Cross-generational effects of climate change on expression of a sexually selected trait.

Sexually selected traits and early breeding are often correlated with quality in birds: individuals that breed earlier in the season have more elaborate traits and raise more surviving offspring [1, 2]. As global climate warms, breeding date for many temperate birds is advancing [3, 4], but we lack corresponding information on climate-induced variation in sexual selection. Here, we investigated influences of climate on a sexually selected plumage trait in a Himalayan warbler (Phylloscopus humei). We found that when spring is warm, birds breed early. Subsequent to an early-breeding year, adults express relatively large sexually selected traits and rear offspring that also develop large traits. The positive effects of early breeding, plus the across-year correlation between parent and offspring cohorts, predict that warmer climates should lead to increases in trait size. However, trait size has not increased over the past 25 years, even though mean breeding date has advanced. We show that whereas warm springs have positive effects on trait size, warm summers have negative effects due to increased feather wear. Apparent stasis in the size of a sexually selected trait thus masks large, conflicting influences of climate change. Continued climate warming has the potential to affect the honesty of sexual signals, as trait expression and condition become increasingly disassociated.

Function of the tetraspanin CD151-alpha6beta1 integrin complex during cellular morphogenesis.

Upon plating on basement membrane Matrigel, NIH3T3 cells formed an anastomosing network of cord-like structures, inhibitable by anti-alpha6beta1 integrin antibodies. For NIH3T3 cells transfected with human CD151 protein, the formation of a cord-like network was also inhibitable by anti-CD151 antibodies. Furthermore, CD151 and alpha6beta1 were physically associated within NIH3T3 cells. On removal of the short 8-amino acid C-terminal CD151 tail (by deletion or exchange), exogenous CD151 exerted a dominant negative effect, as it almost completely suppressed alpha6beta1-dependent cell network formation and NIH3T3 cell spreading on laminin-1 (an alpha6beta1 ligand). Importantly, mutant CD151 retained alpha6beta1 association and did not alter alpha6beta1-mediated cell adhesion to Matrigel. In conclusion, the CD151-alpha6beta1 integrin complex acts as a functional unit that markedly influences cellular morphogenesis, with the CD151 tail being of particular importance in determining the "outside-in" functions of alpha6beta1-integrin that follow ligand engagement. Also, antibodies to alpha6beta1 and CD151 inhibited formation of endothelial cell cord-like networks, thus pointing to possible relevance of CD151-alpha6beta1 complexes during angiogenesis.