When good enough is best

In this issue of Neuron, Rinberg et al. show that mice use a speed-accuracy tradeoff in odor discrimination. Shorter sampling results in high performance for easy problems, and enforced longer sampling results in higher accuracy for difficult problems, but mice freely choose intermediate sampling durations and accuracy varies with difficulty. Reward value and task requirements may determine sampling time choice and performance levels.     

When enough is not enough: shorebirds and shellfishing

In a number of extensive coastal areas in northwest Europe, large numbers of long-lived migrant birds eat shellfish that are also commercially harvested. Competition between birds and people for this resource often leads to conflicts between commercial and conservation interests. One policy to prevent shellfishing from harming birds is to ensure that enough food remains after harvesting to meet most or all of their energy demands. Using simulations with behaviour-based models of five areas, we show here that even leaving enough shellfish to meet 100% of the birds' demands may fail to ensure that birds survive in good condition. Up to almost eight times this amount is needed to protect them from being harmed by the shellfishery, even when the birds can consume other kinds of non-harvested prey.     

Oogenesis: when most is good enough

In male meiosis an unaligned chromosome blocks meiotic progression. However, oocytes with one or more misaligned chromosomes can complete meiosis. This difference reflects a more permissive role of the spindle assembly checkpoint, rather than solely reflecting the ability of some univalents to adopt a meiosis II-like orientation on the spindle.     

When enough is enough: genetic diseases associated with transcriptional derepression

For many human genetic diseases, the underlying genetic defect has been determined. Thus, although traditionally a field only for researchers in medicine or human genetics, human diseases are now opening up to molecular biologists, cell biologists and biochemists. Here we discuss four human genetic disorders, Familial Alzheimer's disease, Rett syndrome, Klippel-Trenaunay syndrome and Facioscapulohumeral muscular dystrophy, and how investigations into these diseases are providing important lessons about human biology.     

When enough is enough: Detrimental effects of excess histones

Comment on: Singh RK, et al. Cell Cycle 2010; 9:4236-44.     

SLE and malaria: another look at an old idea

An alternative view of the relationship between autoimmune disease and malaria is provided in the following article by Geoff Butcher and Ian Clark. Here they reassess the evidence that favours an earlier suggestion that where parasitic infections are common, autoimmune disease is rare. They suggest that malaria may exert a protective effect against the autoimmune nephritis in systemic lupus erythematosus (SLE).     

A second look at the second messenger hypothesis

Several hundred hormones, neurotransmitters, growth factors and other "first messengers" bind to specific cell membrane receptors and induce a myriad of effects: short term, transport, metabolic, mitotic and regulation of thousands of specific genes. Yet, less than a dozen "second messengers" have been clearly established to date. Even allowing for the discovery of a large number of additional second messengers, there remains a paradox in terms of information-transfer within the cell: how can so many specific signals produce so many effects through so few relatively nonspecific intermediates? We consider several possible solutions to this paradox, including the hypothesis that signal specificity is encoded in part in the primary structure of the receptor.     

HIV-1 attachment: another look

HIV-1 attachment to host cells is generally considered to take place via high-affinity binding between CD4 and gp120. However, the binding of virion-associated gp120 to cellular CD4 is often weak, and most cell types that are permissive for HIV-1 infection express little CD4. Thus, other interactions between the virion and the cell surface could dominate the attachment process.     

When BAD is good for beta cells

BAD, a proapoptotic member of the Bcl-2 family of proteins, is regulated by phosphorylation. A recent study (Danial et al., 2008) suggests a phosphorylation-state-dependent bifunctional role of BAD in the regulation of glucose-stimulated insulin secretion and beta cell mass.     

Dealing with DNA lesions: When one cell cycle is not enough

Subversion of genome integrity fuels cellular adaptation and is a prerequisite for organismal evolution, yet genomic lesions are also the harmful driving force of cancer and other age-related human diseases. Genome integrity maintenance is inherently linked to genome organization and nuclear architecture, which are substantially remodeled during the cell cycle. Here we discuss recent findings on how actively dividing cells cope with endogenous genomic lesions that occur frequently at repetitive, heterochromatic, and late replicating regions as byproducts of genome duplication. We discuss how such lesions, rather than being resolved immediately when they occur, are dealt with in subsequent cell cycle phases, and even after mitotic cell division, and how this in turn affects genome organization, stability, and function.