Rapid evolution of metabolic traits explains thermal adaptation in phytoplankton

Understanding the mechanisms that determine how phytoplankton adapt to warming will substantially improve the realism of models describing ecological and biogeochemical effects of climate change. Here, we quantify the evolution of elevated thermal tolerance in the phytoplankton, Chlorella vulgaris. Initially, population growth was limited at higher temperatures because respiration was more sensitive to temperature than photosynthesis meaning less carbon was available for growth. Tolerance to high temperature evolved after ≈ 100 generations via greater down-regulation of respiration relative to photosynthesis. By down-regulating respiration, phytoplankton overcame the metabolic constraint imposed by the greater temperature sensitivity of respiration and more efficiently allocated fixed carbon to growth. Rapid evolution of carbon-use efficiency provides a potentially general mechanism for thermal adaptation in phytoplankton and implies that evolutionary responses in phytoplankton will modify biogeochemical cycles and hence food web structure and function under warming. Models of climate futures that ignore adaptation would usefully be revisited

Engineering a DNA damage response without DNA damage

DNA damage response signaling has been achieved experimentally in the absence of double-strand DNA breaks

Travail pendant les études et abandon scolaire : Causes, conséquences et politiques d'intervention

The deterioration of the wage conditions of non-qualified workers has been the subject of considerable attention over the past few years. Unfortunately, it is not the sole preoccupation of public decision-makers. In this class of workers, the employment rate is particularly low, while unemployment tends to remain rather high. The first cause of non-qualification of young workers being their dropping out of school (the Canadian rate of dropouts from high school is 18%), any policy likely to reduce the dropout rates will be an effective means of improving the working situation of the youth. Our research identifies several determinants of dropping out and different policies which can be put into action by the governments in order to reduce dropout. We mention particularly the role played by the minimum wage in the dropout phenomenon: it is clear that a high minimum wage tends to increase dropout significantly La détérioration des conditions salariales des travailleurs non qualifiés sur le marché du travail a été l'objet d'une attention considérable au cours des dernières années. Malheureusement, elle n'est pas la seule source de préoccupations pour les décideurs publics. S'agissant de cette catégorie de travailleurs, le ratio emploi/population demeure singulièrement bas et le taux de chômage se0501ntient à des niveaux le plus souvent élevés. La première source de la non qualification des jeunes travailleurs étant l'abandon des études secondaires (à l'échelle canadienne, le taux d'abandon au secondaire est estimé à 18 %), toute politique susceptible de réduire les taux d'abandon représentera un moyen efficace d'améliorer la situation des jeunes sur le marché du travail. Notre recherche identifie plusieurs déterminants de l'abandon et différentes politiques qui pourront être mises de l'avant par les gouvernements pour réduire l'abandon scolaire. En particulier, mentionnons le rôle du salaire minimum dans le phénomène du décrochage : il est clair que le salaire minimum, quand il est élevé, contribue de façon significative à accroître l'abandon scolaire.School dropout, hours of work during study, minimum wage, Abandon scolaire, heures travaillées pendant les études, salaire minimum

PP4 is a γH2AX phosphatase required for recovery from the DNA damage checkpoint

Phosphorylation of histone H2AX on Ser 139 (γH2AX) is one of the earliest events in the response to DNA double-strand breaks; however, the subsequent removal of γH2AX from chromatin is less understood, despite being a process tightly coordinated with DNA repair. Previous studies in yeast have identified the Pph3 phosphatase (the PP4C orthologue) as important for the dephosphorylation of γH2AX. By contrast, work in human cells attributed this activity to PP2A. Here, we report that PP4 contributes to the dephosphorylation of γH2AX, both at the sites of DNA damage and in undamaged chromatin in human cells, independently of a role in DNA repair. Furthermore, depletion of PP4C results in a prolonged checkpoint arrest, most likely owing to the persistence of mediator of DNA damage checkpoint 1 (MDC1) at the sites of DNA lesions. Taken together, these results indicate that PP4 is an evolutionarily conserved γH2AX phosphatase

Comparative experimental evolution reveals species-specific idiosyncrasies in marine phytoplankton adaptation to warming

A number of experimental studies have demonstrated that phytoplankton can display rapid thermal adaptation in response to warmed environments. While these studies provide insight into the evolutionary responses of single species, they tend to employ different experimental techniques. Consequently, our ability to compare the potential for thermal adaptation across different, ecologically relevant, species remains limited. Here, we address this limitation by conducting simultaneous long-term warming experiments with the same experimental design on clonal isolates of three phylogenetically diverse species of marine phytoplankton; the cyanobacterium Synechococcus sp., the prasinophyte Ostreococcus tauri and the diatom Phaeodoactylum tricornutum. Over the same experimental time period, we observed differing levels of thermal adaptation in response to stressful supra-optimal temperatures. Synechococcus sp. displayed the greatest improvement in fitness (i.e., growth rate) and thermal tolerance (i.e., temperature limits of growth). Ostreococcus tauri was able to improve fitness and thermal tolerance, but to a lesser extent. Finally, Phaeodoactylum tricornutum showed no signs of adaptation. These findings could help us understand how the structure of phytoplankton communities may change in response to warming, and possible biogeochemical implications, as some species show relatively more rapid adaptive shifts in their thermal tolerance

Saccharomyces cerevisiae Rad9 Acts as a Mec1 Adaptor to Allow Rad53 Activation

SummaryBackground: The DNA damage checkpoint is a protein kinase-based signaling system that detects and signals physical alterations in DNA. Despite having identified many components of this signaling cascade, the exact mechanisms by which checkpoint kinases are activated after DNA damage, as well as the role of the checkpoint mediators, remain poorly understood.Results: To elucidate the mechanisms that underlie the MEC1 and RAD9-dependent activation of Rad53, the Saccharomyces cerevisiae ortholog of Chk2, we mapped and characterized in vivo phosphorylation sites present on Rad53 after DNA damage by mass spectrometry. We find that Rad53 requires for its activation multisite phosphorylation on a number of typical and atypical Mec1 phosphorylation sites, thus confirming that Rad53 is a direct target of Mec1, the mammalian ATR homolog. Moreover, by using biochemical reconstitution experiments, we demonstrate that efficient and direct phosphorylation of Rad53 by Mec1 is only observed in the presence of purified Rad9, the archetypal checkpoint mediator. We find that the stimulatory activity of Rad9 requires a phospho- and FHA-dependent interaction with Rad53, which allows Rad53 to be recognized as a substrate for Mec1.Conclusions: Our results indicate that Rad9 acts as a bona fide signaling adaptor that enables Rad53 phosphorylation by Mec1. Given the high degree of conservation of checkpoint signaling in eukaryotes, we propose that one of the critical functions of checkpoint mediators such as MDC1, 53BP1, or Brca1 is to act as PIKK adaptors during the DNA damage response

CDC5 Inhibits the Hyperphosphorylation of the Checkpoint Kinase Rad53, Leading to Checkpoint Adaptation

The mechanistic role of the yeast kinase CDC5, in allowing cells to adapt to the presence of irreparable DNA damage and continue to divide, is revealed