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
Wednesday, October 14, 2009
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
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
Tuesday, October 6, 2009
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.
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
Fungi;
Dikarya;
Ascomycota;
Pezizomycotina;
Sordariomycetes;
Hypocreomycetidae;
Hypocreales;
mitosporic Hypocreales;
Fusarium;
Fusarium oxysporum species complex;
Fusarium oxysporum
Monday, October 5, 2009
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
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
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
Thursday, September 10, 2009
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.
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.
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