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Merlet, J.

Publications and source records attributed to Merlet, J..

5 recordsLinked to original sources

Multiple pathways prevent bi-parental mitochondria transmission in C. elegans

The uniparental transmission of the maternal mitochondrial genome is achieved by the disposal of the sperm mitochondria and their DNA (mtDNA) around fertilization. C. elegans embryo allowed the identification of several factors and mechanisms involved after fertilization. The discovery that the autophagy pathway and its adaptor ALLO-1 are implicated represented a major progress. In addition, studies in fish and fly have implicated CPS-6, a sperm mitochondrial endonuclease, in the degradation of C. elegans sperm-derived mtDNA. The sperm mitochondria-associated proteins FNDC-1 and PHB-2 were also implicated in efficiently removing sperm-derived mitochondria. Despite these recent findings, it is still not clear whether they account for the complete degradation and if we can experimentally prevent sperm-mitochondria clearance and induce sperm-mtDNA transmission to the progeny. Here, we investigated the genetic interactions and tested the impact of simultaneous inactivation of known factors on the fate of sperm-derived mitochondria and their mtDNA. We revealed an additive effect of ALLO-1 and CPS-6 loss of function. Furthermore, the inactivation of known factors acting in sperm mitochondria clearance was not sufficient to avoid sperm mitochondria removal and to allow paternal mtDNA inheritance across generations. These findings reveal that C. elegans employs at least two parallel pathways to ensure the degradation of paternal mitochondria and suggest the presence of unidentified mechanism(s) safeguarding maternal mitochondrial inheritance.

developmental biology↗

Effects of host sex, age and behaviour on co-infection patterns in a wild ungulate

Recent zoonotic disease emergences reveal the importance of studying wildlife parasite communities. As wild hosts frequently harbour diverse parasite species, understanding the drivers of multiple infection patterns in free-ranging hosts is critical for elucidating the ecological and epidemiological dynamics of parasite communities. In this study, we analysed co-infection patterns in European roe deer (Capreolus capreolus) inhabiting a fragmented rural landscape in southwestern France. Using data from 130 GPS-tracked roe deer, we examined the influence of proximity to livestock, host activity levels, age, sex, and between-parasite interactions on the presence of 11 parasitic taxa. Hierarchical modelling of species communities (HMSC) revealed that proximity to livestock significantly increased the likelihood of infection with orofecally transmitted parasites (Toxoplasma gondii, gastrointestinal parasites). Sex and age were other key predictors, with males and juveniles exhibiting a higher frequency of parasite presence, likely influenced by hormonal and immune system differences. Activity levels showed distinct age-related effects, with higher activity levels being positively associated with increased parasite prevalence in yearlings, but not in adults. In contrast, parasite association patterns within individual hosts were weak, suggesting minimal interactions between parasite species. Our findings highlight the interplay between exposure and susceptibility in shaping co-infection patterns and underscore the value of hierarchical modelling approaches in multi-parasite systems. Key FindingsO_LIParasite communities, studied in 130 GPS monitored roe deer, revealed frequent co-infection. C_LIO_LIProximity to livestock increased the risk of infection by parasite taxa shared with domestic animals. C_LIO_LIFor several parasitic taxa, males and younger roe deer had a higher probability of infection. C_LIO_LIThe effect of host activity on parasite infection was dependent on roe deer age. C_LIO_LIOnly slight between-parasite interactions were detected within individual hosts. C_LI

ecology↗

Age and spatio-temporal variations in food resources modulate stress-immunity relationships in three populations of wild roe deer

Living in variable and unpredictable environments, organisms face recurrent stressful situations. The endocrine stress response, which includes the secretion of glucocorticoids, helps organisms to cope with these perturbations. Although short-term elevations of glucocorticoid levels are often associated with immediate beneficial consequences for individuals, long-term glucocorticoid elevation can compromise key physiological functions such as immunity. While laboratory works highlighted the immunosuppressive effect of long-term elevated glucocorticoids, it remains largely unknown, especially in wild animals, whether this relationship is modulated by individual and environmental characteristics. In this study, we explored the co-variation between baseline cortisol levels, assessed non-invasively using faecal cortisol metabolites (FCMs), and 12 constitutive indices of innate, inflammatory, and adaptive immune functions, in wild roe deer living in three populations with contrasting environmental conditions. Using longitudinal data on 564 individuals, we further investigated whether age and spatio-temporal variations in the quantity and quality of food resources affect the relationship between FCMs and immunity. Negative covariation with glucocorticoids was evident only for innate and inflammatory markers of immunity, while adaptive immunity appeared to be positively or not linked to glucocorticoids. In addition, the negative covariations were generally exacerbated, or revealed, in individuals facing harsh environmental constraints and in old individuals. Therefore, our results highlight the importance of measuring multiple immune markers of immunity in individuals from contrasted environments to unravel the complex relationships between glucocorticoids and immunity in wild animals. Our results also help explain conflicting results found in the literature and could improve our understanding of the long-term consequences of elevated glucocorticoid levels on disease spread and population dynamics.

ecology↗

RAD-sequencing for estimating GRM-based heritability in the wild: a case study in roe deer

Estimating the evolutionary potential of quantitative traits and reliably predicting responses to selection in wild populations are important challenges in evolutionary biology. The genomic revolution has opened up opportunities for measuring relatedness among individuals with precision, enabling pedigree-free estimation of trait heritabilities in wild populations. However, until now, most quantitative genetic studies based on a genomic relatedness matrix (GRM) have focused on long-term monitored populations for which traditional pedigrees were also available, and have often had access to knowledge of genome sequence and variability. Here, we investigated the potential of RAD-sequencing for estimating heritability in a free-ranging roe deer population for which no prior genomic resources were available. We propose a step-by-step analytical framework to optimize the quality and quantity of the genomic data and explore the impact of the SNP calling and filtering processes on the GRM structure and GRM-based heritability estimates. As expected, our results show that sequence coverage strongly affects the number of recovered loci, the genotyping error rate and the amount of missing data. Ultimately, this had little effect on heritability estimates and their standard errors, provided that the GRM was built from a minimum number of loci (above 7000). GRM-based heritability estimates thus appear robust to a moderate level of genotyping errors in the SNP dataset. We also showed that quality filters, such as the removal of low-frequency variants, affect the relatedness structure of the GRM, generating lower h2 estimates. Our work illustrates the huge potential of RAD-sequencing for estimating GRM-based heritability in virtually any natural population.

genomics↗

Fluctuating pathogen-mediated selection drives the maintenance of innate immune gene polymorphism in a widespread wild ungulate

Toll-like Receptors (TLR) play a central role in recognition and host frontline defence against a wide range of pathogens. A number of recent studies have shown that TLR genes (Tlrs) often exhibit a large polymorphism in natural populations. Yet, there is little knowledge on how this polymorphism is maintained and how it influences disease susceptibility in the wild. In a previous work, we showed that some Tlrs exhibit similarly high levels of genetic diversity than Mhc and contemporary signatures of balancing selection in roe deer (Capreolus capreolus), an abundant and widespread ungulate in Europe. Here, we tested whether Mhc-Drb or Tlr (Tlr2, Tlr4 and Tlr5) diversity is driven by pathogen-mediated selection. We examined the relationships between their genotype (heterozygosity status and presence of specific alleles) and infections with Toxoplasma and Chlamydia, two intracellular pathogens known to cause reproductive failure in ungulates. We showed that Toxoplasma and Chlamydia exposures vary significantly across year and landscape structure with few co-infection events detected, and that the two pathogens act antagonistically on Tlr2 polymorphism. By contrast, we found no evidence of association with Mhc-Drb and a limited support for Tlr heterozygosity advantage. Our study confirmed the importance of looking beyond Mhc genes in wildlife immunogenetic studies. It also emphasized the necessity to consider multiple pathogen challenges and their spatiotemporal variation to improve our understanding of vertebrate defence evolution against pathogens.

evolutionary biology↗