Abscisic acid (ABA), the major plant stress hormone, plays a crucial role in the response to the most pervasive causes of loss of crop productivity worldwide, including drought and high salinity. Serine/arginine-rich (SR) proteins are RNA-binding proteins that play crucial roles in the regulation of alternative splicing (AS), a key posttranscriptional mechanism for expanding proteome diversity and a flexible means of regulating gene expression in higher eukaryotes. While its functional relevance in plants remains largely unknown, mounting evidence suggests a central role for AS in the response to abiotic stress, in particular by targeting the ABA hormonal pathway. Using gene expression analyses, subcellular localization studies and reverse genetics approaches, this project will investigate the functional significance of six ABA-regulated Arabidopsis SR genes in stress responses mediated by the ABA phytohormone. To gain mechanistic insight into the mode of action of the SR proteins implicated in the ABA pathway, the physiological transcripts targeted by these splicing factors to achieve plant stress tolerance will be identified using a combination of genome-wide and biochemical approaches. In brief, next-generation sequencing technologies will be applied to whole transcriptome analysis (RNA-seq) of plants with altered levels of an SR protein and to RNA immunoprecipitation (RIP-seq) in plants expressing a tagged version of the SR protein. In discovering new plant genes that determine the ability to cope with unfavorable environmental conditions and by revealing the molecular mechanisms underlying their mode of action, this work will pave the way for the development of new efficient strategies to improve crop productivity in specific world regions.

Gut microbiota support intestinal tract development, immune system maturation, and protection against pathogens. Imbalanced microbiota (dysbiosis) has a role in inflammatory bowel disease (IBD). To control inflammation, patients take antibiotics, exacerbating dysbiosis, leading to loss of colonization resistance against pathogens and proliferation of pathobionts, disease development and progression. Microbiota composition has, therefore, a very important role in host health, and strategies to manipulate this composition are lacking. Microbiota-produced molecules, like quorum sensing (QS) signal autoinducer-2, can influence gut composition. Bacteria use QS to regulate populational gene expression. We intend to take advantage of microbial interactions mediated by QS to tackle IBD dysbiosis. We will design biotherapies to attenuate the detrimental dysbiotic effects on host health, focusing on gut QS in IBD. The microbiota imbalance observed in IBD leads to high inflammation, expansion of pathobionts, and loss of protection against infections. In previous work, we have shown that by committing the gut microbiota to inter-species QS we could increase members of the microbiota affected by antibiotics, highlighting the potential of QS manipulation to counteract dysbiosis. We propose to manipulate QS of native gut microbes to counteract IBD-associated dysbiosis, and thus inflammation and loss of protection associated with it, rescuing normal microbiota functions. We will tackle dysbiosis by manipulating QS signalling and by fostering specific beneficial interactions amongst microbes. The potential of this therapy, as an alternative or complement to antibiotics, is centred on bypassing the worsening of dysbiosis, like loss of protection against the expansion of inflammation-driving pathobionts and infections, as well as the attenuation of inflammation.