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.