INVESTIGADORES
CAMPOS BERMUDEZ Valeria Alina
congresos y reuniones científicas
Título:
Epigenetic regulation associated with systemic resistance induced by Trichoderma in Zea mays leaves
Autor/es:
AGOSTINI, RB.; BUONO, G.; ARIEL, F.; VARGAS, WA.; RIUS, SP.; CAMPOS BERMUDEZ, VA.
Reunión:
Congreso; XXXIII Argentinian Meeting of Plant Physiology; 2021
Resumen:
Trichoderma spp. are considered as promising biological control agents since, during its symbiosis with plants, they induce them a systemic priming state of defenses. Therefore, the primed plants are able to mount a quicker and robust immune response to effectively ward off a broad spectrum of pathogens. Priming of plant defenses is marked by changes at transcriptional, metabolic, and epigenetic level. Epigenetic regulation involves the restructuring of chromatin through covalent modifications of DNA and histones that modulate its accessibility.Here we investigate the epigenetic reprogramming in leaves from maize plants inoculated with T. atrovidire and infected with Colletotrichum graminicola. The hemibiotrophic fungal pathogen, C. graminicola causes anthracnose in maize (corn) and is a major problem of maize susceptible to infection resulting in increasing economic concerns.We have previously selected the group of maize genes whose expression is modulated in priming state induced by T. atroviride (Agostini et al., 2019). The aim of this research is to determine the changes in the structure of chromatine of promoters of some selected priming genes, trough FAIRE-qPCR (chromatin compaction/relaxation state) and ChIP-qPCR (histone post-translational modifications).In conclusion, the systemic resistance induced by T. atroviride in maize plant leaves generates an open chromatin state in the promoters of relevant genes linked to hormone defense and signaling. Furthermore, it increases the acetylation of H3K9 and decreases the triple methylation of H3K27. This would indicate that these promoters are transcriptionally active to respond to a stress situation such a pathogen attack.