Biology subjects

Girard, F.

Publications and source records attributed to Girard, F..

6 recordsLinked to original sources

bioRxiv2026

Genome-wide chromatin reset at the onset of leg regeneration in pancrustaceans

Regeneration requires injured tissues to selectively reactivate certain developmental programs while triggering regeneration-specific mechanisms and responding to the immediate consequences of tissue damage. How chromatin states are reorganized during this transition, and whether the underlying sequence of regulatory events is conserved across regenerating animals, remain poorly understood. We address these questions in the two-spotted cricket Gryllus bimaculatus, in which limb regeneration progressively declines during nymphal development and is absent in adults, and extend our analysis to the crustacean Parhyale hawaiensis. We first establish a chromosome-scale genomic and epigenomic framework for the cricket and then follow chromatin and transcriptional changes after limb amputation. Amputation triggers a striking genome-wide shutdown of enhancer-associated chromatin, marked by loss of accessible regulatory regions and depletion of H3K27ac and H3K4me1. This is followed, in regeneration-competent tissue, by selective reopening of a restricted population of regulatory elements and strong induction of the pioneer transcription factor Zelda (GbZelda). The GbZelda locus is unusually marked by both H3K27me3 and H3K9me3 in intact leg tissue; after injury, H3K9me3 is reduced broadly, whereas H3K27me3 is selectively relieved in regenerating nymphs. Finally, analysis of Parhyale reveals the same sequence of chromatin events during appendage regeneration: an initial enhancer shutdown followed by selective regulatory reopening concomitant with Zelda upregulation. Thus, rather than restoring the pre-injury regulatory landscape wholesale, appendage regeneration in these two pancrustacean models proceeds through a conserved sequence of genome-wide chromatin resetting, selective regulatory reopening and activation of a pioneer transcription factor.

developmental biology↗

bioRxiv2025

Bacteriophage PAK_P3 genome structuration and dynamics during infection of Pseudomonas aeruginosa reveal specific interactions patterns

Bacteriophages, or phages, are highly abundant and diverse genomic entities that play an important role in microbial ecology, evolution, and horizontal gene transfer. While the dynamic changes in genome organization in cellular organisms have been well described, the 3D folding of phage genomes during the infection of their host is extremely limited. Understanding how phage genomes fold, invade and rearrange the genome of their host to functionally organize the optimal expression of their genes remains unknown. Here, we explore the spatial dynamics of the virulent double-stranded DNA phage PAK_P3 during infection of its host Pseudomonas aeruginosa and reveal how its genome rapidly decondenses to adopt a specific 3D organization that reflects its transcriptional program. Concomitantly, the host genome decondenses as gene expression wanes and transcription induced domains vanish. We also uncover specific and discrete bridging of the host and the phage genomes, showing how the phage genome exploits the spatial genome architecture of its host to succeed in its infection cycle. Our data highlights an unprecedented level of genome folding and gene expression regulation during a viral infection.

microbiology↗

bioRxiv2025

High-severity fires undermine resilience of black spruce-dominated boreal forests in eastern North America

Climate-induced fire regime shifts may reduce post-fire resilience of black spruce-dominated (BS; Picea mariana) North American boreal forests. While post-fire vulnerability of immature BS stands has been extensively studied, no study has evaluated simultaneous effects of fire severity and seasonality on the post-fire regeneration of mature (> 60-year-old) BS stands. This study aims to quantify post-fire regeneration levels of BS and co-occurring tree species to assess ecosystem recovery and possible loss of resilience due to regeneration failure. We analyzed effects of seed bank conditions, fire regime characteristics (fire severity and seasonality), and seedbed conditions on BS post-fire regeneration in mature forests in Quebec, Canada. Post-fire regeneration density was extensively surveyed across [~]50 400 km2 through a network of 536 plots that were distributed in 21 fires, which burned between 1995 and 2016. One-third of plots failed to regenerate (< 1750 conifer seedlings/ha) at levels adequate to produce closed-crown forest, whereas one-fifth experienced compositional changes, mainly towards jack pine (JP; Pinus banksiana) dominance. Pre-fire basal area of BS and living Sphagnum ground cover increased BS post-fire regeneration, whereas high-severity crown fires and spring fires reduced it. These findings suggest that mature BS-dominated forests may lose resilience in response to high-severity and spring fires. Given the projected increase in fire severity, and the extension towards an early-fire season in response to climate change, our study suggests that post-fire regeneration failure may become more frequent over the coming decades, with potential negative consequences on ecosystem services that are provided by BS-dominated boreal forests.

ecology↗

bioRxiv2023

Anchoring of parasitic plasmids to inactive regions of eukaryotic chromosomes through nucleosome signal

Natural plasmids are common in prokaryotes but few have been documented in eukaryotes. The natural 2{micro} plasmid present in budding yeast Saccharomyces cerevisiae is one of the most well characterized. This highly stable genetic element coexists with its host for millions of years, efficiently segregating at each cell division through a mechanism that remains poorly understood. Using proximity ligation (Hi-C, Micro-C) to map the contacts between the 2{micro} and yeast chromosomes under dozens of different biological conditions, we found that the plasmid tether preferentially on regions with low transcriptional activity, often corresponding to long inactive genes. Common players in chromosome structure such as members of the structural maintenance of chromosome complexes (SMC) are not involved in these contacts which depend instead on a nucleosomal signal associated with a depletion of RNA Pol II. These contacts are stable throughout the cell cycle, and can be established within minutes. This strategy may involve other types of DNA molecules and species other than S. cerevisiae, as suggested by the binding pattern of the natural plasmid along the silent regions of the chromosomes of Dictyostelium discoideum.

genomics↗

bioRxiv2020

Cohesin regulates homology search during recombinational DNA repair

Homologous recombination (HR) is a ubiquitous DNA double-strand break (DSB) repair mechanism that promotes cell survival. It entails a potentially genome-wide homology search step, carried out along a conserved RecA/Rad51-ssDNA nucleoprotein filament (NPF) assembled on each DSB ends1-3. This search is subdued to NPF-dsDNA collision probability, dictated in part by chromatin conformation2,4. In contrast to the extensive knowledge about chromatin composition and mobility changes elicited by the DNA damage checkpoint (DDC)5-7, whether, how, and to which extent a DSB impacts spatial chromatin organization, and whether this organization in turns influences the homology search process, remains ill-defined8,9. Here we characterize two layers of spatial chromatin reorganization following DSB formation in S. cerevisiae. While cohesin folds chromosomes into cohesive arrays of 10-20 kb long chromatin loops as cells arrest in G2/M10,11, the DSB-flanking regions locally interact in a resection- and 9-1-1 clamp-dependent manner, independently of cohesin and HR proteins. This local structure blocks cohesin progression, constraining the extending NPF at loop base. Functionally this organization promotes side-specific cis DSB-dsDNA interactions that scales with loop expansion span, and provides a kinetic advantage for identification of intra- over inter-chromosomal homologies. We propose that cohesins regulate homology search by promoting cis dsDNA over-sampling, both upon loop expansion-coupled unidimensional dsDNA scanning, NPF trapping, and chromosome individualization, largely independent of their role in sister chromatid cohesion.

genetics↗

bioRxiv2020

The enrichment of breakpoints in late-replicating chromatin provides novel insights into chromoanagenesis mechanisms

The rise of pangenomic molecular assays allowed uncovering complex rearrangements named chromoanagenesis that were hypothesized to result from catastrophic shattering events. Constitutional cases have typically been reported individually preventing identification of common features and uncovering the mechanisms at play. We characterized 20 new chromoanagenesis and discovered yet undescribed features. While literature differentiates chromothripsis and its shattering event repaired through non-homologous end joining from chromoanasynthesis born to aberrant replicative processes, we identified shattered chromosomes repaired through a combination of mechanisms. In particular, three samples present with "rearrangement hubs" comprising a fragmented kilobase-long sequence threaded throughout the rearrangement. To assess the mechanisms at play, we merged our data with those of 20 published constitutional complex chromosomal rearrangement cases. We evaluated if the distribution of their 1032 combined breakpoints was distinctive using bootstrap simulations and found that breakpoints tend to keep away from haplosensitive genes suggesting selective pressure. We then compared their distribution with that of 13,310 and 468 breakpoints of cancer complex chromosomal rearrangements and constitutional simple rearrangement samples, respectively. Both complex rearrangement groups showed breakpoint enrichment in late replicating regions suggesting similar origins for constitutional and cancer cases. Simple rearrangement breakpoints but not complex ones were depleted from lamina-associated domains (LADs), possibly as a consequence of reduced mobility of DNA ends bound to lamina. The enrichment of breakpoints in late-replicating chromatin for both constitutional and cancer chromoanagenesis provides an orthogonal support to the premature chromosome condensation hypothesis that was put forward to explain chromoanagenesis.

genomics↗