The evolution of trait correlations constrains phenotypic adaptation to high CO2 in a eukaryotic alga

Microbes form the base of food webs and drive biogeochemical cycling. Predicting the effects of microbial evolution on global elemental cycles remains a significant challenge due to the sheer number of interacting environmental and trait combinations. Here, we present an approach for integrating multivariate trait data into a predictive model of trait evolution. We investigated the outcome of thousands of possible adaptive walks parameterized using empirical evolution data from the alga Chlamydomonas exposed to high CO2. We found that the direction of historical bias (existing trait correlations) influenced both the rate of adaptation and the evolved phenotypes (trait combinations). Critically, we use fitness landscapes derived directly from empirical trait values to capture known evolutionary phenomena. This work demonstrates that ecological models need to represent both changes in traits and changes in the correlation between traits in order to accurately capture phytoplankton evolution and predict future shifts in elemental cycling

Multivariate trait analysis reveals diatom plasticity constrained to a reduced set of biological axes

AbstractTrait-based approaches to phytoplankton ecology have gained traction in recent decades as phenotypic traits are incorporated into ecological and biogeochemical models. Here, we use high-throughput phenotyping to explore both intra- and interspecific constraints on trait combinations that are expressed in the cosmopolitan marine diatom genus Thalassiosira. We demonstrate that within Thalassiosira, phenotypic diversity cannot be predicted from genotypic diversity, and moreover, plasticity can create highly divergent phenotypes that are incongruent with taxonomic grouping. Significantly, multivariate phenotypes can be represented in reduced dimensional space using principal component analysis with 77.7% of the variance captured by two orthogonal axes, here termed a ‘trait-scape’. Furthermore, this trait-scape can be recovered with a reduced set of traits. Plastic responses to the new environments expanded phenotypic trait values and the trait-scape, however, the overall pattern of response to the new environments was similar between strains and many trait correlations remained constant. These findings demonstrate that trait-scapes can be used to reveal common constraints on multi-trait plasticity in phytoplankton with divergent underlying phenotypes. Understanding how to integrate trait correlational constraints and trade-offs into theoretical frameworks like biogeochemical models will be critical to predict how microbial responses to environmental change will impact elemental cycling now and into the future.</jats:p

p53-regulated transcriptional program associated with genotoxic stress-induced apoptosis

10.1074/jbc.M311912200Journal of Biological Chemistry2792021183-21192JBCH

Conformational Change of Human Checkpoint Kinase 1 (Chk1) Induced by DNA Damage

Phosphorylation of Chk1 by ataxia telangiectasia-mutated and Rad3-related (ATR) is critical for checkpoint activation upon DNA damage. However, how phosphorylation activates Chk1 remains unclear. Many studies suggest a conformational change model of Chk1 activation in which phosphorylation shifts Chk1 from a closed inactive conformation to an open active conformation during the DNA damage response. However, no structural study has been reported to support this Chk1 activation model. Here we used FRET and bimolecular fluorescence complementary techniques to show that Chk1 indeed maintains a closed conformation in the absence of DNA damage through an intramolecular interaction between a region (residues 31–87) at the N-terminal kinase domain and the distal C terminus. A highly conserved Leu-449 at the C terminus is important for this intramolecular interaction. We further showed that abolishing the intramolecular interaction by a Leu-449 to Arg mutation or inducing ATR-dependent Chk1 phosphorylation by DNA damage disrupts the closed conformation, leading to an open and activated conformation of Chk1. These data provide significant insight into the mechanisms of Chk1 activation during the DNA damage response