Does experimentally altered plumage ornamentation of female passerines influence nestling quality? A test in female tree swallows

It is widely recognized that female animals in a variety of taxa display ornamental traits, such as elaborate plumage, but elucidating whether such traits evolve by selection or genetic correlation remains a challenge because more ornamented females are often found to produce low‐quality offspring. While resource trade‐offs between the production of ornaments and offspring may underlie this negative relationship, it is not an adequate explanation for species where the timing of production of ornaments and offspring does not overlap. Instead, costs associated with engaging in agonistic interactions with conspecifics, which maintains the honesty of signals of quality, may also reduce resources available to invest in offspring. In this study, we enhanced and reduced the plumage brightness of female tree swallows (Tachycineta bicolor) relative to controls to test whether social costs associated with displaying bright plumage is a potential mechanism underlying the observation that more ornamented females produce low‐quality nestlings. Our results showed that nestlings reared by females in the enhanced plumage brightness treatment were structurally smaller, having shorter lengths of the combined head and bill than nestlings in the reduced plumage brightness treatment, and tended to grow their head and bills more slowly than nestlings in the reduced and control plumage brightness treatments. Nestlings in the enhanced plumage brightness treatment also tended to gain mass more slowly than nestlings in control treatment. Overall, that females with enhanced plumage brightness produced structurally smaller nestlings provides evidence that social costs paid by females may lead to the production of low‐quality offspring and should be considered in future studies.     

Protein abundance of AKT and ERK pathway components governs cell type‐specific regulation of proliferation

Signaling through the AKT and ERK pathways controls cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell cycle progression, is poorly understood. Here, we study different hematopoietic cell types, in which AKT and ERK signaling is triggered by erythropoietin (Epo). Although these cell types share the molecular network topology for pro‐proliferative Epo signaling, they exhibit distinct proliferative responses. Iterating quantitative experiments and mathematical modeling, we identify two molecular sources for cell type‐specific proliferation. First, cell type‐specific protein abundance patterns cause differential signal flow along the AKT and ERK pathways. Second, downstream regulators of both pathways have differential effects on proliferation, suggesting that protein synthesis is rate‐limiting for faster cycling cells while slower cell cycles are controlled at the G1‐S progression. The integrated mathematical model of Epo‐driven proliferation explains cell type‐specific effects of targeted AKT and ERK inhibitors and faithfully predicts, based on the protein abundance, anti‐proliferative effects of inhibitors in primary human erythroid progenitor cells. Our findings suggest that the effectiveness of targeted cancer therapy might become predictable from protein abundance.