G-QUADRUPLEX: POTENTIAL EPIGENETIC MEMORY INVOLVED IN PRIMING INDUCED BY TRICHODERMA IN MAIZE PLANTS

PIGA, E.; VARGAS, W.A.; ARMAS, P.; CAMPOS BERMUDEZ, V.A.; AGOSTINI, R.B.; RIUS, S.P.

Congreso; Plant Biology 2020; 2020

American Society of Plant Biologists

Trichoderma spp. is considered as promising biological control agents. They can trigger Induced Systemic Resistance (ISR) to prevent future pathogenic attacks. Priming of plant defenses is marked by changes in transcriptional, metabolic, and epigenetic levels after stimulus perception. The primed plants have an epigenetic environmental memory that upon pathogenic attack, they are able to mount a quicker and/or robust immune response to effectively ward off pathogenic infections and/or develop stress tolerance.Epigenetic regulation involves the restructuring of chromatin through covalent modifications of DNA and histones and the accessibility of chromatin. G-quadruplexes (G4) comprise a class of nucleic acid secondary structures formed by stacking of guanine base tetrads in a quadruple helix. G4 structures have been shown to affect a vast array of genetic functions, including transcription, translation, replication, recombination, and DNA repair. Interestingly, recent works suggest roles for G4, in association with G4-interacting proteins, in epigenetics regulating both DNA and histone modifications.In this work we sought to investigate the G4 epigenetic reprogramming in leaves from maize plantsinoculated with T. atrovidire. The main goal of our research was to determine the global presence of G4 structures at genomic DNA using G4 specific antibody in Dot-Blot assays and to evaluate the enrichment of putative Quadruplex forming G-Rich Sequences (QGRS) in previously selected priming genes promoters. The results obtained reveal that at 6 days post-inoculation with Trichoderma, there is an increase in the levels of genomic G4 with respect to the control condition. In addition, in silico analysis of the promoters revealed a significant enrichment of QGRS mainly in promoters involved in hormone signalling prevoiusly detected as involved in ISR