Ismael Rodrigo Bravo
Email: irodrig@ibmcp.upv.es
Phone: '+34 963 877 862
Position: Investigador en Plantilla / Profesor Titular UPV
Group: Signalling and response to biotic stress
ORCID: 0000-0002-8994-6112
Biography
My scientific career has always been oriented toward Plant Biochemistry and Molecular Biology. Since the beginning of my PhD thesis in 1988, under the supervision of Professor Vicente Conejero in the Department of Biotechnology at the Universitat Politècnica de València, my studies have focused on the biochemical and molecular aspects of plant-pathogen interactions. In 1994, I became part of the Institute for Plant Molecular and Cellular Biology (IBMCP), a joint research center between UPV and CSIC, together with our research group. From 1996 to 1998, I carried out a postdoctoral stay in the laboratory of Professor Daniel F. Klessig at the Waksman Institute, State University of New Jersey (USA), studying plant transcription factors involved in pathogen signaling.
I have participated in several competitive research projects within Vicente Conejero’s group, focused on plant-pathogen interactions in various study systems (viroids, viruses, bacteria, wounding) using tomato as a model plant. One of the PR proteins described by our group (P23, with in vitro antifungal activity) was overexpressed in citrus plants, conferring resistance to the fungus Phytophthora citrophthora. The wound-inducible protein TCI21 showed strong activity as a chymotrypsin inhibitor and, when overexpressed in tomato, caused significant mortality in herbivorous insect larvae (Lisón et al., 2006). Our group has characterized gentisic acid (GA, 2,5-dihydroxybenzoic acid) as a signaling molecule for pathogenesis, complementary and alternative to salicylic acid (SA), that mediates plant defense responses to pathogens causing systemic infections (Bellés et al., 2006). We also isolated and characterized a glycosyltransferase that specifically conjugates GA to xylose (Tárraga et al., 2010). Furthermore, we showed that resistance mediated by both SA and GA is linked to the activation of gene silencing mechanisms (Campos et al., 2014). Related to the conjugation of phenolic compounds and plant pathogenesis, we recently described a glycosyltransferase in tomato (Twi1) that glycosylates flavonoids and also plays a role in antiviral defense (Campos et al., 2019).
In recent years, we have incorporated various “omics” approaches to gain a broader understanding of the molecular processes involved in plant responses to pathogens. Our first proteomic studies focused on the differential expression patterns of proteins triggered by viroid infection in tomato (Lisón et al., 2013). The use of metabolomic methodologies has allowed us to study alterations in metabolic profiles and to characterize metabolites involved in the defense response (López-Gresa et al., 2012). Among our achievements is the characterization of t-FNA, a phenolic compound induced in tomato upon bacterial infection, which has outstanding antioxidant activity and for which we obtained patent P201030693 (López-Gresa et al., 2011), as well as the protective effect of compound HB, covered by patent P201730685 (López-Gresa et al., 2017). Recently, we described that HB also promotes stomatal closure and accelerates the ripening of grapes and other climacteric fruits (Payá et al., 2020), and the compound has been licensed by a biotechnology company.
Our first proteomic studies aimed at analyzing the differential protein expression induced by CEVd viroid infection in tomato plants. We found alterations in the expression of ribosomal proteins and eukaryotic nuclear factors (Lisón et al., 2013). We have further explored this line of research and demonstrated that CEVd infection induces ribosomal stress in tomato (Cottilli et al., 2019), producing changes in the polysome profiles of viroid-infected plants. The viroid itself was found associated with ribosomes in diseased plants. The viroid appears to interfere with rRNA processing in a symptom-dependent manner. Therefore, the plant ribosome emerges as a target for viroid pathogenesis, triggering ribosomal stress in which ethylene plays an important role, as we have recently shown (Vázquez-Prol et al., 2020).