This project aims at studying how plants gene regulatory networks are rewired in response to abiotic constraints in different tissues. To this end, I will use maize response to water deficit as a model. I will use data from the [AMAZING GeneATLAS project](https://amaizing.fr/), to infer the gene regulatory networks of several tissues in well-watered and water-deficit conditions. I am particularly interested in the role of enhancers in such a response.
Polygenic adaptation, in which small changes in allele frequencies co-occur at multiple variants, has been proposed to be a major adaptive mechanism for polygenic traits. Because 90% of genetic variants associated to polygenic traits are located in non-coding, regulatory regions, I am interested in studying the extent to which polygenic selection targets regulatory regions of the human genome. I propose to combine network biology and population genetics methods in order to develop a new approach to detect signatures of polygenic adaptation in regulatory regions.
This project aims at deciphering the enhancer-mediated tissue-specific regulation of gene expression in maize tissues during leaf development. To this end, I contrasted the gene regulatory networks of two leaf tissues, dividing seedling leaves and mature husk modified leaves that protect the cob. Using a systems biology approach, I showed that these two leaf tissues both share a part of their regulatory network, and feature tissue-specific regulatory modules such as response to growth hormone in seedlings, and stress response in husk. I also investigated the molecular origin of such tissue-specific enhancer-driven regulatory networks, and showed that two different transposable elements from families were shaping the tissue-specific gene regulatory networks of seedlings and husks.
During my first postdoc, I investigated the genetic bases of the regulation of the expression of polygenic traits, using systems biology approaches based on bipartite network representation. I notably characterized the regulatory role of germinal mutations increasing the risk to develop cancers.