Diseases and reproductive success in a wild mammal: example in the alpine chamois

Density-dependent and climatic factors affect reproduction and dynamics of wild ungulates. Parasites can also decrease reproductive success through either a direct abortive effect or a negative impact on host growth and body condition. However, few studies have investigated the effect of parasitism on fecundity of ungulates in natural conditions. We studied three bacterial infections caused by Salmonella enterica serovar Abortusovis, Chlamydophila abortus and Coxiella burnetii. These bacteria are leading causes of reproductive failure in sheep, goat and cattle, which raises the question of their influence on population dynamics of wild ungulates. A long-term study of demography and epidemiology of an alpine chamois (Rupicapra rupicapra, L.) population (Les Bauges Reserve, France) and a generalized linear modeling approach were used to analyze the reproductive success of chamois according to population density, weather conditions and the prevalence of antibodies against the three bacteria in females. This approach enabled us to identify the confounding effect of weather and parasitism on fecundity in a natural population. After accounting for density, the prevalence of antibodies against the three bacteria explained 36% of the annual variation in reproductive success, and weather conditions explained an additional 31%. This study was, to our knowledge, the first to compare the decrease in fecundity due to bacterial infections and weather conditions in a population of wild mountain ungulates.     

Secondary response of in vitro primed human lymphocytes to allogeneic cells

The secondary response of human lymphocytes primed in vitro with allogeneic lymphocytes is reported. Accelerated proliferation is observed ' both against the specific priming cell and against unrelated third party cells, but the intensity of proliferation against the specific cell is usually, but not always, higher than that against third party cells. To clarify the respective roles ofHL-A andMLR-S in the development of this secondary proliferative response, three kinds of cells were used from which MLR-S activity was supposed to have been abolished while serologically-defined HL-A antigens were present: (a) heattreated cells, (b) UV-treated cells, and (c) a recombinant betweenHL-A andMLR-S. Heat treated cells were unsatisfactory for this study, but UV-treated and recombinant cells showed thatMLR-S was sufficient and necessary both for priming and for eliciting a secondary proliferative response. No role could be found forHL-A or for a secondMLR-S locus positioned between the first and secondHL-A loci.     

Two-component systems in Pseudomonas aeruginosa: why so many?

Screening the Pseudomonas aeruginosa genome has led to the identification of the highest number of putative genes encoding two-component regulatory systems of all bacterial genomes sequenced to date (64 and 63 encoding response regulators and histidine kinases, respectively). Sixteen atypical kinases, among them 11 devoid of an Hpt domain, and three independent Hpt modules were retrieved. These data suggest that P. aeruginosa possesses complex control strategies with which to respond to environmental challenges.     

A Recessive Skeletal Dysplasia, SEMD Aggrecan Type, Results from a Missense Mutation Affecting the C-Type Lectin Domain of Aggrecan

Analysis of a nuclear family with three affected offspring identified an autosomal-recessive form of spondyloepimetaphyseal dysplasia characterized by severe short stature and a unique constellation of radiographic findings. Homozygosity for a haplotype that was identical by descent between two of the affected individuals identified a locus for the disease gene within a 17.4 Mb interval on chromosome 15, a region containing 296 genes. These genes were assessed and ranked by cartilage selectivity with whole-genome microarray data, revealing only two genes, encoding aggrecan and chondroitin sulfate proteoglycan 4, that were selectively expressed in cartilage. Sequence analysis of aggrecan complementary DNA from an affected individual revealed homozygosity for a missense mutation (c.6799G → A) that predicts a p.D2267N amino acid substitution in the C-type lectin domain within the G3 domain of aggrecan. The D2267 residue is predicted to coordinate binding of a calcium ion, which influences the conformational binding loops of the C-type lectin domain that mediate interactions with tenascins and other extracellular-matrix proteins. Expression of the normal and mutant G3 domains in mammalian cells showed that the mutation created a functional N-glycosylation site but did not adversely affect protein trafficking and secretion. Surface-plasmon-resonance studies showed that the mutation influenced the binding and kinetics of the interactions between the aggrecan G3 domain and tenascin-C. These findings identify an autosomal-recessive skeletal dysplasia and a significant role for the aggrecan C-type lectin domain in regulating endochondral ossification and, thereby, height.