RESUMEN
Programmed cell death (PCD) plays an important role in plant environmental stress and has the potential to be manipulated to enhance disease resistance. Plants have innate immunity and, following pathogen perception, the host induces a Hypersensitive Response PCD (HR-PCD), leading to pattern (PTI) or effector triggered immunity (ETI). Here we report a non-HR type or Apoptotic-Like PCD (AL-PCD) in pathogen infected wheat and potato based on apoptotic-like DNA fragmentation. A deletion mutation in the gene encoding histidine rich calcium binding protein (TaHRC) in FHB-resistant wheat (R-NIL) failed to induce AL-PCD. Similarly, the CRISPR-Cas9 based silencing of StHRC gene in Russet Burbank potato failed to induce apoptotic-like DNA fragmentation, proved based on DNA laddering and TUNEL assays. The absence of AL-PCD in wheat R-NIL reduced pathogen biomass and mycotoxins, increasing the accumulation of resistance metabolites and FHB-resistance, and in potato it enhanced resistance to multiple pathogens. In addition, the reduced expressions of metacaspase (StMC7) and Ca2+ dependent endonuclease 2 (StCaN2) genes in potato with Sthrc indicated an involvement of a hierarchy of genes in the induction of AL-PCD. The HRC in commercial varieties of different crops, if functional, can be silenced by genome editing possibly to enhance resistance to multiple pathogens.