Wagner's canalization model

Wagner (1996, Does evolutionary plasticity evolve? Evolution 50, 1008-1023.) and Siegal and Bergman, 2002 and Azevedo et al., 2006 have studied a simple model of the evolution of a network of N genes, in order to explain the observed phenomenon that systems evolve to be robust. These authors primarily considered the case N=10 and used simulations to reach their conclusions. Here we investigate this model in more detail, considering systems of different sizes with and without recombination, and with selection for convergence instead of to a specified limit. For the simpler evolutionary model lacking recombination, we analyze the system as a neutral network. This allows us to describe the equilibrium distribution networks within genotype space. Our results show that, given a sufficiently large population size, the qualitative observation that systems evolve to be robust, is itself robust, as it does not depend on the details of the model. In simple terms, robust systems have more viable offspring, so the evolution of robustness is merely selection for increased fecundity, an observation that is well known in the theory of neutral networks.     

Coevolutionary cycling of host sociality and pathogen virulence in contact networks

Infectious diseases may place strong selection on the social organization of animals. Conversely, the structure of social systems can influence the evolutionary trajectories of pathogens. While much attention has focused on the evolution of host sociality or pathogen virulence separately, few studies have looked at their coevolution. Here we use an agent-based simulation to explore host-pathogen coevolution in social contact networks. Our results indicate that under certain conditions, both host sociality and pathogen virulence exhibit continuous cycling. The way pathogens move through the network (e.g., their interhost transmission and probability of superinfection) and the structure of the network can influence the existence and form of cycling.     

Most nonclinicalKlebsiella strains are notK. pneumoniae sensu stricto

Twenty-nine bacterial isolates identified by routine biochemical procedures asKlebsiella pneumoniae and included in a recent numerical, taxonomy study were analyzed for molecular heterogeneity by DNA hybridization competition experiments. The isolates were obtained from clinical sources, from potable drinking water, trees, sawdust, pulp mill environs, and fresh vegetables. Three distinct groups were formed based on hybridization levels to three reference, cultures. One group exhibited 73–100% relative reassociation (RR) to a fecal coliform-positive reference, organism; a second group exhibited 60–100% RR to a fecal coliform-negative reference culture, while the third group exhibited 84–100% RR to an indole-producing, pectate-degrading, fecal coliformnegative reference, culture. The first group is designated asK. pneumoniae sensu stricto, and the third group asK. oxytoca. The, other isolates comprise at least one, and perhaps three additionalKlebsiella species. The present groups correlate, well with a numerical taxonomy study and with a biotyping scheme, which illustrated that mostK. pneumoniae sensu stricto are of clinical origin,Klebsiella “species” are primarilly of nonclinical orgin, andK. oxytoca are found in both environments. The fecal coliform test response is relevant in the genusKlebsiella for both taxonomic and ecological information in assessing the origin and health significance ofKlebsiella strains derived from nonclinical sources.     

Phosphorylation of rhodopsin: Most rhodopsin molecules are not phosphorylated

Phosphorylation of rod membrane proteins is a light-dependent reaction. Most rhodopsin molecules, however, are not phosphorylated. The protein that is highly phosphorylated (>3 moles phosphate per mole phosphorylated protein) appears to be a rhodopsin species that is different from the rest or is located in different parts of the rod membrane system.     

Epidemic cycling in a multi-strain SIRS epidemic network model

Background

One common observation in infectious diseases caused by multi-strain pathogens is that both the incidence of all infections and the relative fraction of infection with each strain oscillate with time (i.e., so-called Epidemic cycling). Many different mechanisms have been proposed for the pervasive nature of epidemic cycling. Nevertheless, the two facts that people contact each other through a network rather than following a simple mass-action law and most infectious diseases involve multiple strains have not been considered together for their influence on the epidemic cycling.

Methods

To demonstrate how the structural contacts among people influences the dynamical patterns of multi-strain pathogens, we investigate a two strain epidemic model in a network where every individual randomly contacts with a fixed number of other individuals. The standard pair approximation is applied to describe the changing numbers of individuals in different infection states and contact pairs.

Results

We show that spatial correlation due to contact network and interactions between strains through both ecological interference and immune response interact to generate epidemic cycling. Compared to one strain epidemic model, the two strain model presented here can generate epidemic cycling within a much wider parameter range that covers many infectious diseases.

Conclusion

Our results suggest that co-circulation of multiple strains within a contact network provides an explanation for epidemic cycling.

     

Metabolic networks are NP-hard to reconstruct

High-throughput data from various omics and sequencing techniques have rendered the automated metabolic network reconstruction a highly relevant problem. Our approach reflects the inherent probabilistic nature of the steps involved in metabolic network reconstruction. Here, the goal is to arrive at networks which combine probabilistic information with the possibility to obtain a small number of disconnected network constituents by reduction of a given preliminary probabilistic metabolic network. We define automated metabolic network reconstruction as an optimization problem on four-partite graph (nodes representing genes, enzymes, reactions, and metabolites) which integrates: (1) probabilistic information obtained from the existing process for metabolic reconstruction from a given genome, (2) connectedness of the raw metabolic network, and (3) clustering of components in the reconstructed metabolic network. The practical implications of our theoretical analysis refer to the quality of reconstructed metabolic networks and shed light on the problem of finding more efficient and effective methods for automated reconstruction. Our main contributions include: a completeness result for the defined problem, polynomial-time approximation algorithm, and an optimal polynomial-time algorithm for trees. Moreover, we exemplify our approach by the reconstruction of the sucrose biosynthesis pathway in Chlamydomonas reinhardtii.     

How scale-free are biological networks.

The concept of scale-free network has emerged as a powerful unifying paradigm in the study of complex systems in biology and in physical and social studies. Metabolic, protein, and gene interaction networks have been reported to exhibit scale-free behavior based on the analysis of the distribution of the number of connections of the network nodes. Here we study 10 published datasets of various biological interactions and perform goodness-of-fit tests to determine whether the given data is drawn from the power-law distribution. Our analysis did not identify a single interaction network that has a nonzero probability of being drawn from the power-law distribution.     

Betaherpesvirus sequences in eastern spiny mice and Wagner's dipodils

Eastern spiny mice (Acomys dimidiatus; also known as Sinai spiny mice) have been extensively studied in terms of the influence of parasite load on population size and reproductive fitness. The physical isolation of these rodent populations makes them interesting models for disease interactions in a real-life population as opposed to a laboratory. We identify betaherpesvirus sequences in eastern spiny mice and Wagner's dipodils (Dipodillus dasyurus), species that inhabit dry montane wadis (dry creek valleys) of the Sinai, highlighting the need for a comprehensive analysis of the full pathogen repertoire of these rodents in long-term studies.     

Most ultraviolet irradiation induced mutations in the nematode Caenorhabditis elegans are chromosomal rearrangements

In this study we have determined the utility of 254-nm ultraviolet light (UV) as a mutagenic tool in C. elegans. We have demonstrated that irradiation of adult hermaphrodites provides a simple method for the induction of heritable chromosomal rearrangements. A screening protocol was employed that identifies either recessive lethal mutations in the 40 map unit region balanced by the translocation eT1(III;V), or unc-36(III) duplications. Mutations were recovered in 3% of the chromosomes screened after a dose of 120 J/m2. This rate resembles that for 1500 R gamma-ray-induced mutations selected in a similar manner. The mutations were classified either as lethals [mapping to Linkage Group (LG)III or LGV] or as putative unc-36 duplications. In contrast to the majority of UV-induced mutations analysed in microorganisms, we found that a large fraction of the C. elegans UV-induced mutations are not simple intragenic lesions, but are deficiencies for more than one adjacent gene or more complex events. Preliminary evidence for this conclusion came from the high frequency of mutations that had a dominant effect causing reduced numbers of adult progeny. Subsequently 6 out of 9 analysed LGV mutations were found to be deficiencies. Other specific rearrangements also identified were: one translocation, sT5(II;III), and two unc-36 duplications, sDp8 and sDp9. It was concluded that UV irradiation can easily be used as an additional tool for the analysis of C. elegans chromosomes, and that C. elegans should prove to be a useful organism in which to study the mechanisms whereby UV acts as a mutagen in cells of complex eukaryotes.     

Sun-dried raisins are a cost-effective alternative to Sports Jelly Beans in prolonged cycling

The purpose of this study was to examine the effects of a natural carbohydrate (CHO) source in the form of sun-dried raisins (SDRs) vs. Sports Jelly Beans? (SJBs) on endurance performance in trained cyclists and triathletes. Ten healthy men (18-33 years) completed 1 water-only acclimatization exercise trial and 2 randomized exercise trials administered in a crossover fashion. Each trial consisted of a 120-minute constant-intensity glycogen depletion period followed by a 10-km time trial (TT). During each experimental trial, participants consumed isocaloric amounts of SDRs or SJBs in 20-minute intervals. Measurements included time to complete 10-km TT, power output during 10-km TT, blood glucose levels and respiratory exchange ratio during glycogen depletion period, rate of perceived exertion (RPE), 'flow' questionnaire responses, and a hedonic (i.e., pleasantness) sensory acceptance test. There were no significant differences in endurance performance for TT time (SDRs vs. SJBs, 17.3 ± 0.4 vs. 17.3 ± 0.4 seconds) or power (229.3 ± 13.0 vs. 232.0 ± 13.6 W), resting blood glucose levels (5.8 ± 04 mmol·L(-1) for SDRs and 5.4 ± 0.2 mmol·L(-1) for SJBs), RPE, or flow experiences between SDR and SJB trials. However, the mean sensory acceptance scores were significantly higher for the SDRs compared to the SJBs (50.7 ± 1.7 vs. 44.3 ± 2.7). Consuming SDRs or SJBs during 120 minutes of intense cycling results in similar subsequent TT performances and are equally effective in maintaining blood glucose levels during exercise. Therefore, SDRs are a natural, pleasant, cost-effective CHO alternative to commercial SJBs that can be used during moderate- to high-intensity endurance exercise.