An appraisal of how the vitamin A‐redox hypothesis can maintain honesty of carotenoid‐dependent signals

The vitamin A‐redox hypothesis provides an explanation for honest signaling of phenotypic quality by carotenoid‐dependent traits. A key aspect of the vitamin A‐redox hypothesis, applicable to both yellow and red coloration, is the hypothesized negative feedback of tightly regulated Vitamin A plasma levels on the enzyme responsible for sequestering both Vitamin A and carotenoids from the gut. We performed a meta‐analysis and find that vitamin A levels are positively related to carotenoid plasma levels (r = 0.50, P = 0.0002). On the basis of this finding and further theoretical considerations, we propose that the vitamin A‐redox hypothesis is unlikely to explain carotenoid‐dependent honest signaling.     

Authors' reply

Article: http://dx.doi.org/10.1002/bimj.200410172 Letter to the Editor: http://dx.doi.org/10.1002/bimj.200710416     

Yolk androgens do not appear to mediate sexual conflict over parental investment in the collared flycatcher Ficedula albicollis

Males and females are in conflict over parental care, as it would be favourable for one parent to shift labour to the other. Yolk hormones may offer a mechanism through which female birds could influence offspring traits in ways that increase the relative investment by the male. We studied the role of yolk androgens in mediating sexual conflict over parental care in the collared flycatcher (Ficedula albicollis). In a cross-fostering experiment, the male's proportion of total feeding visits increased with increasing androgen levels in the foster eggs. This could suggest that sexual conflict over parental care may be influenced by the female's differential allocation of yolk androgens or a maternal effect associated with yolk androgens. However, when we experimentally elevated yolk androgen levels, male feeding rates did not differ between control and androgen-manipulated nests. This suggests that other egg components correlated with yolk androgen levels, rather than yolk androgen levels per se, may influence male parental effort. In conclusion, yolk androgens per se do not appear to mediate sexual conflict over parental investment in the collared flycatcher.     

Yolk androgens and begging behaviour in black-headed gull chicks: an experimental field study

Black-headed gulls, Larus ridibundus, produce clutches of three eggs, which contain high levels of maternal androgens in the yolk. These levels increase with laying order and the eggs hatch asynchronously. Experiments have supported the hypothesis that this within-clutch variation in maternal androgens mitigates the disadvantage of last-hatched chicks in sibling competition, by enhancing embryonic development and early posthatching growth. We hypothesized that these effects come about by the stimulating effects of maternal androgens on begging behaviour and competitive ability. In the field, we injected first-laid eggs of a clutch (which have a low androgen level) with either an androgen solution (T eggs) or vehicle (Oil eggs). We then created pairs of chicks hatched from Oil and T eggs, matched for egg mass and hatching date. Parent-chick interactions were recorded from observation hides. Chicks from T eggs hatched almost half a day sooner than those from Oil eggs. Furthermore, chicks from T eggs were more active during the first week after hatching, were more often the first to react to the approaching parent, begged more frequently, and obtained the larger share of food. We conclude that the enhancing effect of yolk androgens on growth in this species arises at least partly through androgen-mediated effects on the chicks' behaviour. Copyright 2003 The Association for the Study of Animal Behaviour. Published by Elsevier Ltd. All rights reserved.      

Plasma membrane specialization and intracellular polarity of freshly isolated rat hepatocytes

It was investigated whether rat hepatocytes maintain their plasma membrane specialization (sinusoidal, lateral and bile canalicular sites) and their intracellular polarity (peribiliary region, rich in lysosomes and poor in mitochondria) after isolation. The morphology of the hepatocytes and the cytochemical localization of marker enzymes for the bile canalicular membrane (alkaline phosphatase, adenosine triphosphatase and 5' nucleotidase), for the lysosomes (acid phosphatase) and for the mitochondria (beta-hydroxybutyrate dehydrogenase and succinate dehydrogenase) were studied in situ and directly after isolation using both light and electron microscopy. The morphology of the cells and the cytochemical activity of acid phosphatase, succinate dehydrogenase and beta-hydroxybutyrate dehydrogenase showed that in isolated cells, as in situ, the lysosomes were concentrated in bands, devoid of mitochondria. Unlike in situ the reaction product of alkaline phosphatase, adenosine triphosphatase and 5'nucleotidase was evenly distributed along the entire plasma membrane of the isolated cells. Morphologically, no tight or gap junctions or desmosomes could be detected in the isolated cells, while the plasma membrane appeared to be homogeneously covered with uniform microvilli. In conclusion it can be stated that during isolation the hepatocytes loose their distinct plasma membrane specialization, but maintain their peribiliary region rich in lysosomes and poor in mitochondria.     

Testosterone Reduces Promiscuity of Female Blue Tits (Cyanistes caeruleus): An Experimental Study

In many animal species, extra‐pair copulations (EPCs) are common and can increase fitness in both sexes. In males, EPCs can increase total reproductive output, whereas in females benefits of EPCs can be indirect through improving the genetic quality of their offspring. Males and females of many vertebrates show an increase in levels of the hormone testosterone (T) during the mating period. In males, T plays an important role in regulating mating behaviour including increasing their EPC rate. While much is known about the role of T in male mating behaviour, the role of T in female reproduction remains unclear. To study the influence of T on extra‐pair paternity rates in females in a field setting, we created three experimental groups of female blue tits (Cyanistes caeruleus): treated with either T, flutamide (Flu; an androgen receptor blocker) or empty implants before egg laying. Subsequently, we scored the number of extra‐pair offspring (EPO) in their broods. We also assessed the attractiveness of females treated with either T or Flu to males in mate choice trials in the laboratory. The overall proportion of EPO was lower for the T‐implanted group compared with the control group, whereas Flu had no effect. Given that males did not show a preference for Flu‐ vs. T‐treated females in the mate choice trials, it appears less likely that the reduction in EPO in the T‐implanted females was due to a reduction in their attractiveness. T levels may have negatively influenced EPO rate by affecting female within‐pair and/or extra‐pair mating behaviour. Future behavioural studies should investigate how elevated T levels reduce the number of EPO.     

Effects of 17-beta-estradiol treatment of female zebra finches on offspring sex ratio and survival

Treatment of female zebra finches (Taeniopygia guttata) with 17-beta-estradiol leads to a female-biased sex ratio in their offspring at the age of independence [Horm. Behav. 35 (1999) 135]. It is unclear whether this is due to a bias of the primary sex ratio or to sex-specific survival. We replicated this experiment and found again a significantly higher total number of daughters than sons at independence in the estradiol-treated group. This was due to higher embryonic survival of daughters compared with sons in the estradiol-treated group and the reverse in the control group. There was no effect of the hormone treatment on the primary sex ratio. Treatment with 17-beta-estradiol led to a significantly shorter hatching time and to heavier offspring at day 7 after hatching. This weight was correlated with maternal plasma estradiol levels on the day of the first egg, which were significantly higher in the estradiol-treated group than in the control group. The results do not support the idea that maternal estradiol levels influence the primary sex ratio. They indicate that maternal estradiol differentially affects survival of sons and daughters via an influence on the embryonic environment, possibly enhancing offspring growth.     

Experimental evidence for genetic heritability of maternal hormone transfer to offspring

In many animal species, embryos are exposed to maternal hormones that affect their development. Maternal hormone transfer varies with environmental conditions of the mother and is often interpreted as being shaped by natural selection to adjust the offspring to prevailing environmental conditions. Such hormone transfer requires genetic variability, which has not yet been experimentally demonstrated. Our study reports direct evidence for additive genetic variance of maternal androgens through a bidirectional selection on yolk testosterone (T) levels in Japanese quail. Lines selected for high egg T (HET) and low egg T (LET) concentration differed in yolk levels of this androgen, resulting in high realized heritability (h2 = 0.42)Correlated responses to selection on other gonadal hormones indicated that selection specifically targeted biologically active androgens. Eggs of HET quail contained higher androstenedione and lower estradiol concentrations than did those of LET quail, with no line differences in yolk progesterone concentration. Plasma T concentrations in adult females were not affected by selection, seriously challenging the hypothesis that transfer of maternal hormones to offspring is constrained by hormone levels in a mother's circulation. Our results suggest that transfer of maternal T represents an indirect genetic effect that has important consequences for the evolution of traits in offspring.     

A dynamic ubiquitin equilibrium couples proteasomal activity to chromatin remodeling

Protein degradation, chromatin remodeling, and membrane trafficking are critically regulated by ubiquitylation. The presence of several coexisting ubiquitin-dependent processes, each of crucial importance to the cell, is remarkable. This brings up questions on how the usage of this versatile regulator is negotiated between the different cellular processes. During proteotoxic stress, the accumulation of ubiquitylated substrates coincides with the depletion of ubiquitylated histone H2A and chromatin remodeling. We show that this redistribution of ubiquitin during proteotoxic stress is a direct consequence of competition for the limited pool of free ubiquitin. Thus, the ubiquitin cycle couples various ubiquitin-dependent processes because of a rate-limiting pool of free ubiquitin. We propose that this ubiquitin equilibrium may allow cells to sense proteotoxic stress in a genome-wide fashion.