Data from: Timing manipulations reveal the lack of a causal link across timing of annual-cycle stages in a long-distance migrant

Organisms need to time their annual-cycle stages, like breeding and migration, to occur at the right time of the year. Climate change has shifted the timing of annual-cycle stages at different rates, thereby tightening or lifting time constraints of these annual-cycle stages, a rarely studied consequence of climate change. The degree to which these constraints are affected by climate change depends on whether consecutive stages are causally linked (I) or whether the timing of each stage is independent of other stages (II). Under (I), a change in timing in one stage has knock-on timing effects on subsequent stages, whereas under (II) a shift in the timing of one stage affects the degree of overlap with previous and subsequent stages. For testing this we combined field manipulations, captivity measurements and geolocation data. We advanced and delayed hatching dates in pied flycatchers (Ficedula hypoleuca) and measured how the timing of subsequent stages (male moult and migration) were affected. There was no causal effect of manipulated hatching dates on the onset of moult and departure to Africa. Thus, advancing hatching dates reduced the male moult-breeding overlap with no effect on the moult-migration interval. Interestingly, the wintering location of delayed males was more westwards, suggesting that delaying the termination of breeding carries-over to winter location. Because we found no causal linkage of the timing of annual-cycle stages, climate change can shift these stages at different rates, with the risk that the time available for some become so short that this will have major fitness consequences

Expression of truncated utrophin leads to major functional improvements in dystrophin-deficient muscles of mice

Dystrophin-deficient mice (mdx) expressing a truncated (trc) utrophin transgene show amelioration of the dystrophic phenotype. Here we report a multifunctional study demonstrating that trcutrophin expression leads to major improvements of the mechanical performance of muscle (that is, force development, mechanical resistance to forced lengthenings and maximal spontaneous activity) and of the maintenance of the intracellular calcium homeostasis. These are two essential functions of muscle fibers, known to be impaired in mdx mouse muscles and Duchenne muscular dystrophy (DMD) patients. Our results bring strong support to the hypothesis that muscle wasting in dystrophin-deficient DMD patients could be prevented by upregulation of utrophin