Biology subjects

Lepoittevin, C.

Publications and source records attributed to Lepoittevin, C..

4 recordsLinked to original sources

bioRxiv2025

Variation in aggressiveness plasticity between northern and southern European populations of Hymenoscyphus fraxineus, an invasive fungal pathogen of ash

Hymenoscyphus fraxineus is an invasive fungal pathogen responsible for the ash dieback epidemic, which continues to cause severe mortality of common ash (Fraxinus excelsior L.) across Europe. Following its likely introduction in northeastern Europe, the pathogen rapidly colonized most regions where common ash is present. As it spread southward, H. fraxineus encountered warmer climates and a higher occurrence of Fraxinus ornus L.), a species resistant to the disease, which may have imposed novel selective pressures on H. fraxineus at the epidemic front. Virulence is a key trait that is expected to evolve during epidemics and to exhibit plasticity in response to environmental variation. We investigated whether the plasticity of virulence in response to temperature and ash species has evolved in H. fraxineus. Using leaf inoculations, we characterized individual reaction norms for virulence in a long-established Lithuanian population and a recently established Italian population of H. fraxineus. At moderate temperature, the two H. fraxineus populations showed similar levels of virulence on F. excelsior. Virulence decreased to a similar extent on F. ornus in both pathogen populations, indicating similar plasticity of their virulence in relation to ash species. Interestingly, increasing temperature reduced virulence in the Lithuanian population but did not significantly change the virulence expressed by the Italian population, which remained stable across temperatures. Although these findings warrant further investigation, they suggest that ash populations in southern Europe may be more vulnerable to ash dieback under warm conditions than previously anticipated.

evolutionary biology↗

bioRxiv2025

Near-infrared spectroscopy-based models correctly classify Abies alba seed origin and predict germination properties

Forestry industry requires high-quantity and quality seeds for afforestation and assisted migration programs. Finding reliable non-destructive methods to characterize seeds would significantly enhance efforts to identify climate-adapted populations. This study presents near-infrared (NIR) spectroscopy models to classify seed origin and predict germination characteristics at different temperatures non-destructively. We focus on Abies alba Mill., a key European forest tree with genetic variation along climatic gradients and seeds with shallow physiological dormancy. Seeds from six populations were analyzed using NIR spectroscopy, and germination was tested at 15{degrees}C, 20{degrees}C, and 25{degrees}C after stratification treatments at 4{degrees}C (0 or 3 weeks). Population classification accuracy using Partial Least Squares Discriminant Analysis was 69%, with significant NIR peaks at 1712, 1929, and 2111 nm, linked to moisture content and storage compounds. NIR spectra explained 51% and 65% of the variation in germination probability and timing using Partial Least Squares Regression, with significant peaks at 1712, 1929, 2111, 1632, and 2073 nm. General Linear Mixed-Effects Models showed that a NIR predictor contributed to 39% of the germination probability variance explained by fixed-effects, and the stratification treatment was the most important driver explaining germination time. Our results proved the utility of NIR-based tools to effectively classify bulked seeds and predict germination, opening new perspectives to nursery and forestry sectors and populations adaptation and adjustments to warming climate. This study will facilitate further investigations on the physiological processes that occur during dormancy, a critical process for forest regeneration given the expected impact of shorter and warmer winters on seed behavior.

ecology↗

bioRxiv2023

Demographic and genetic impacts of powdery mildew in a young oak cohort

The demographic and genetic impacts of powdery mildew on the early stages of an oak population were studied in an ad hoc field design with two disease exposures. This enabled a detailed phenotypic monitoring of 1,733 emerging individuals from 15 progenies over nine years, and the genotyping of 68% of them. The pathogen induced high levels of seedling mortality several years after sowing, associated with reduced growth and capacity to overwinter. The probability of juvenile survival could be predicted from mean disease severity in early years and acorn weight. Fast-growing families showed the highest survival rate under both natural and protected disease exposure. Correlatively, no equalizing effect of increased powdery mildew pressure on the relative contribution of mother trees to the next generation could be detected. Contrary to a possible trade-off hypothesis between growth and defense, family height potential was not negatively related to disease resistance across the studied oak mother trees. Overall, our results suggest that in Quercus robur natural populations, infection levels (related to resistance sensu stricto) may be less determinant than growth-related tolerance to infection for the fate of seedlings. However, an equalizing effect of powdery mildew on relative oak genotype performances cannot be excluded at later stages since such an effect was already visible on height. Average genomic diversity was not significantly affected by mortality associated with powdery mildew. However, our study brings support to a deleterious effect of very low individual heterozygosity on the probability of survival across the different families. Finally, our study points to a few candidate genes for several fitness-related traits.

plant biology↗

bioRxiv2018

High-quality SNPs from genic regions highlight introgression patterns among European white oaks (Quercus petraea and Q. robur).

The Src homology-2 domain containing phosphatase SHP2 is a critical regulator of signal transduction, being implicated in cell growth and differentiation. Activating mutations cause developmental disorders and act as oncogenic drivers in hematologic cancers. SHP2 is activated by phosphopeptide binding to the N-SH2 domain, triggering the release of N-SH2 from the catalytic PTP domain. Based on early crystallographic data, it has been widely accepted that opening of the binding cleft of N-SH2 serves as the key "allosteric switch" driving SHP2 activation. To test the putative coupling between binding cleft opening and SHP2 activation as assumed by the "allosteric switch" model, we critically reviewed structural data of SHP2 and we used extensive molecular dynamics (MD) simulation and free energy calculations of isolated N-SH2 in solution, SHP2 in solution, and SHP2 in a crystal environment. Our results demonstrate that the binding cleft in N-SH2 is constitutively flexible and open in solution, and that a closed cleft found in certain structures is a consequence of crystal contacts. The degree of opening of the binding cleft has only a negligible effect on the free energy of SHP2 activation. Instead, SHP2 activation is greatly favored by the opening of the central {beta}- sheet of N-SH2. We conclude that opening of the N-SH2 binding cleft is not the key allosteric switch triggering SHP2 activation. Significance StatementSHP2 is a multi-domain protein, playing an important role in up-regulating cellular processes such as cell survival, proliferation, and programmed cell death. SHP2 mutations cause developmental disorders and were found in many cancer types, including neuroblastoma, breast cancer, and leukemia. In healthy cells, SHP2 mainly takes an autoinhibited, inactive form, and SHP2 is activated upon binding of phosphopeptides to the N-SH2 domain. For the past two decades, the widening of the binding cleft upon peptide binding has been considered as the key event driving SHP2 activation. Here, by analyzing crystallographic data and molecular simulations, we demonstrate that the binding cleft in N-SH2 is, instead, already open and accessible in solution, and its degree of opening does not influence SHP2 activation.

evolutionary biology↗