Role of recombination in the evolution of the model plant pathogen Pseudomonas syringae pv. tomato DC3000, a very atypical tomato strain

Pseudomonas syringae pv. tomato strain DC3000 (PtoDC3000) is one of the most intensively studied bacterial plant pathogens today. Here we report a thorough investigation into PtoDC3000 and close relatives isolated from Antirrhinum majus (snapdragon), Apium graveolens (celery), and Solanaceae and Brassicaceae species. Multilocus sequence typing (MLST) was used to resolve the precise phylogenetic relationship between isolates and to determine the importance of recombination in their evolution. MLST data were correlated with an analysis of the locus coding for the type III secreted (T3S) effector AvrPto1 to investigate the role of recombination in the evolution of effector repertoires. Host range tests were performed to determine if closely related isolates from different plants have different host ranges. It was found that PtoDC3000 is located in the same phylogenetic cluster as isolates from several Brassicaceae and Solanaceae species and that these isolates have a relatively wide host range that includes tomato, Arabidopsis thaliana, and cauliflower. All other analyzed tomato isolates from three different continents form a distinct cluster and are pathogenic only on tomato. Therefore, PtoDC3000 is a very unusual tomato isolate. Several recombination breakpoints were detected within sequenced gene fragments, and population genetic tests indicate that recombination contributed more than mutation to the variation between isolates. Moreover, recombination may play an important role in the reassortment of T3S effectors between strains. The data are finally discussed from a taxonomic standpoint, and P. syringae pv. tomato is proposed to be divided into two pathovars.     

Absence of male reproductive skew,along with high frequency of polyandry and conspecific brood parasitism in the lekking Houbara bustard Chlamydotis undulata undulata

Behavioural studies have led to the perception that lekking species experience a high male reproductive skew as a consequence of females’ selective mate choice. In addition, observations suggest that females copulate only once and therefore polyandry seems unlikely as females are supposed to choose the best male available. In order to analyse the mating strategy of the Houbara bustard, an endangered lekking species under reinforcement in eastern Morocco, we used microsatellite data to perform paternity analyses. None of our observations followed common expectations under a lek mating system: we found no male reproductive skew suggesting no apparent selective female mate choice and no apparent male benefit from lekking. In contrast, a high level of polyandry (60 % of the nests) was recorded suggesting that sperm competition may operate. In addition, we present another case of conspecific brood parasitism in a lekking species and this was an unexpected alternative strategy for a species presenting high parental cost and low fecundity. The increasing number of studies contradicting common assumptions on lekking species suggests that alternative breeding strategies such as males pursuing an off‐lek mating strategy, female polyandry and even conspecific brood parasitism might be more widespread in lekking species than previously thought.     

Parameter inference for biochemical systems that undergo a Hopf bifurcation

The increasingly widespread use of parametric mathematical models to describe biological systems means that the ability to infer model parameters is of great importance. In this study, we consider parameter inferability in nonlinear ordinary differential equation models that undergo a bifurcation, focusing on a simple but generic biochemical reaction model. We systematically investigate the shape of the likelihood function for the model's parameters, analyzing the changes that occur as the model undergoes a Hopf bifurcation. We demonstrate that there exists an intrinsic link between inference and the parameters’ impact on the modeled system's dynamical stability, which we hope will motivate further research in this area.     

Adaptive Changes in Postsynaptic Dopamine Receptors Despite Unaltered Dopamine Dynamics in Mice Lacking Monoamine Oxidase B

Monoamine oxidase (MAO) B is considered a key enzyme in dopamine metabolism. The present studies, conducted in MAO B knockout mice, show that lack of MAO B does not alter extracellular levels of dopamine in striatum. Similarly, the synthesis, storage, uptake, and release of dopamine are also unaltered. However, autoradiography revealed a significant up-regulation of the D2-like dopamine receptors in the striatum of MAO B knockout mice. Mutant mice also exhibit a functional supersensitivity of D1-dopamine receptors in the nucleus accumbens. Thus, the agonist SKF 38,393-induced c-Fos immunoreactivity was significantly increased in knockout mice as compared with wild-type controls. In view of the apparently normal basal dopamine dynamics observed in MAO B knockout mice, we hypothesize that a dopamine-independent mechanism underlies adaptations in dopamine receptor function that occur as a consequence of MAO B depletion. Finally, these findings suggest that chronic administration of MAO inhibitors, as occurs in the treatment of Parkinson's disease and depression, may be associated with an increased responsiveness of CNS neurons to dopamine receptor ligands.     

Disturbances in glucose-tolerance, insulin-release, and stress-induced hyperglycemia upon disruption of the Ca(v)2.3 (alpha 1E) subunit of voltage-gated Ca(2+) channels

Multiple types of voltage-activated Ca(2+) channels (T, L, N, P, Q, R type) coordinate Ca(2+)-dependent processes in neurons and neuroendocrine cells. Expressional and functional data have suggested a role for Ca(v)2.3 Ca(2+) channels in endocrine processes. To verify its role in vivo, Ca(v)2.3(-/-) mutant mice were generated, thus deficient in alpha 1E/R-type Ca(2+) channel. Intraperitoneal injection of D-glucose showed that glucose tolerance was markedly reduced, and insulin release into plasma was impaired in Ca(v)2.3-deficient mice. In isolated islets of Langerhans from these animals, no glucose-induced insulin release was detected. Further, in stressed Ca(v)2.3-deficient mice, the rate of glucose release into the blood was only 29% of that observed for wild-type animals. Thus, the deletion of Ca(v)2.3 causes deficits not only in insulin release but also in stress-induced hyperglycemia. The complex phenotype of Ca(v)2.3-deficient mice has dual components related to endocrine and neurological defects. The present findings provide direct evidence of a functional role for the Ca(v)2.3 subunit in hormone secretion and glucose homeostasis.     

Genes associated with the end of dormancy in grapes

A grape bud EST library was constructed and 4,270 ESTs sequenced. The library clones were arrayed for the purpose of investigating the level of gene expression over time, particularly leading up to the buds release from dormancy. The arrays were hybridized with P³³-labeled probes produced from samples of buds collected at weekly intervals. These probes covered the time from 9 weeks prior to bud burst until just after the emergence of the shoots. Expression patterns from these genes have been examined. It was found that 74% of the genes in the data set were homologous to known proteins. Genes were then assigned to functional categories according to their primary BLAST match. Of these 13% were involved with photosynthesis, 13% with disease resistance and defense, 5% energy, 12% metabolism, 20% protein production and processing, 25% cell structure and plant growth and the remaining 12% were unclassified The expression pattern of a selection of candidate genes retrieved from literature previously reporting an association with dormancy changes was assessed. On closer examination most of these genes relate to the oxidative processes and stress responses within the cell. The results of this study show that even in the dormant state, gene expression in the buds is high.     

Increased salt sensitivity secondary to leptin resistance in SHHF rats is mediated by endothelin

A link between leptin resistance, obesity, and salt sensitivity has been suggested. SHHF/Mcc-fa ^cp rats (SHHF) were used to study the effect of gene dosage of a null mutation of the leptin receptor (cp) on salt sensitivity and response to a combined endothelin A and B receptor antagonist (bosentan). Obese (cp/cp), heterozygous (+/cp), and homozygous lean (+/+) male SHHF were fed a low salt diet (0.3% NaCl) for 7 days, followed by a high salt diet (8.0% NaCl) for 7 days. There were no significant differences in systolic blood pressure between genotypes on low salt. In response to high salt, cp/cp had significantly greater systolic pressure than +/cp and +/+. On high salt diet, cp/cp showed a significant increase in 24 h urinary endothelin excretion and increased renal expression of preproendothelin mRNA. There was no effect of high salt diet on renal excretion of nitric oxide (NOx) or on gene expression of endothelial, neuronal, or cytokine-induced nitric oxide synthase isoforms (eNOS, nNOS, iNOS, respectively). Treatment with bosentan prevented the high salt-induced increment in systolic blood pressure in cp/cp. This was associated with a doubling of renal NOx excretion, but without changes in eNOS, nNOS, or iNOS expression. Endothelin receptor antagonism did not normalize systolic pressure in any of the genotypes. Our studies indicate that obesity secondary to leptin resistance (cp/cp) results in increased salt sensitivity that is mediated by endothelin in the SHHF rat.