Biology subjects

Pages, C.

Publications and source records attributed to Pages, C..

3 recordsLinked to original sources

bioRxiv2024

Interplay between the Xer recombination system and the dissemination of antibioresistance in Acinetobacter baumannii

Antibiotic-resistant infections pose a pressing challenge in clinical settings. Plasmids are widely recognized for hastening the emergence of resistance by facilitating horizontal gene transfer of antibiotic resistance genes among bacteria. We explore this inquiry in Acinetobacter baumannii, a globally emerging nosocomial pathogen responsible for a wide array of infections with worrying accumulation of resistances, notably involving plasmids. In this specie, plasmids of the Rep_3 family harbor adaptive genes within variable regions edged by potential site-specific recombination sites recognized by the XerCD recombinase. We first show that the Xer system of Acinetobacter baumannii functions as described in Escherichia coli, resolving chromosome dimers at the dif site as well as recombining plasmid-borne sites. The multiple Xer recombination sites found in Rep_3 plasmids do not, however, allow excising plasmid fragments. They rather recombine to co-integrate plasmids, which may then further evolve to exchange genes. Co-integrates represent a significative part of the plasmid population and their formation is controlled by the sequence of the recombination sites determining their compatibility between the recombining sites. We conclude that plasmids frequently exchange genes in Acinetobacter baumannii using Xer recombination, allowing a high level yet controlled plasticity involved in the acquisition and combination of resistance genes.

microbiology↗

bioRxiv2024

A mechanistic step in the genesis of secondary chromosomes from plasmids

Bacterial genomes contain a plethora of secondary replicons of divergent size. Circular replicons must carry a system for resolving dimeric forms, resulting from recombination between sister copies. These systems use site-specific recombinases. Among these, the XerCD recombinase resolves dimers of chromosomes and certain plasmids using different controls. We have analyzed the dimer resolution functions in enterobacterial secondary replicons and show that, in addition to the main chromosomes, XerCD is preferentially used by small plasmids and by the largest secondary replicons, megaplasmids and secondary chromosomes. Indeed, all replicons longer than 250 kb host an active XerCD recombination site. These sites, in contrast to those of small plasmids, use the same control as chromosomes, coupled to cell division by the FtsK protein. We conclude that a chromosome-like mode of dimer resolution is mandatory for the faithful inheritance of large plasmids and chromids, its acquisition being a prerequisite for the genesis of secondary chromosomes from plasmids.

microbiology↗

bioRxiv2017

Challenges in estimating heritability of phase polyphenism: Insights from measured and simulated data in the desert locust

Quantitative genetics experiments aim at understanding and predicting the evolution of phenotypic traits. Running such experiments often bring the same questions: Should I bother with maternal effects? Could I estimate those effects? What is the best crossing scheme to obtain reliable estimates? Can I use molecular markers to spare time in the complex task of keeping track of the experimental pedigree?\n\nWe explored those practical issues in the desert locust, Schistocerca gregaria using morphologic and coloration traits, known to be influenced by maternal effects. We ran quantitative genetic analyses with an experimental dataset and used simulations to explore i) the efficiency of animal models to accurately estimate both heritability and maternal effects, ii) the influence of crossing schemes on the precision of estimates and iii) the performance of a marker-based method compared to the pedigree-based method.\n\nThe simulations indicated that maternal effects deeply affect heritability estimates and very large datasets are required to properly distinguish and estimate maternal effects and heritabilities. In particular, ignoring maternal effects in the animal model resulted in overestimation of heritabilities and a high rate of false positives whereas models specifying maternal variance suffer from lack of power. Maternal effects can be estimated more precisely than heritabilities but with low power. To obtain better estimates, bigger datasets are required and, in the presence of maternal effects, increasing the number of families over the number of offspring per families is recommended. Our simulations also showed that, in the desert locust, using relatedness based on available microsatellite markers may allow reasonably reliable estimates while rearing locusts in group.\n\nIn the light of the simulation results, our experimental dataset suggested that maternal effects affected various phase traits. However the statistical limitations, revealed by the simulation approach, didnt allow precise variance estimates. We stressed out that doing simulations is a useful step to design an experiment in quantitative genetics and interpret the outputs of the statistical models.

evolutionary biology↗