Climate change drives poleward increases and equatorward declines in marine species

Marine environments have increased in temperature by an average of 1°C since preindustrial (1850) times [1]. Given that species ranges are closely allied to physiological thermal tolerances in marine organisms [2], it may therefore be expected that ocean warming would lead to abundance increases at poleward range edges, and abundance declines towards the equator [3]. Here we report a global analysis of abundance tends of 304 widely distributed marine species over the last century, across a range of taxonomic groups from phytoplankton to fish and marine mammals. Specifically, using a literature database we investigate the extent that the direction and strength of longterm species abundance changes depend on the sampled location within the latitudinal range of species. Our results show that abundance increases have been most prominent where sampling has taken place at the poleward edges of species ranges, while abundance declines have been most prominent where sampling has taken place at the equatorward edge of species ranges. These data provide evidence of omnipresent large-scale changes in abundance of marine species consistent with warming over the last century, and suggest that adaptation has not provided a buffer against the negative effects of warmer conditions at the equatorward extent of species ranges. On the basis of these results we suggest that projected sea temperature increases of up to 1.5°C over pre-industrial levels by 2050 [4] will continue to drive latitudinal abundance shifts in marine species, including those of importance for coastal livelihoods

Competition of Escherichia coli DNA Polymerases I, II and III with DNA Pol IV in Stressed Cells

Escherichia coli has five DNA polymerases, one of which, the low-fidelity Pol IV or DinB, is required for stress-induced mutagenesis in the well-studied Lac frameshift-reversion assay. Although normally present at ∼200 molecules per cell, Pol IV is recruited to acts of DNA double-strand-break repair, and causes mutagenesis, only when at least two cellular stress responses are activated: the SOS DNA-damage response, which upregulates DinB ∼10-fold, and the RpoS-controlled general-stress response, which upregulates Pol IV about 2-fold. DNA Pol III was also implicated but its role in mutagenesis was unclear. We sought in vivo evidence on the presence and interactions of multiple DNA polymerases during stress-induced mutagenesis. Using multiply mutant strains, we provide evidence of competition of DNA Pols I, II and III with Pol IV, implying that they are all present at sites of stress-induced mutagenesis. Previous data indicate that Pol V is also present. We show that the interactions of Pols I, II and III with Pol IV result neither from, first, induction of the SOS response when particular DNA polymerases are removed, nor second, from proofreading of DNA Pol IV errors by the editing functions of Pol I or Pol III. Third, we provide evidence that Pol III itself does not assist with but rather inhibits Pol IV-dependent mutagenesis. The data support the remaining hypothesis that during the acts of DNA double-strand-break (DSB) repair, shown previously to underlie stress-induced mutagenesis in the Lac system, there is competition of DNA polymerases I, II and III with DNA Pol IV for action at the primer terminus. Up-regulation of Pol IV, and possibly other stress-response-controlled factor(s), tilt the competition in favor of error-prone Pol IV at the expense of more accurate polymerases, thus producing stress-induced mutations. This mutagenesis assay reveals the DNA polymerases operating in DSB repair during stress and also provides a sensitive indicator for DNA polymerase competition and choice in vivo

Measures of frailty in population-based studies: An overview

Although research productivity in the field of frailty has risen exponentially in recent years, there remains a lack of consensus regarding the measurement of this syndrome. This overview offers three services: first, we provide a comprehensive catalogue of current frailty measures; second, we evaluate their reliability and validity; third, we report on their popularity of use