Stress and Gene Regulation

Understanding the molecular mechanisms that determine virus-host compatibility and disease is a major driving force for biologists and plant pathologists. Bearing this idea in mind, we investigate the crosstalk between virus infection and plant innate immunity. Thus, while normal, coevolved interactions of viruses with the host plant 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 is disturbed.

Plant immunity allows to perceive non-self and mount responses to keep microbes in check. Growing evidence indicates that viruses elicit immune responses, which may contribute to combat viral infections in plants. We used reverse genetics tools to study the role of multiple immune (co)receptor and immune regulators in this antiviral response. Among them, we identified the cell-surface receptor-like kinase BIR1 as a negative regulator of antiviral immunity. Virus infection stimulates the accumulation of SA, which in turn triggers transcriptional activation of BIR1. Since BIR1 is an essential component for immune attenuation in plants, our works has been focused to understand the mechanisms of BIR1 homeostasis. We found that DNA methylation constitutively regulates BIR1 transcription, while post-transcriptional RNA silencing removes the excess of BIR1 transcripts when BIR1 is transcriptionally activated, demonstrating that RNA silencing is a regulatory checkpoint of the immune response. We have further explored the consequences of BIR1 induction. BIR1 induction at physiological levels interferes with both the expression pattern-triggered immunity (PTI)-related genes and deposition of callose at the plasmodesmata triggered by immune elicitors. BIR1 induction may be a pathogen-driven mechanism to modulate plant defenses during infections, helping to maintain host-pathogen equilibrium. We found that non-physiological expression of BIR1 results in severe growth defects and cell-death and a broad misregulation of immunity. In recent years, we also put the focus in deciphering novel components of the BIR1-dependent antiviral signaling and how they function.

We identified several master regulators of PTI and effector triggered immunity (ETI) signaling cascades, including EDS1 and SOBIR1, that are required for the ETI-like of cell death phenotypes observed when BIR1 is expressed at non-physiological levels. We hypothesize that BIR1, previously thought to represent a negative regulator of plant immunity, is a guarded protein surveilled by unknown TNL-type resistant proteins. Thus, TNLs may monitor the integrity of BIR1 or BIR1-co-receptor complexes, with SOBIR1 working alongside EDS1 to transduce signals downstream of TNL.

Recently, we set up an experimental pipeline to search for novel BIR1-interacting protein candidates in infected plants as well as BIR1-responsive genes. Also of interest, we study how plant viruses are perceived by extracellular immune receptors and how the perception of plant viruses connects to the downstream immune signaling pathways.

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”.