Evolution and plasticity of photosynthetic thermal tolerance, specific leaf area and leaf size: congeneric species from desert and coastal environments

• We examined whether increased high temperature photosynthetic thermal tolerance (PT), reduced specific leaf area (SLA) and reduced leaf size represent correlated and convergent adaptations for recently diverged Encelia, Salvia, Atriplex and Eriogonumcongeneric species pairs from contrasting thermal and water environments (the Mojave Desert and coastal California). We also studied whether variation in PT is associated with inducible small heat shock protein expression (sHsp). • Traits were measured in a common environment (CE) and in the field to partition effects of phenotypic plasticity and genetic divergence. • We found little evidence for convergent adaptation of PT (CE measurements). Field measurements revealed significant plasticity for PT, which was also associated with increased sHsp expression. Compared to coastal congeners desert species had lower SLA in the CE. These differences were magnified in the field. There was a negative correlation between SLA and PT. Desert species also tended to have smaller leaves both in the CE and in the field. • SLA and leaf size reductions represent repeated evolutionary divergences and are perhaps convergent adaptations for species radiating into the desert, while PT is highly plastic and shows little evidence for convergent adaptation in the congeneric species pairs we studied

The integrated stress response contributes to tRNA synthetase-associated peripheral neuropathy.

Dominant mutations in ubiquitously expressed transfer RNA (tRNA) synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth (CMT) disease. Genetic evidence in mouse and Drosophila models suggests a gain-of-function mechanism. In this study, we used in vivo, cell type-specific transcriptional and translational profiling to show that mutant tRNA synthetases activate the integrated stress response (ISR) through the sensor kinase GCN2 (general control nonderepressible 2). The chronic activation of the ISR contributed to the pathophysiology, and genetic deletion or pharmacological inhibition of Gcn2 alleviated the peripheral neuropathy. The activation of GCN2 suggests that the aberrant activity of the mutant tRNA synthetases is still related to translation and that inhibiting GCN2 or the ISR may represent a therapeutic strategy in CMT