Why is the microtubule lattice helical?

Microtubules polymerize from identical tubulin heterodimers, which form a helical lattice pattern that is the microtubule. This pattern always has left-handed chirality, but it is not known why. But as tubulin, similar to other proteins, evolved for a purpose, the question of the title of this artcile appears to be meaningful. In a computer simulation that explores the 'counterfactual biology' of microtubules without helicity, we demonstrate that these have the same mechanical properties as Nature's microtubules with helicity. Thus only a dynamical reason for helicity is left as potential explanation. We find that helicity solves 'the problem of the blind mason', i.e. how to correctly build a structure, guided only by the shape of the bricks. This answer in turn raises some new questions for researchers to address.     

Why is the polymerase chain reaction resistant to in vitro evolution?

A variety of methods have been developed to amplify DNA and RNA. These methods vary in their susceptibility to evolve new molecular species differing from the starting template. PCR is exceptionally resistant to in vitro evolution, whereas methods such as Q replicase and 3SR are much less robust. This paper develops some simple mathematical models which suggest that PCR is resistant to in vitro evolution because the reaction controls replication in discrete cycles: fast replication is of little advantage during PCR because the reaction limits fast replicators as well as slow ones to a single copy per cycle. In contrast, continuous (isothermal) reactions, as in the Q replicase reaction, favor fast replicators. The advantage of fast replication is compounded in continuous reactions, because a fast replicator can complete many generations of replication during the time it takes a slow replicator to complete one generation. These models suggest that continuous amplication protocols will never achieve the robustness against in vitro evolution observed with PCR.Correspondence to: J.J. Bull     

Why is metabolic labour divided in nitrification?

Winogradsky discovered in 1890 that nitrification is carried out in two consecutive steps by two distinct groups of bacteria: ammonia-oxidizing bacteria and nitrite-oxidizing bacteria. An explanation for this division of labour is offered based on the kinetic theory of optimal design of metabolic pathways, which postulates the existence of an optimal length for a pathway that maximizes the rate of ATP production. Shortening long pathways could, therefore, increase growth rate. However, this would reduce growth yield if the shorter pathway has fewer ATP-generating steps. High yields would be advantageous when bacteria grow in clonal clusters, as is typical for biofilms. It is postulated that bacteria that completely oxidize ammonia to nitrate exist in such environments.     

Dead or gone? Bayesian inference on mortality for the dispersing sex

Estimates of age‐specific mortality are regularly used in ecology, evolution, and conservation research. However, estimating mortality of the dispersing sex, in species where one sex undergoes natal dispersal, is difficult. This is because it is often unclear whether members of the dispersing sex that disappear from monitored areas have died or dispersed. Here, we develop an extension of a multievent model that imputes dispersal state (i.e., died or dispersed) for uncertain records of the dispersing sex as a latent state and estimates age‐specific mortality and dispersal parameters in a Bayesian hierarchical framework. To check the performance of our model, we first conduct a simulation study. We then apply our model to a long‐term data set of African lions. Using these data, we further study how well our model estimates mortality of the dispersing sex by incrementally reducing the level of uncertainty in the records of male lions. We achieve this by taking advantage of an expert's indication on the likely fate of each missing male (i.e., likely died or dispersed). We find that our model produces accurate mortality estimates for simulated data of varying sample sizes and proportions of uncertain male records. From the empirical study, we learned that our model provides similar mortality estimates for different levels of uncertainty in records. However, a sensitivity of the mortality estimates to varying uncertainty is, as can be expected, detectable. We conclude that our model provides a solution to the challenge of estimating mortality of the dispersing sex in species with data deficiency due to natal dispersal. Given the utility of sex‐specific mortality estimates in biological and conservation research, and the virtual ubiquity of sex‐biased dispersal, our model will be useful to a wide variety of applications.     

Why is algaculture still incipient in Brazil?

Macroalgae represent 26 % of the global production of cultivated organisms, with Gracilaria spp. representing 12 % of that production; Eucheuma spp. and Kappaphycus alvarezii account for 34 % of world’s algae production. Despite the potential for cultivating seaweed in Brazil, and with its more than 8000 km of coastline, there is neither marine algaculture nor detailed knowledge even among aquaculture farmers concerning the utility of algae in agriculture, industry, and gastronomy, with the result that algaculture represents only the smallest fraction of national aquaculture production. The main cultivated species of seaweed sold in Brazil include the exotic K. alvarezii and native species of Gracilaria that are grown on small scales and do not meet national industrial demands, which must be supplemented by imports. We discuss Brazilian algaculture here, pointing out some of the problems that restrict commercial production of algae in that country and offer solutions that could be shared with other nations.     

Why is mutual mate choice not the norm? Operational sex ratios,sex roles and the evolution of sexually dimorphic and monomorphic signalling.

Biases in the operational sex ratio (OSR) are seen as the fundamental reason behind differential competition for mates in the two sexes, and as a strong determinant behind differences in choosiness. This view has been challenged by Kokko and Monaghan, who argue that sex-specific parental investment, mortalities, mate-encounter rates and quality variation determine the mating system in a way that is not reducible to the OSR. We develop a game-theoretic model of choosiness, signalling and parental care, to examine (i) whether the results of Kokko and Monaghan remain robust when its simplifying assumptions are relaxed, (ii) how parental care coevolves with mating strategies and the OSR and (iii) why mutual mate choice is observed relatively rarely even when both sexes vary in quality. We find qualitative agreement with the simpler approach: parental investment is the primary determinant of sex roles instead of the OSR, and factors promoting choosiness are high species-specific mate-encounter rate, high sex-specific mate-encounter rate, high cost of breeding (parental investment), low cost of mate searching and highly variable quality of the opposite sex. The coevolution of parental care and mating strategies hinders mutual mate choice if one parent can compensate for reduced care by the other, but promotes it if offspring survival depends greatly on biparental care. We argue that the relative rarity of mutual mate choice is not due to biases in the OSR. Instead, we describe processes by which sexual strategies tend to diverge. This divergence is prevented, and mutual mate choice maintained, if synergistic benefits of biparental care render parental investment both high and not too different in the two sexes.     

Does increasing mortality change the response of fish populations to environmental fluctuations?

Fluctuations of fish populations abundances are shaped by the interplay between population dynamics and the stochastic forcing of the environment. Age-structured populations behave as a filter of the environment. This filter is characterised by the species-specific life cycle and life-history traits. An increased mortality of mature individuals alters these characteristics and may therefore induce changes in the variability of populations. The response of a generic age-structured model was analysed to investigate the expected changes in the fluctuations of fish populations in response to decreased adult survival. These expectations were then tested on an extensive dataset. In accordance with theory, the analyses revealed that decreased adult survival and mean age of spawners were linked to an increase in the relative importance of short-term fluctuations. It suggests that intensive exploitation can lead to a change in the variability of fish populations, an issue of central interest from both conservation and management perspectives.     

Why is the Number of DNA Bases 4?

In this paper we construct a mathematical model for DNA replication based on Shannon's mathematical theory for communication. We treat DNA replication as a communication channel. We show that the mean replication rate is maximal with four nucleotide bases under the primary assumption that the pairing time of the G–C bases is between 1.65 and 3 times the pairing time of the A–T bases.     

Why is epigenetics important in understanding the pathogenesis of inflammatory musculoskeletal diseases?

In its widest sense, the term epigenetics describes a range of mechanisms in genome function that do not solely result from the DNA sequence itself. These mechanisms comprise DNA and chromatin modifications and their associated systems, as well as the noncoding RNA machinery. The epigenetic apparatus is essential for controlling normal development and homeostasis, and also provides a means for the organism to integrate and react upon environmental cues. A multitude of functional studies as well as systematic genome-wide mapping of epigenetic marks and chromatin modifiers reveal the importance of epigenomic mechanisms in human pathologies, including inflammatory conditions and musculoskeletal disease such as rheumatoid arthritis. Collectively, these studies pave the way to identify possible novel therapeutic intervention points and to investigate the utility of drugs that interfere with epigenetic signalling not only in cancer, but possibly also in inflammatory and autoimmune diseases.     

Disease-related versus polymorphic mutations in human mitochondrial tRNAs: Where is the difference?

A number of point mutations in human mitochondrial (mt) tRNA genes are correlated with a variety of neuromuscular and other severe disorders including encephalopathies, myopathies, cardiopathies and diabetes. The complexity of the genotype/phenotype relationships, the diversity of possible molecular impacts of the different mutations at the tRNA structure/function levels, and the exponential discovery of new mutations call for the search for unifying features. Here, the basic features (at the levels of primary and secondary structure) of 68 ‘pathogenic’ mutations are compared with those of 64 ‘polymorphic’ neutral mutations, revealing that these standard parameters for mutant analysis are not sufficient to predict the pathogenicity of mt tRNA mutations. Thus, case by case molecular investigation remains the only means of assessing the growing family of pathogenic mutations in mt tRNAs. New lines of research are suggested.     

Why is the cystic fibrosis gene so frequent?

Summary The high incidence of cystic fibrosis (CF) in most European populations (and populations of European descent) can be explained by different hypotheses that can be tested using the available data concerning this disorder. Among the five hypotheses discussed (genetic heterogeneity, high rate of mutation, meiotic drive, drift and heterozygote advantage), only the last is supported by experimental data. The following conclusions can be drawn from the evidence that we have reviewed: (1) CF is a single gene disorder (genetically homogeneous). (2) Haplotypes associated with the CF gene suggest that only a few mutations (the same gene located in 7q13 is always affected) are responsible for the disorder. (3) CF with pancreatic insufficiency is mainly associated with a single haplotype, whereas CF with pancreatic sufficiency is more frequently associated with different haplotypes. (4) A selective advantage consisting of higher resistance to Cl^–-secreting diarrhoeas might have favored, in the past, survival of infants heterozygous for the CF gene.