Biology subjects

Burban, C.

Publications and source records attributed to Burban, C..

3 recordsLinked to original sources

bioRxiv2024

Insect-habitat-plant interaction networks provide guidelines to mitigate the risk of transmission of Xylella fastidiosa to grapevine in Southern France

O_LIXylella fastidiosa (Xf) is a xylem-limited bacterium that has been recorded in several European countries since its detection in 2013 in Apulia (Italy). Given the prominence of the wine industry in many southern European countries, a big threat is the development of Pierces disease in grapevines. Yet, the insect-habitat and insect-plant interaction networks in which xylem feeders, possible vectors of Xf, are involved around European vineyards are largely unknown. C_LIO_LIHere we describe these networks in three important wine-growing regions of southern France (Provence-Alpes-Cote dAzur, Occitanie, Nouvelle-Aquitaine) to identify the main source habitats of xylem feeders, and to gather information about their specialization degree at the habitat, plant family, and plant species levels. A total of 92 landscapes (and 700 sites) were studied over three sampling sessions in the fall 2020, the spring 2021, and the fall 2021. C_LIO_LIAmong the habitats sampled, meadows hosted the largest xylem feeder communities, followed by alfalfa fields. Vineyard headlands and inter-rows hosted slightly smaller xylem feeder communities, indicating that potential Xf vectors were thriving in the close vicinity of vulnerable plants. Finally woody habitats in general and grapevines in particular hosted very few xylem feeders, showing that transfer on vulnerable plants are rare, but not inexistent. In terms of specialization degrees, Philaenus spumarius, Aphrophora alni, Lepyronia coleoptrata, and Cicadella viridis were all similarly generalists at the habitat, plant family or plant species level. The only specialist was Aphrophora grp. salicina, which was restricted to riparian forests, and more specifically to Salicaceae. Neophilaenus spp. were extremely specialist at the plant family level (Poaceae), but rather generalist at the habitat and plant species levels. All 1017 insects screened for the presence of Xf tested negative, showing that Xf is not widespread in the studied regions. C_LIO_LIOur study provides new basic ecological information on potential vectors of Xf, especially on their specialization and feeding preferences, as well as practical information that may be relevant for the design of epidemiological surveillance plans. C_LI

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↗