Stress and Gene Regulation

Understanding the molecular mechanisms that determine virus-host compatibility and disease is major driving force for biologists and plant pathologists. Bearing this idea in mind, our most recent research interest puts the focus on the crosstalk between RNA silencing and plant innate immunity during viral infections in plants. Thus, while normal, coevolved interactions of viruses with the host RNA silencing and plant immunity are optimally balanced such that infection is achieved without causing damage to the host, viruses may cause dangerous outbreaks and disease if this subtle equilibrium between virus multiplication and host integrity is disturbed. In our previous projects we learnt that RNA silencing is critical to maintain the immune regulator BIR1 under optimal expression limits. This regulation is necessary to avoid the constitutive expression of plant defenses, which otherwise would cause severe autoimmune phenotypes that compromise plant integrity and fitness. Once proven that several immune receptors involved in BIR1 signaling pathways largely influence viral susceptibility, we explore the molecular mechanisms of post-transcriptional regulation of BIR1 during viral infection, and the role of BIR1-dependent signaling pathways on the antiviral response.In our work, we use a large range of molecular and genetic experimental approaches, including high-throughput stretegies, using the model plant Arabidopsis thaliana and the model Tobacco rattle virus. Recently, we study the contribution of site-specific mRNA cleavage on BIR1 regulation and the collaborative work of nonsense-RNA mediated decay (NMD) and RNA silencing as underlying mechanisms of BIR1 post-transcriptional regulation. This is substantiated by the finding that BIR1 transcripts are significantly upregulated in NMD mutants. In recent years, we also put the focus in deciphering novel components of the BIR1-dependent antiviral signaling and how they function. We study the role of the BIR1 partners BAK1 and SOBIR1, two positive regulators of plant immunity, on autoimmune phenotypes associated to BIR1 overexpression and on antiviral responses. We proved that both regulators are misregulated during virus infections and loss-of-function mutants exhibit altered susceptibility to virus infection. Furthermore, the autoimmune phenotypes observed in BIR1 overexpressor transgenics are rescued in a sobir1-12mutant background, corroborating previous findings that indicate that SOBIR1 is a suppresor of bir1-1 phenotypes. Interestingly, the antiviral phenotype of bir1-1 mutants is independent of BAK1 and SOBIR1, suggesting alternative BIR1-dependent signaling pathways of antiviral immmunity. Recently, we set up an experimental pipeline to search for novel BIR1-interacting protein candidates in infected plants as well as BIR1-responsive genes. We have seen that misregulation of BIR1 leads to the induction of several receptor-like proteins (RLPS) whose expression is normally down-regulated. Their functions are unknown for most of them. We are investigating whether these RLPs forms protein receptor-complexes with master immune regulators and their contribution to loss-of-function BIR1-associated phenotypes.

BIR1, due to its role as a repressor of basal- and effector-triggered immunity, is a promising tool for engineering resistance against pathogen infections in plants. Since future sustainable agriculture should rely on knowledge-based approaches that make use of an in-depth understanding of plant-virus interactions, our results are expected to contribute to the development of sustained crop production that uses improved plant cultivars avoiding treatments with environmentally toxic chemicals. Our research is oriented toward the challenge identified as “Bioeconomía: sostenibilidad de los sistemas de producción primaria y forestales, seguridad y calidad alimentaria, investigación marina y marítima y bioproductos”.