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Thesis

English

ID: <

10670/1.qv08ak

>

Where these data come from
Genetic bases of natural variation of Arabidopsis thaliana response to Ralstonia solanacearum in a global warming context

Abstract

In the context of climate warming, global surface temperature is predicted to increase from 1.5 to 4.8°C by the end of the century and extreme climatic events are expected to become more frequent. These changes will affect plant development and favor the poleward geographic migration of pathogens. Thus, plants will be facing an increased risk of epidemics as well as the emergence of new highly aggressive pathogen species. As a consequence, crop yields losses are anticipated and food security is put at risk. Alarmingly, several studies showed that an increase of temperature inhibits most of the major known resistance mechanisms. However, the underlying molecular mechanisms are still poorly characterized. In my thesis project, by exploiting natural genetic variation in Arabidopsis thaliana, I aimed to identify and characterize the genetic bases of resistance mechanisms remaining efficient at elevated temperature to Ralstonia solanacearum, one of the most harmful pathogenic phytobacteria causing bacterial wilt. To uncover quantitative trait loci (QTLs) associated with natural variation of response to R. solanacearum under heat stress, I adopted genome wide association (GWA) approaches using two geographically complementary collections of accessions of A. thaliana. In the worldwide collection, a single accession was totally resistant to the R. solanacearum GMI1000 strain under heat stress. Using a bulk segregant analysis approach, we identified the genetic basis of this total resistance that turned out to be controlled by a specific allelic form of the RPS4/RRS1 immunoreceptor pair. Beyond this simple genetic architecture, GWA analysis revealed a polygenic architecture underlying disease symptom progression. By adopting a reverse genetic approach, I functionally validated two genes encoding strictosidine synthase-like proteins (SSL) involved in early plant defense response to R. solanacearum. Using a local French collection revealed a genetic architecture of quantitative disease resistance (QDR) to R. solanacearum that totally differs from the one obtained with the worldwide collection. In particular, a complex genetic network of interacting loci was detected under heat stress. Among the detected QTLs, I functionally validated the atypical meiotic cyclin SOLO DANCERS gene as involved in QDR to R. solanacearum. By adopting an interdisciplinary approach between quantitative genetics and molecular biology, I highlighted in A. thaliana the diversity of molecular functions underlying natural variation of resistance to R. solanacearum under stress, which may in turn provide candidate genes for crop resistance to pathogens in the context of climate warming.

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