Growth factor erv1-like modulates Drp1 to preserve mitochondrial dynamics and function in mouse embryonic stem cells.

The relationship of mitochondrial dynamics and function to pluripotency are rather poorly understood aspects of stem cell biology. Here we show that growth factor erv1-like (Gfer) is involved in preserving mouse embryonic stem cell (ESC) mitochondrial morphology and function. Knockdown (KD) of Gfer in ESCs leads to decreased pluripotency marker expression, embryoid body (EB) formation, cell survival, and loss of mitochondrial function. Mitochondria in Gfer-KD ESCs undergo excessive fragmentation and mitophagy, whereas those in ESCs overexpressing Gfer appear elongated. Levels of the mitochondrial fission GTPase dynamin-related protein 1 (Drp1) are highly elevated in Gfer-KD ESCs and decreased in Gfer-overexpressing cells. Treatment with a specific inhibitor of Drp1 rescues mitochondrial function and apoptosis, whereas expression of Drp1-dominant negative resulted in the restoration of pluripotency marker expression in Gfer-KD ESCs. Altogether, our data reveal a novel prosurvival role for Gfer in maintaining mitochondrial fission-fusion dynamics in pluripotent ESCs.

Sexual selection and canine dimorphism in New World monkeys.

Social and ecological factors are important in shaping sexual dimorphism in Anthropoidea, but there is also a tendency for body-size dimorphism and canine dimorphism to increase with increased body size (Rensch's rule) (Rensch: Evolution Above the Species Level. London: Methuen, 1959.) Most ecologist interpret Rensch's rule to be a consequence of social and ecological selective factors that covary with body size, but recent claims have been advanced that dimorphism is principally a consequence of selection for increased body size alone. Here we assess the effects of body size, body-size dimorphism, and social structure on canine dimorphism among platyrrhine monkeys. Platyrrhine species examined are classified into four behavioral groups reflecting the intensity of intermale competition for access to females or to limiting resources. As canine dimorphism increases, so does the level of intermale competition. Those species with monogamous and polyandrous social structures have the lowest canine dimorphism, while those with dominance rank hierarchies of males have the most canine dimorphism. Species with fission-fusion social structures and transitory intermale breeding-season competition fall between these extremes. Among platyrrhines there is a significant positive correlation between body size and canine dimorphism However, within levels of competition, no significant correlation was found between the two. Also, with increased body size, body-size dimorphism tends to increase, and this correlation holds in some cases within competition levels. In an analysis of covariance, once the level of intermale competition is controlled for, neither molar size nor molar-size dimorphism accounts for a significant part of the variance in canine dimorphism. A similar analysis using body weight as a measure of size and dimorphism yields a less clear-cut picture: body weight contributes significantly to the model when the effects of the other factors are controlled. Finally, in a model using head and body length as a measure of size and dimorphism, all factors and the interactions between them are significant. We conclude that intermale competition among platyrrhine species is the most important factor explaining variations in canine dimorphism. The significant effects of size and size dimorphism in some models may be evidence that natural (as opposed to sexual) selection also plays a role in the evolution of increased canine dimorphism.

Early social exposure in wild chimpanzees: mothers with sons are more gregarious than mothers with daughters.

In many mammals, early social experience is critical to developing species-appropriate adult behaviors. Although mother-infant interactions play an undeniably significant role in social development, other individuals in the social milieu may also influence infant outcomes. Additionally, the social skills necessary for adult success may differ between the sexes. In chimpanzees (Pan troglodytes), adult males are more gregarious than females and rely on a suite of competitive and cooperative relationships to obtain access to females. In fission-fusion species, including humans and chimpanzees, subgroup composition is labile and individuals can vary the number of individuals with whom they associate. Thus, mothers in these species have a variety of social options. In this study, we investigated whether wild chimpanzee maternal subgrouping patterns differed based on infant sex. Our results show that mothers of sons were more gregarious than mothers of daughters; differences were especially pronounced during the first 6 mo of life, when infant behavior is unlikely to influence maternal subgrouping. Furthermore, mothers with sons spent significantly more time in parties containing males during the first 6 mo. These early differences foreshadow the well-documented sex differences in adult social behavior, and maternal gregariousness may provide sons with important observational learning experiences and social exposure early in life. The presence of these patterns in chimpanzees raises questions concerning the evolutionary history of differential social exposure and its role in shaping sex-typical behavior in humans.

Mitochondrial fusion is regulated by Reaper to modulate Drosophila programmed cell death.

In most multicellular organisms, the decision to undergo programmed cell death in response to cellular damage or developmental cues is typically transmitted through mitochondria. It has been suggested that an exception is the apoptotic pathway of Drosophila melanogaster, in which the role of mitochondria remains unclear. Although IAP antagonists in Drosophila such as Reaper, Hid and Grim may induce cell death without mitochondrial membrane permeabilization, it is surprising that all three localize to mitochondria. Moreover, induction of Reaper and Hid appears to result in mitochondrial fragmentation during Drosophila cell death. Most importantly, disruption of mitochondrial fission can inhibit Reaper and Hid-induced cell death, suggesting that alterations in mitochondrial dynamics can modulate cell death in fly cells. We report here that Drosophila Reaper can induce mitochondrial fragmentation by binding to and inhibiting the pro-fusion protein MFN2 and its Drosophila counterpart dMFN/Marf. Our in vitro and in vivo analyses reveal that dMFN overexpression can inhibit cell death induced by Reaper or γ-irradiation. In addition, knockdown of dMFN causes a striking loss of adult wing tissue and significant apoptosis in the developing wing discs. Our findings are consistent with a growing body of work describing a role for mitochondrial fission and fusion machinery in the decision of cells to die.