The adult sex ratio (ASR) is a key parameter of the demography of human and other animal populations, yet the causes of variation in ASR, how individuals respond to this variation, and how their response feeds back into population dynamics remain poorly understood. A prevalent hypothesis is that ASR is regulated by intrasexual competition, which would cause more mortality or emigration in the sex of increasing frequency. Our experimental manipulation of populations of the common lizard (Lacerta vivipara) shows the opposite effect. Male mortality and emigration are not higher under male-biased ASR. Rather, an excess of adult males begets aggression toward adult females, whose survival and fecundity drop, along with their emigration rate. The ensuing prediction that adult male skew should be amplified and total population size should decline is supported by long-term data. Numerical projections show that this amplifying effect causes a major risk of population extinction. In general, such an ''evolutionary trap'' toward extinction threatens populations in which there is a substantial mating cost for females, and environmental changes or management practices skew the ASR toward males.adult sex ratio ͉ Lacerta vivipara ͉ male behavior ͉ population extinction ͉ sexual coercion

The coevolution of parental investment and offspring solicitation is driven by partly different evolutionary interests of genes expressed in parents and their offspring. In species with biparental care, the outcome of this conflict may be influenced by the sexual conflict over parental investment. Models for the resolution of such family conflicts have made so far untested assumptions about genetic variation and covariation in the parental resource provisioning response and the level of offspring solicitation. Using a combination of cross-fostering and begging playback experiments, we show that, in the great tit (Parus major), (i) the begging call intensity of nestlings depends on their common origin, suggesting genetic variation for this begging display, (ii) only mothers respond to begging calls by increased food provisioning, and (iii) the size of the parental response is positively related to the begging call intensity of nestlings in the maternal but not paternal line. This study indicates that genetic covariation, its differential expression in the maternal and paternal lines and/or early environmental and parental effects need to be taken into account when predicting the phenotypic outcome of the conflict over investment between genes expressed in each parent and the offspring.

Autophagy is an essential recycling pathway implicated in neurodegeneration either as a pro-survival or a pro-death mechanism. Its role after axonal injury is still uncertain. Axotomy of the optic nerve is a classical model of neurodegeneration. It induces retinal ganglion cell death, a process also occurring in glaucoma and other optic neuropathies. We analyzed autophagy induction and cell survival following optic nerve transection (ONT) in mice. Our results demonstrate activation of autophagy shortly after axotomy with autophagosome formation, upregulation of the autophagy regulator Atg5 and apoptotic death of 50% of the retinal ganglion cells (RGCs) after 5 days. Genetic downregulation of autophagy using knockout mice for Atg4B (another regulator of autophagy) or with specific deletion of Atg5 in retinal ganglion cells, using the Atg5 flox/flox mice reduces cell survival after ONT, whereas pharmacological induction of autophagy in vivo increases the number of surviving cells. In conclusion, our data support that autophagy has a cytoprotective role in RGCs after traumatic injury and may provide a new therapeutic strategy to ameliorate retinal diseases. Retinal ganglion cells (RGCs) are the only projecting neurons of the retina. Their axons form the optic nerve and transmit visual information to the brain. RGCs undergo apoptotic cell death in a stereotyped manner during development and in response to injury, in glaucoma and other optic neuropathies. 1 Degeneration of RGCs is often modeled by optic nerve transection (ONT), which leads to the death of these central nervous system neurons. 2 The mechanisms of RGC death are still a matter of intense investigation, and several factors including growth factor deprivation and oxidative stress have been proposed to participate in RGC degeneration in glaucoma and after ONT. 1,3 Autophagy is an intracellular catabolic pathway, which degrades cell components, toxic aggregates and damaged organelles and recycles them as basic building blocks in order to maintain cellular homeostasis. 4 Autophagy begins with the formation of a double membrane, sequestering parts of the cytosol and finally closing to form an autophagosome. This autophagosome subsequently fuses with lysosomes, thus, enabling degradation of the engulfed material. 4 Autophagy represents a cytoprotective response in many cell types 5 and its deregulation is implicated in many pathological conditions, including cancer, infectious diseases and neurodegeneration. 6 The role of autophagy in neuronal physiology is still far from being completely understood. 7,8 On one hand, autophagy is essential in preventing spontaneous neurodegeneration in mice, as deletion of the autophagy regulators Atg5, Atg7 and FIP200 in neuronal precursors induces cell death, accumulation of damaged ubiquitinated proteins and premature lethality. 9-11 Similarly, upregulation of autophagy decreases the accumulation of protein aggregates in several neurodegenerative proteinopathies. 12,13 Conversely autophagy triggers neuronal death under seve...