracking of RNAP along the DNA template (Komissarova and Kashlev 1997b; Nudler et al. 1997). Annealing of antisense oligonucleotides to the nascent RNA would be able to recapitulate indirect effects of hairpins, but not direct effects.


Interaction of a nascent RNA structure with RNA polymerase is required for hairpin-dependent transcriptional pausing but not for transcript release
Irina Artsimovitch and Robert Landick1
Genes & Dev. 1998. 12: 3110-3122