What does race do?

In writing on ‘John Rex's Main Mistake’, Michael Banton reveals more about Banton than he does about Rex. I use Banton's discussion of the differences between his own and John Rex's ‘mistakes’ to explore why, in my view, race continues to have analytical purchase in a purportedly ‘post-racial’ age     

Subfunctionalization: How often does it occur? How long does it take?

The mechanisms responsible for the preservation of duplicate genes have been debated for more than 70 years. Recently, Lynch and Force have proposed a new explanation: subfunctionalization--after duplication the two gene copies specialize to perform complementary functions. We investigate the probability that subfunctionalization occurs, the amount of time after duplication that it takes for the outcome to be resolved, and the relationship of these quantities to the population size and mutation rates.     

What does 'chromatin remodeling' mean?

The regulated alteration of chromatin structure, termed 'chromatin remodeling', can be accomplished by covalent modification of histones or by the action of ATP-dependent remodeling complexes. A variety of mechanisms can be used to remodel chromatin; some act locally on a single nucleosome and others act more broadly. It is critical to establish a direct connection between the remodeling events observed in vivo and the mechanistic capabilities of remodeling complexes in vitro.     

How does Drosophila melanogaster overwinter?

In temperate regions low temperatures seem to be the most restrictive factor for survival of Drosophila natural populations, which depends on the capacity of one or more developmental stages to resist unfavourable winter conditions. In this study we have attempted to answer the question of how D. melanogaster overwinters under natural temperature conditions. Only adults overwintered and no diapause was observed in any developmental stage. Thus, developmental duration becomes a decisive component with respect to overwintering potential and, therefore, the preadult stages are unlikely to overwinter. Possible evolutionary steps in adaptation to cold regions are discussed.     

How does a virus bud?

How does a virus bud from the plasma membrane of its host? Here we investigate several possible rate-limiting processes, including thermal fluctuations of the plasma membrane, hydrodynamic interactions, and diffusion of the glycoprotein spikes. We find that for bending moduli greater than 3 x 10(-13) ergs, membrane thermal fluctuations are insufficient to wrap the viral capsid, and the mechanical force driving the budding process must arise from some other process. If budding is limited by the rate at which glycoprotein spikes can diffuse to the budding site, we compute that the budding time is 10-20 min, in accord with the experimentally determined upper limit of 20 min. In light of this, we suggest some alternative mechanisms for budding and provide a rationale for the observation that budding frequently occurs in regions of high membrane curvature.     

How does radiation kill cells?

Recent advances in the understanding of intracellular signaling after genotoxic injury have led to a better understanding of the pathways that influence radiation-induced cell death. Particular progress has been made in defining molecular controls of apoptosis and radiation-induced cell cycle arrest, as well as the possible role of telomerase activity in stabilizing DNA breaks.     

When does grazing benefit plants?

Many recent studies have attempted to support the hypothesis that grazing can have positive effects on plant growth and fitness. However, a recent critical survey has shown that many of these studies suffer from poor experimental design, and consequently that the hypothesis may only be tenable under very particular circumstances.     

When does coevolution promote diversification?

Coevolutionary interactions between species are thought to be an important cause of evolutionary diversification. Despite this general belief, little theoretical basis exists for distinguishing between the types of interactions that promote diversification and those types that have no effect or that even restrict it. Using analytical models and simulations of phenotypic evolution across a metapopulation, we show that coevolutionary interactions promote diversification when they impose a cost of phenotype matching, as is the case for competition or host-parasite antagonism. In contrast, classical coevolutionary arms races have no tendency to promote or inhibit diversification, and mutualistic interactions actually restrict diversification. Together with the results of recent phylogenetic and ecological studies, these results suggest that the causes of diversification in many coevolutionary systems may require reassessment.     

Deficiency of lymphotoxin-α does not exacerbate high-fat diet-induced obesity but does enhance inflammation in mice

Lymphotoxin-α (LTα) is secreted by lymphocytes and acts through tumor necrosis factor-α receptors and the LTβ receptor. Our goals were to determine whether LT has a role in obesity and investigate whether LT contributes to the link between obesity and adipose tissue lymphocyte accumulation. LT deficient (LT(-/-)) and wild-type (WT) mice were fed standard pelleted rodent chow or a high-fat/high-sucrose diet (HFHS) for 13 wk. Body weight, body composition, and food intake were measured. Glucose tolerance was assessed. Systemic and adipose tissue inflammatory statuses were evaluated by quantifying plasma adipokine levels and tissue macrophage and T cell-specific gene expression in abdominal fat. LT(-/-) mice were smaller (20%) and leaner (25%) than WT controls after 13 wk of HFHS diet feeding. LT(-/-) mice showed improved glucose tolerance, suggesting that, in WT mice, LT may impair glucose metabolism. Surprisingly, adipose tissue from rodent chow- and HFHS-fed LT(-/-) mice exhibited increased T lymphocyte and macrophage infiltration compared with WT mice. Despite the fact that LT(-/-) mice exhibited an enhanced inflammatory status at the systemic and tissue level even when fed rodent chow, they were protected from enhanced diet-induced obesity and insulin resistance. Thus, LT contributes to body weight and adiposity and is required to modulate the accumulation of immune cells in adipose tissue.