To breed, or not to breed? Predation risk induces breeding suppression in common voles

Breeding suppression hypothesis (BSH) predicts that, in several vole species, females will suppress breeding in response to high risk of mustelid predation; compared to breeding females, suppressing females would gain higher chances of survival. Seminal evidence for BSH was obtained in the laboratory, but attempts to replicate breeding suppression under field conditions were less conclusive. We tested whether breeding suppression occurs in common voles (Microtus arvalis), and how population density and predation risk combined affect voles’ reproductive activity. We found that, in contrast to males, female common voles suppress reproductive activity when faced with high predation risk. Population size was not reduced despite breeding suppression. A model of the interaction between predation risk and population density revealed that predator-induced breeding suppression depends on the density of conspecifics. We concluded that breeding suppression is a viable adaptation only at low vole densities, when per capita predation risk is high. Finally, we identified the key issues of experimental design required for the consistency of future studies on breeding suppression.     

To model or not to model?

In theory, the combination of mathematical modeling with experimental studies can be a powerful and compelling approach to understanding cell biology. In practice, choosing appropriate problems, identifying willing and able collaborators, and publishing the resulting research can be remarkably challenging. To provide perspective on the question of whether and when to combine modeling and experiments, a panel of experts at the 2010 ASCB Annual Meeting shared their personal experiences and advice on how to use modeling effectively.     

To charge or not to charge?

The ability to engineer proteins with increased thermostability will profoundly broaden their practical applications. Recent experimental results show that optimization of charge-charge interactions on the surface of proteins can be a useful strategy in the design of thermostable enzymes. Results also indicate a possibility that such optimized interactions provide structural determinants for enhanced stability of proteins from thermophilic organisms. In this article, the general strategy for design of thermostable proteins and perspectives for future studies are discussed.     

To B,or not to B: Is calcium the answer?

B lymphocytes are an important component of the adaptive and innate immune system because of their ability to secrete antibodies and to present antigens to T cells, which is critical for immune responses to many pathogens. Abnormal B cell function is the cause of diseases including autoimmune, paraneoplastic, and immunodeficiency disorders. The development, survival, and function of B cells depend on signaling through the B cell receptor (BCR) and costimulatory receptors. One of the signaling pathways induced by antigen binding to the BCR is store-operated Ca²⁺ entry (SOCE), which depends on the Ca²⁺ channel ORAI1 and its activators stromal interaction molecule (STIM) 1 and 2. A recent study by Berry et al. [1] reports that B cells lacking STIM1 and STIM2 fail to survive and proliferate because abolished SOCE results in impaired expression of two key anti-apoptotic genes and blunted activation of mTORC1 and c-Myc signaling. The associated Ca²⁺ regulated checkpoints of B cell survival and proliferation can be bypassed, at least partially, by costimulation through CD40 or TLR9. This study provides important new insights on how SOCE controls B cell function.     

To disaggregate or not to disaggregate,injury and cell disaggregation,transient or permanent?

Summary Methods for disaggregating tissues to obtain cells for primary cultures are reviewed and evaluated. The procedures include dissociation with crude and purified enzymes (singly and in various combinations), depletion of cations, and manipulation of pH and osmolality. Presented at the Workshop on Primary Cell Culture, November 1–3, 1973, Convenor Dr. Warren I. Schaeffer, University of Vermont, at the W. Alton Jones Cell Science Center, Lake Placid, N.Y. The editorial assistance of Dr. and Mrs. Joseph Leighton in preparing for press the five papers from that Workshop is gratefullv acknowledged. This work was supported by National Institutes of Health Research Grant CA-11339 from the National Cancer Institute. The Jackson Laboratory is fully accredited by the American Association for Accreditation of Laboratory Animal Care. The experimental work on liver cell dissociation referred to was carried out by Alice T. Noyes, Patricia M. Ward, Ellen Akeson, and Susan Torrey.     

To know or not to know? Genetic ignorance, autonomy and paternalism

This paper examines some arguments which deny the existence of an individual right to remain ignorant about genetic information relating to oneself--often referred to as 'a right to genetic ignorance' or, more generically, as 'a right not to know'. Such arguments fall broadly into two categories: 1) those which accept that individuals have a right to remain ignorant in self-regarding matters, but deny that this right can be extended to genetic ignorance, since such ignorance may be harmful to others, particularly those to whom one is genetically related (the 'harm to others objection') and 2) those which contend that, even if genetic ignorance is only self harming, it is not something to which individuals can rationally or morally claim to have a 'right' at all, since they defend their claims on autonomy-respecting grounds and ignorance is inimical to autonomy (the 'incoherence objection'). I argue that defenders of a right not to know have some plausible responses to the 'harm to others objection', they and their opponents reach an impasse in which both sides are left voicing concerns about the paternalistic implications of the other's point of view. I conclude that defenders of a right not to know would, therefore, advance their position further by analysing it in terms of values other than those of autonomy and rights.     

To be or not to be ubiquitinated?

Levels of p21, a cyclin-dependent kinase (CDK) inhibitor, are controlled in part at the post-translational level by protein degradation. Although the signaling pathways leading to p21 degradation have not yet been fully elucidated, it is evident that p21 ubiquitination is an essential factor in its degradation. We discuss that, with the only notable exception of ornithine decarboxylase, ubiquitination appears to be a prerequisite for proteasomal degradation rather than an unnecessary byproduct of such proteolysis.     

Cellulose: To depolymerize… or not to?

Oxidation of the primary OH groups in cellulose is a pivotal reaction both at lab and industrial scale, leading to the value-added products, i.e. oxidized cellulose which have tremendous applications in medicine, pharmacy and hi-tech industry. Moreover, the introduction of carboxyl moieties creates prerequisites for further cellulose functionalization through covalent attachment or electrostatic interactions, being an essential achievement designed to boost the area of cellulose-based nanomaterials fabrication. Various methods for the cellulose oxidation have been developed in the course of time, aiming the selective conversion of the OH groups. These methods use: nitrogen dioxide in chloroform, alkali metal nitrites and nitrates, strong acids alone or in combination with permanganates or sodium nitrite, ozone, and sodium periodate or lead (IV) tetraacetate. In the case of the last two reagents, cellulose dialdehydes derivatives are formed, which are further oxidized by sodium chlorite or hydrogen peroxide to form dicarboxyl groups. A major improvement in the cellulose oxidation was represented by the introduction of the stable nitroxyl radicals, such as 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO). However, a major impediment for the researchers working in this area is related with the severe depolymerisation occurred during the TEMPO-mediated conversion of CH₂OH into COOH groups. On the other hand, the cellulose depolymerisation represent the key step, in the general effort of searching for alternative strategies to develop new renewable, carbon-neutral energy sources. In this connection, exploiting the biomass feed stocks to produce biofuel and other low molecular organic compounds, involves a high amount of research to improve the overall reaction conditions, limit the energy consumption, and to use benign reagents. This work is therefore focused on the parallelism between these two apparently antagonist processes involving cellulose, building a necessary bridge between them, thinking how the reported drawbacks of the TEMPO-mediated oxidation of cellulose are heading towards to the biomass valorisation, presenting why the apparently undesired side reactions could be turned into beneficial processes if they are correlated with the existing achievements of particular significance in the field of cellulose conversion into small organic compounds, aiming the general goal of pursuing for alternatives to replace the petroleum-based products in human life.     

To move or not to move? Semaphorin signalling in cell migration

Semaphorins were discovered 11 years ago as molecular cues for axon guidance that are conserved from invertebrates to humans. More than 20 semaphorin genes have been identified in mammals and their protein products are now known to be involved in a range of processes from the guidance of cell migration to the regulation of the immune response, angiogenesis and cancer. Plexins, either alone or in association with neuropilins, constitute high-affinity semaphorin receptors. However, other transmembrane molecules have been implicated in semaphorin receptor complexes, and interactions between plexins and a range of intracellular effectors have been reported. These data indicate that semaphorins might be able to elicit responses through more than one signalling pathway. Interestingly, according to recent findings, the semaphorin-dependent control of cell migration crucially involves integrin-based adhesive structures through which polarized cell-membrane protrusion is coupled to cytoskeletal dynamics. This review focuses on the mechanisms whereby semaphorins are thought to regulate cell migration.     

To NO or not to NO: 'where?' is the question

Nitric oxide (NO) is a gaseous radical with unique biological functions essential for the cardiovascular system, host defense and neuro-transmission. For two decades it was thought that NO was able to diffuse freely across relatively long distances and to traverse major parts of the cell, if not multiple cell layers. However, NO has been proven to be extremely reactive: it reacts with other reactive oxygen species, heavy metals, as well as with cysteine and tyrosine residues in proteins. In accordance, it is now widely accepted that once NO is generated, it is very short-lived and diffuses only over a short distance. This urges for the local production of NO and the localization of NO synthases in the proximity of their downstream targets. This review discusses the highly organized localization of NO synthases, with the endothelial isoform (eNOS) as its main focus, since from this synthase most is known about its subcellular localization and regulation.