Male Homosexual Preference: Where,When, Why?

Male homosexual preference (MHP) has long been of interest to scholars studying the evolution of human sexuality. Indeed, MHP is partially heritable, induces a reproductive cost and is common. MHP has thus been considered a Darwinian paradox. Several questions arise when MHP is considered in an evolutionary context. At what point did MHP appear in the human evolutionary history? Is MHP present in all human groups? How has MHP evolved, given that MHP is a reproductively costly trait? These questions were addressed here, using data from the anthropological and archaeological literature. Our detailed analysis of the available data challenges the common view of MHP being a “virtually universal” trait present in humans since prehistory. The conditions under which it is possible to affirm that MHP was present in past societies are discussed. Furthermore, using anthropological reports, the presence or absence of MHP was documented for 107 societies, allowing us to conclude that evidence of the absence of MHP is available for some societies. A recent evolutionary hypothesis has argued that social stratification together with hypergyny (the hypergyny hypothesis) are necessary conditions for the evolution of MHP. Here, the link between the level of stratification and the probability of observing MHP was tested using an unprecedented large dataset. Furthermore, the test was performed for the first time by controlling for the phylogenetic non-independence between societies. A positive relationship was observed between the level of social stratification and the probability of observing MHP, supporting the hypergyny hypothesis.     

The Lengthening of a Giant Protein: When, How, and Why?

Subcommissural organ (SCO)-spondin is a giant glycoprotein of more than 5000 amino acids found in Vertebrata, expressed in the central nervous system and constitutive of Reissner’s fiber. For the first time, in situ hybridization performed on zebrafish (Danio rerio) embryos shows that the gene encoding this protein is expressed transitionally in the floor plate, the ventral midline of the neural tube, and later in the diencephalic third ventricle roof, the SCO. The modular organization of the protein in Echinodermata (Strongylocentrotus purpuratus), Urochordata (Ciona savignyi and C. intestinalis), and Vertebrata (Teleostei, Amphibia, Aves and Mammalia) is also described. As the thrombospondin type 1 repeat motifs represent an increasingly large part of the protein during Deuterostomia evolution, the duplication mechanisms leading to this complex organization are examined. The functional significance of the particularly well-preserved arrangement of the series of SCO-spondin repeat motifs and thombospondin type 1 repeats is discussed. Electronic Supplementary Material The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

RNA–Chromatin Interactome: What? Where? When?

Molecular Biology - It was noticed in the early 1960s that a large amount of RNAs is associated with chromatin. What kind of RNAs are they? Where are they located on chromatin? When and in what...     

Mating Plugs in Polyandrous Giants: Which Sex Produces Them,When, How and Why?

Background

Males usually produce mating plugs to reduce sperm competition. However, females can conceivably also produce mating plugs in order to prevent unwanted, superfluous and energetically costly matings. In spiders–appropriate models for testing plugging biology hypotheses–mating plugs may consist of male genital parts and/or of amorphous covers consisting of glandular or sperm secretions. In the giant wood spider Nephila pilipes, a highly sexually dimorphic and polygamous species, males are known to produce ineffective embolic plugs through genital damage, but nothing is known about the origin and function of additional conspicuous amorphous plugs (AP) covering female genitals.

Methodology

We tested alternative hypotheses of the nature and function of AP in N. pilipes by staging mating trials with varying degrees of polyandry. No APs were ever formed during mating trials, which rules out the possibility of male AP formation. Instead, those females that oviposited produced the AP from a liquid secreted during egg sac formation. Polyandrous females were more likely to lay eggs and to produce the AP, as were those that mated longer and with more total insertions. Our further tests revealed that, in spite of being a side product of egg sac production, AP, when hardened, prevented any subsequent copulation.

Conclusions

We conclude that in the giant wood spider (Nephila pilipes), the amorphous mating plugs are not produced by the males, that repeated copulations (most likely polyandrous) are necessary for egg fertilization and AP formation, and that the AP represents a female adaptation to sexual conflict through prevention of unwanted, excessive copulations. Considering the largely unknown origin of amorphous plugs in spiders, we predict that a similar pattern might be detected in other clades, which would help elucidate the evolutionary interplay of various selection pressures responsible for the origin and maintenance of mating plugs.     

The evolution of endothermy in terrestrial vertebrates: Who? When? Why?

Avian and mammalian endothermy results from elevated rates of resting, or routine, metabolism and enables these animals to maintain high and stable body temperatures in the face of variable ambient temperatures. Endothermy is also associated with enhanced stamina and elevated capacity for aerobic metabolism during periods of prolonged activity. These attributes of birds and mammals have greatly contributed to their widespread distribution and ecological success. Unfortunately, since few anatomical/physiological attributes linked to endothermy are preserved in fossils, the origin of endothermy among the ancestors of mammals and birds has long remained obscure. Two recent approaches provide new insight into the metabolic physiology of extinct forms. One addresses chronic (resting) metabolic rates and emphasizes the presence of nasal respiratory turbinates in virtually all extant endotherms. These structures are associated with recovery of respiratory heat and moisture in animals with high resting metabolic rates. The fossil record of nonmammalian synapsids suggests that at least two Late Permian lineages possessed incipient respiratory turbinates. In contrast, these structures appear to have been absent in dinosaurs and nonornithurine birds. Instead, nasal morphology suggests that in the avian lineage, respiratory turbinates first appeared in Cretaceous ornithurines. The other approach addresses the capacity for maximal aerobic activity and examines lung structure and ventilatory mechanisms. There is no positive evidence to support the reconstruction of a derived, avian-like parabronchial lung/air sac system in dinosaurs or nonornithurine birds. Dinosaur lungs were likely heterogenous, multicameral septate lungs with conventional, tidal ventilation, although evidence from some theropods suggests that at least this group may have had a hepatic piston mechanism of supplementary lung ventilation. This suggests that dinosaurs and nonornithurine birds generally lacked the capacity for high, avian-like levels of sustained activity, although the aerobic capacity of theropods may have exceeded that of extant ectotherms. The avian parabronchial lung/air sac system appears to be an attribute limited to ornithurine birds.     

Rapamycin and Ageing: When,for How Long,and How Much?

正The mechanistic target of rapamycin(mTOR)is a nutrient and growth factor responsive kinase that modulates lifespan in species from yeast to mice(Johnson et al.,2013b).mTOR exists in two complexes within cells,mTOR complexⅠ(mTORC1)and mTOR complex 2(mTORC2)(Laplante and Sabatini,2012).Abundant evidence suggests that mTORC1is the primary mTOR complex involved in regulating longevity:mutations that reduce the     

Proliferation/Quiescence: When to start? Where to stop? What to stock?

ABSTRACT: The cell cycle is a tightly controlled series of events that ultimately lead to cell division. The literature deciphering the molecular processes involved in regulating the consecutive cell cycle steps is colossal. By contrast, much less is known about non-dividing cellular states, even if they concern the vast majority of cells, from prokaryotes to multi-cellular organisms. Indeed, cells decide to enter the division cycle only if conditions are favourable. Otherwise they may enter quiescence, a reversible non-dividing cellular state. Recent studies in yeast have shed new light on the transition between proliferation and quiescence, re-questioning the notion of cell cycle commitment. They also indicate a predominant role for cellular metabolic status as a major regulator of quiescence establishment and exit. Additionally, a growing body of evidence indicates that environmental conditions, and notably the availability of various nutrients, by impinging on specific metabolic routes, directly regulate specific cellular re-organization that occurs upon proliferation/quiescence transitions.     

Poly(ADP-ribose) Polymerase Cleavage during Apoptosis: When and Where?

Poly(ADP-ribose) polymerase-1 (PARP-1) plays the active role of “nick sensor” during DNA repair and apoptosis, when it synthesizes ADP-ribose from NAD⁺ in the presence of DNA strand breaks. Moreover, PARP-1 becomes a target of apoptotic caspases, which originate two proteolytic fragments of 89 and 24 kDa. The precise relationship between PARP-1 activation and degradation during apoptosis is still a matter of debate. In human Hep-2 cells driven to apoptosis by actinomycin D, we have monitored PARP-1 activity by the mAb 10H, which is specific for the ADP-ribose polymers, and we have observed that poly(ADP-ribose) synthesis is a very early response to the apoptotic stimulus. The analysis of the presence and fate of the p89 proteolytic fragment revealed that PARP-1 proteolysis by caspases is concomitant with poly(ADP-ribose) synthesis and that p89 migrates from the nucleus into the cytoplasm in late apoptotic cells with advanced nuclear fragmentation.     

Where,When and Why Do Tsetse Contact Humans? Answers from Studies in a National Park of Zimbabwe

Background

Sleeping sickness, also called human African trypanosomiasis, is transmitted by the tsetse, a blood-sucking fly confined to sub-Saharan Africa. The form of the disease in West and Central Africa is carried mainly by species of tsetse that inhabit riverine woodland and feed avidly on humans. In contrast, the vectors for the East and Southern African form of the disease are usually savannah species that feed mostly on wild and domestic animals and bite humans infrequently, mainly because the odours produced by humans can be repellent. Hence, it takes a long time to catch many savannah tsetse from people, which in turn means that studies of the nature of contact between savannah tsetse and humans, and the ways of minimizing it, have been largely neglected.

Methodology/Principal Findings

The savannah tsetse, Glossina morsitans morsitans and G. pallidipes, were caught from men in the Mana Pools National park of Zimbabwe. Mostly the catch consisted of young G. m. morsitans, with little food reserve. Catches were increased by 4–8 times if the men were walking, not stationary, and increased about ten times more if they rode on a truck at 10 km/h. Catches were unaffected if the men used deodorant or were baited with artificial ox odour, but declined by about 95% if the men were with an ox. Surprisingly, men pursuing their normal daily activities were bitten about as much when in or near buildings as when in woodland. Catches from oxen and a standard ox-like trap were poor indices of the number and physiological state of tsetse attacking men.

Conclusion/Significance

The search for new strategies to minimize the contact between humans and savannah tsetse should focus on that occurring in buildings and vehicles. There is a need to design a man-like trap to help to provide an index of sleeping sickness risk.     

Can Invasive Species Facilitate Native Species? Evidence of How, When, and Why These Impacts Occur

Although the predatory and competitive impacts of biological invasions are well documented, facilitation of native species by non-indigenous species is frequently overlooked. A search through recent ecological literature found that facilitative interactions between invasive and native species occur in a wide range of habitats, can have cascading effects across trophic levels, can re-structure communities, and can lead to evolutionary changes. These are critical findings that, until now, have been mostly absent from analyses of ecological impacts of biological invasions. Here I present evidence for several mechanisms that exemplify how exotic species can facilitate native species. These mechanisms include habitat modification, trophic subsidy, pollination, competitive release, and predatory release. Habitat modification is the most frequently documented mechanism, reflecting the drastic changes generated by the invasion of functionally novel habitat engineers. Further, I predict that facilitative impacts on native species will be most likely when invasive species provide a limiting resource, increase habitat complexity, functionally replace a native species, or ameliorate predation or competition. Finally, three types of facilitation (novel, substitutive, and indirect) define why exotic species can lead to facilitation of native species. It is evident that understanding biological invasions at the community and ecosystem levels will be more accurate if we integrate facilitative interactions into future ecological research. Since facilitative impacts of biological invasions can occur with native endangered species, and can have wide-ranging impacts, these results also have important implications for management, eradication, and restoration.Contribution Number 2293, Bodega Marine Laboratory, University of California at Davis.     

Mitotic death: a mechanism of survival? A review

Mitotic death is a delayed response of p53 mutant tumours that are resistant to genotoxic damage. Questions surround why this response is so delayed and how its mechanisms serve a survival function. After uncoupling apoptosis from G1 and S phase arrests and adapting these checkpoints, p53 mutated tumour cells arrive at the G2 compartment where decisions regarding survival and death are made. Missed or insufficient DNA repair in G1 and S phases after severe genotoxic damage results in cells arriving in G2 with an accumulation of point mutations and chromosome breaks. Double strand breaks can be repaired by homologous recombination during G2 arrest. However, cells with excessive chromosome lesions either directly bypass the G2/M checkpoint, starting endocycles from G2 arrest, or are subsequently detected by the spindle checkpoint and present with the features of mitotic death. These complex features include apoptosis from metaphase and mitosis restitution, the latter of which can also facilitate transient endocycles, producing endopolyploid cells. The ability of cells to initiate endocycles during G2 arrest and mitosis restitution most likely reflects their similar molecular environments, with down-regulated mitosis promoting factor activity. Resulting endocycling cells have the ability to repair damaged DNA, and although mostly reproductively dead, in some cases give rise to mitotic progeny. We conclude that the features of mitotic death do not simply represent aberrations of dying cells but are indicative of a switch to amitotic modes of cell survival that may provide additional mechanisms of genotoxic resistance.