Do changes in climate patterns in wintering areas affect the timing of the spring arrival of trans‐Saharan migrant birds?

The life cycles of plants and animals are changing around the world in line with the predictions originated from hypotheses concerning the impact of global warming and climate change on biological systems. Commonly, the search for ecological mechanisms behind the observed changes in bird phenology has focused on the analysis of climatic patterns from the species breeding grounds. However, the ecology of bird migration suggests that the spring arrival of long‐distance migrants (such as trans‐Saharan birds) is more likely to be influenced by climate conditions in wintering areas given their direct impact on the onset of migration and its progression. We tested this hypothesis by analysing the first arrival dates (FADs) of six trans‐Saharan migrants (cuckoo Cuculus canorus, swift Apus apus, hoopoe Upupa epops, swallow Hirundo rustica, house martin Delichon urbica and nightingale Luscinia megarhynchos), in a western Mediterranean area since from 1952 to 2003. By means of multiple regression analyses, FADs were analysed in relation to the monthly temperature and precipitation patterns of five African climatic regions south of the Sahara where species are thought to overwinter and from the European site from where FADs were collected. We obtained significant models for five species explaining 9–41% of the variation in FADs. The interpretation of the models suggests that: (1) The climate in wintering quarters, especially the precipitation, has a stronger influence on FADs than that in the species' potential European breeding grounds. (2) The accumulative effects of climate patterns prior to migration onset may be of considerable importance since those climate variables that served to summarize climate patterns 12 months prior to the onset of migration were selected by final models. (3) Temperature and precipitation in African regions are likely to affect departure decision in the species studied through their indirect effects on food availability and the build‐up of reserves for migration. Our results concerning the factors that affect the arrival times of trans‐Saharan migrants indicate that the effects of climate change are more complex than previously suggested, and that these effects might have an interacting impact on species ecology, for example by reversing ecological pressures during species' life cycles.     

Hydrogen sulfide:A novel component in Arabidopsis peroxisomes which triggers catalase inhibition

Plant peroxisomes have the capacity to generate different reactive oxygen and nitrogen species(ROS and RNS),such as H_2O_2,superoxide radical(O_2~-),nitric oxide and peroxynitrite(ONOO~-).These organelles have an active nitrooxidative metabolism which can be exacerbated by adverse stress conditions.Hydrogen sulfide(H_2S)is a new signaling gasotransmitter which can mediate the posttranslational modification(PTM)persulfidation.We used Arabidopsis thaliana transgenic seedlings expressing cyan fluorescent protein(CFP)fused to a canonical peroxisome targeting signal 1(PTS1)to visualize peroxisomes in living cells,as well as a specific fluorescent probe which showed that peroxisomes contain H_2S.H_2S was also detected in chloroplasts under glyphosate-induced oxidative stress conditions.Peroxisomal enzyme activities,including catalase,photorespiratory H_2O_2-generating glycolate oxidase(GOX)and hydroxypyruvate reductase(HPR),were assayed in vitro with a H_2S donor.In line with the persulfidation of this enzyme,catalase activity declined significantly in the presence of the H_2S donor.To corroborate the inhibitory effect of H_2S on catalase activity,we also assayed pure catalase from bovine liver and pepper fruit-enriched samples,in which catalase activity was inhibited.Taken together,these data provide evidence of the presence of H_2S in plant peroxisomes which appears to regulate catalase activity and,consequently,the peroxisomal H_2O_2 metabolism.     

The Genetic Basis of Escherichia coli Pathoadaptation to Macrophages

Antagonistic interactions are likely important driving forces of the evolutionary process underlying bacterial genome complexity and diversity. We hypothesized that the ability of evolved bacteria to escape specific components of host innate immunity, such as phagocytosis and killing by macrophages (MΦ), is a critical trait relevant in the acquisition of bacterial virulence. Here, we used a combination of experimental evolution, phenotypic characterization, genome sequencing and mathematical modeling to address how fast, and through how many adaptive steps, a commensal Escherichia coli (E. coli) acquire this virulence trait. We show that when maintained in vitro under the selective pressure of host MΦ commensal E. coli can evolve, in less than 500 generations, virulent clones that escape phagocytosis and MΦ killing in vitro, while increasing their pathogenicity in vivo, as assessed in mice. This pathoadaptive process is driven by a mechanism involving the insertion of a single transposable element into the promoter region of the E. coli yrfF gene. Moreover, transposition of the IS186 element into the promoter of Lon gene, encoding an ATP-dependent serine protease, is likely to accelerate this pathoadaptive process. Competition between clones carrying distinct beneficial mutations dominates the dynamics of the pathoadaptive process, as suggested from a mathematical model, which reproduces the observed experimental dynamics of E. coli evolution towards virulence. In conclusion, we reveal a molecular mechanism explaining how a specific component of host innate immunity can modulate microbial evolution towards pathogenicity.     

Small-world networks decrease the speed of Muller's ratchet

Muller's ratchet is an evolutionary process that has been implicated in the extinction of asexual species, the evolution of non-recombining genomes, such as the mitochondria, the degeneration of the Y chromosome, and the evolution of sex and recombination. Here we study the speed of Muller's ratchet in a spatially structured population which is subdivided into many small populations (demes) connected by migration, and distributed on a graph. We studied different types of networks: regular networks (similar to the stepping-stone model), small-world networks and completely random graphs. We show that at the onset of the small-world network - which is characterized by high local connectivity among the demes but low average path length - the speed of the ratchet starts to decrease dramatically. This result is independent of the number of demes considered, but is more pronounced the larger the network and the stronger the deleterious effect of mutations. Furthermore, although the ratchet slows down with increasing migration between demes, the observed decrease in speed is smaller in the stepping-stone model than in small-world networks. As migration rate increases, the structured populations approach, but never reach, the result in the corresponding panmictic population with the same number of individuals. Since small-world networks have been shown to describe well the real contact networks among people, we discuss our results in the light of the evolution of microbes and disease epidemics.     

Conserved intron positions in ancient protein modules

Background  

The timing of the origin of introns is of crucial importance for an understanding of early genome architecture. The Exon theory of genes proposed a role for introns in the formation of multi-exon proteins by exon shuffling and predicts the presence of conserved splice sites in ancient genes. In this study, large-scale analysis of potential conserved splice sites was performed using an intron-exon database (ExInt) derived from GenBank.     

Mitogen activated protein kinase plays a significant role in metaphase II arrest, spindle morphology, and maintenance of maturation promoting factor activity in bovine oocytes

Mammalian oocytes are arrested at the G2/M transition of the first meiotic division from which, after reaching full size and subsequent to an LH surge, they undergo final maturation. Oocyte maturation, which involves germinal vesicle breakdown, progression through metaphase I (MI), and arrest at MII, is triggered and regulated by the coordinated action of two kinases, maturation promoting factor (MPF) and mitogen activated protein kinase (MAPK). The importance of the role of MPF in mammalian oocyte maturation is well established, while the role of MAPK, although well understood in mouse oocytes, has not been fully elucidated in oocytes of large domestic species, especially bovine oocytes. Here we show that injection of MKP-1 mRNA, which encodes a dual specificity MAPK phosphatase, into germinal vesicle stage bovine oocytes prevents the activation of MAPK during maturation. Despite the lack of MAPK activity, MKP-1-injected oocytes resume and progress through meiosis, although they are unable to arrest at MII stage and, by 22-26-hour post-maturation, exhibit decondensed pronucleus-like chromatin, a clear sign of parthenogenetic activation. MKP-1-injected bovine oocytes exhibit normal activation of MPF activity; however, by 18-hour post-maturation, MPF activity starts to decline and by 22-26 hr MPF activity is absent. MKP-1-injected oocytes also show disorganized MII spindles with poorly aligned chromosomes. In summary, our results demonstrate that in bovine oocytes MAPK activity is required for MII arrest, maintenance of MPF activity, and spindle organization.     

Injection of sperm cytosolic factor into mouse metaphase II oocytes induces different developmental fates according to the frequency of [Ca(2+)](i) oscillations and oocyte age

Intracellular calcium ([Ca(2+)](i)) rises are a hallmark of mammalian fertilization and are associated with normal activation of embryonic development. Injection of mammalian sperm cytosolic factor (SCF) into oocytes has been shown to trigger [Ca(2+)](i) rises similar to those observed during fertilization, and to initiate normal embryonic development. However, Ca(2+) release has also been shown to be associated with cell death, but the mechanisms of the detrimental effects of Ca(2+) stimulation on development have not yet been investigated. Thus, studies were undertaken using SCF to test the effects of [Ca(2+)](i) oscillations on oocyte activation in freshly ovulated and aged oocytes. Injections of 1 mg/ml SCF into freshly ovulated mouse metaphase II oocytes, which evoked Ca(2+) responses with low frequency and short duration, induced normal activation and cleavage to the two-cell stage. Conversely, injection of 15 mg/ml SCF, which triggered high-frequency and persistent Ca(2+) responses, induced abnormal activation that was characterized by abnormal chromatin configurations, inhibition of DNA synthesis, and lack of first mitotic spindle assembly. More importantly, fertilization-like Ca(2+) responses induced by injection of 1 mg/ml SCF triggered cell death, rather than activation, in in vitro-aged oocytes. These oocytes exhibited extensive cytoplasmic and DNA fragmentation that was accompanied by activation of protein caspases, all of which are signs of apoptotic cell death. Fewer similarly aged oocytes that were either unstimulated or activated with 7% ethanol underwent fragmentation. Together, these results suggest that [Ca(2+)](i) oscillations are required to activate freshly ovulated oocytes, but if initiated at abnormally high frequency and duration or if induced in aged oocytes, the [Ca(2+)](i) oscillations may trigger premature termination of embryonic development.     

RATES OF FITNESS DECLINE AND REBOUND SUGGEST PERVASIVE EPISTASIS

Unraveling the factors that determine the rate of adaptation is a major question in evolutionary biology. One key parameter is the effect of a new mutation on fitness, which invariably depends on the environment and genetic background. The fate of a mutation also depends on population size, which determines the amount of drift it will experience. Here, we manipulate both population size and genotype composition and follow adaptation of 23 distinct Escherichia coli genotypes. These have previously accumulated mutations under intense genetic drift and encompass a substantial fitness variation. A simple rule is uncovered: the net fitness change is negatively correlated with the fitness of the genotype in which new mutations appear—a signature of epistasis. We find that Fisher's geometrical model can account for the observed patterns of fitness change and infer the parameters of this model that best fit the data, using Approximate Bayesian Computation. We estimate a genomic mutation rate of 0.01 per generation for fitness altering mutations, albeit with a large confidence interval, a mean fitness effect of mutations of ?0.01, and an effective number of traits nine in mutS^? E. coli. This framework can be extended to confront a broader range of models with data and test different classes of fitness landscape models.     

The speed of Muller's ratchet with background selection, and the degeneration of Y chromosomes.

The rate of accumulation of deleterious mutations by Muller's ratchet is investigated in large asexual haploid populations, for a range of parameters with potential biological relevance. The rate of this process is studied by considering a very simple model in which mutations can have two types of effect: either strongly deleterious or mildly deleterious. It is shown that the rate of accumulation of mildly deleterious mutations can be greatly increased by the presence of strongly deleterious mutations, and that this can be predicted from the associated reduction in effective population size (the background selection effect). We also examine the rate of the ratchet when there are two classes of mutation of similar but unequal effects on fitness. The accuracy of analytical approximations for the rate of this process is analysed. Its possible role in causing the degeneration of Y and neo-Y chromosomes is discussed in the light of our present knowledge of deleterious mutation rates and selection coefficients.