Biology subjects

Saclier, N.

Publications and source records attributed to Saclier, N..

5 recordsLinked to original sources

bioRxiv2026

Protein response to deleterious episodes of GC-biased gene conversion in mammals of different Ne

GC-biased gene conversion (gBGC) is a widespread recombination-associated process that favours the fixation of GC alleles independently of their fitness. In coding regions, it can oppose purifying selection and favour the accumulation of deleterious AT to GC mutations. In mammals where recombination hotspots are predominantly determined by PRDM9, the deleterious effect of gBGC is expected to be episodic due to the rapid turnover of hotspots. The deleterious impact of gBGC episodes on proteins has been well documented, particularly in rodents and primates. However, the evolutionary response of the affected proteins after the episodes end has been scarcely investigated. Theory predicts that a decline in gBGC intensity should trigger a compensatory response that enables previous damage to be repaired. Recently, we reported evidence for pervasive compensatory evolution following gBGC episodes in Hydromyini rodents. Here, we aimed to investigate whether this post- gBGC compensation is widespread among mammals in which gBGC is episodic. Using a phylogenetic approach, we analysed substitution patterns in coding exons from five mammalian taxa spanning a range of effective population size (Ne): Murini, Rattini, Cetacea, Cercopithecidae and Hominoidae. We detected thousands of gBGC episodes, characterised by an increased rate of non-synonymous AT to GC substitutions. We found evidence for compensatory evolution in non-primate taxa, and a lack of signal in Primates. Although the influence of Ne remains unclear, our study highlights both the evolutionary significance of post-gBGC compensation and the methodological challenges in detecting it.

genomics↗

bioRxiv2025

Emergence and stabilisation of a neo-Y chromosome in nematode species with rare males

How do sex chromosomes evolve in the transition to asexuality? So far, species that depart from canonical sexual reproduction - for example, parthenogens with rare sex, or species where the paternal genome is set aside - have been found to carry either no sex chromosomes, or sex chromosomes but no male-specific sex chromosome (i. e., no Y). Here we reveal that, in Mesorhabditis nematodes, a new Y chromosome emerged once, from sexual ancestors, in species that have transitioned into an unconventional mode of reproduction called autopseudogamy. In this reproductive system, females produce clonal females plus rare ([~]10%) males that are needed for fertilisation, but that do not contribute to the female genome. Analysing the Y chromosomes of two autopseudogamous species, we found high levels of degeneration, most likely due to loss of recombination, and two additional conserved features: i) they accumulated male-beneficial genes, and ii) they display a strong fertilisation drive, in that mainly Y-bearing sperm fertilise female oocytes. Both features are likely evolutionarily favourable in the context of autopseudogamy. Our results suggest that male-specific chromosomes can still be maintained in systems with rare, and possibly genetically useless, males.

evolutionary biology↗

bioRxiv2025

Molecular re-adaptation: compensatory evolution following deleterious episodes of GC-biased gene conversion in rodents

GC-biased gene conversion (gBGC) is a widespread evolutionary force associated with meiotic recombination that favours the accumulation of deleterious AT to GC substitutions in proteins, moving them away from their fitness optimum. In many mammals recombination hotspots have a rapid turnover, leading to episodic gBGC, with the accumulation of deleterious mutations stopping when the recombination hotspot dies. Selection is therefore expected to act to repair the damage caused by gBGC episodes through compensatory evolution. However, this process has never been studied or quantified so far. Here, we analysed the nucleotide substitution pattern in coding sequences of a highly diversified group of Murinae rodents. Using phylogenetic analyses of about 70,000 coding exons, we identified numerous exon-specific, lineage-specific gBGC episodes, characterised by a clustering of synonymous AT to GC substitutions and by an increasing rate of non-synonymous AT to GC substitutions, many of which are potentially deleterious. Analysing the molecular evolution of the affected exons in downstream lineages, we found evidence for pervasive compensatory evolution after deleterious gBGC episodes. Compensation appears to occur rapidly after the end of the episode, and to be driven by the standing genetic variation rather than new mutations. Our results demonstrate the impact of gBGC on the evolution of amino-acid sequences, and underline the key role of epistasis in protein adaptation. This study contributes to a growing body of literature emphasizing that adaptive mutations, which arise in response to environmental changes, are just one subset of beneficial mutations, alongside mutations resulting from oscillations around the fitness optimum.

genomics↗

bioRxiv2024

Transcriptomic bases of within- and trans-generational predator-induced plasticity in the freshwater snail Physa acuta

Inducible defences in response to predation risk are a well-known example of adaptive phenotypic plasticity. Although inducible defences have been studied mainly within a generation (within-generational plasticity), there is now clear evidence that ancestral exposure to predation risk can influence the defences expressed by offspring, even if they have not been exposed themselves (transgenerational plasticity). The molecular mechanisms allowing the transmission of environmental information across generations are not well understood. In this study, we combined measures of antipredator responses (behavioural and morphological) with transcriptomic investigations across two generations in the freshwater snail Physa acuta. We hypothesised that both within- and transgenerational plasticity would induce phenotypic changes associated with differential gene expression. Our results confirmed within- and transgenerational plasticity: F1 snails respond to predator-cue exposure by increasing escape behaviour, reducing shell length, and developing thicker and slenderer shells, whereas F2 snails from exposed parents have longer and thicker shells with narrower apertures. Within- and transgenerational plasticity were accompanied by the differential expression of 112 genes (101 up- and 11 downregulated) and 23 differentially expressed genes (17 up- and 6 downregulated), respectively. Within- and transgenerational plasticity did not share common differentially expressed genes, but the associated molecular functions, involving metabolism and transcription regulation, were similar. These results suggest that predator-induced within-generational plasticity and transgenerational plasticity may result from different genomic pathways and may evolve independently.

evolutionary biology↗

bioRxiv2020

Bedrock radioactivity influences the rate and spectrum of mutation

All organisms on Earth are exposed to low doses of natural radioactivity but some habitats are more radioactive than others. Yet, documenting the influence of natural radioactivity on the evolution of biodiversity is challenging. Here, we addressed whether organisms living in naturally more radioactive habitats accumulate more mutations across generations using 14 species of waterlice living in subterranean habitats with contrasted levels of radioactivity. We found that the mitochondrial and nuclear mutation rates across a waterlouse species genome increased on average by 60 and 30%, respectively, when radioactivity increased by a factor of three. We also found a positive correlation between the level of radioactivity and the probability of G to T (and complementary C to A) mutations, a hallmark of oxidative stress. We conclude that even low doses of natural bedrock radioactivity influence the mutation rate through the likely accumulation of oxidative damage, in particular in the mitochondrial genome.

evolutionary biology↗