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Plant defence suppression is mediated by a fungal sirtuin during rice infection by M agnaporthe oryzae
Author(s) -
Fernandez Jessie,
MarroquinGuzman Margarita,
Nandakumar Renu,
Shijo Sara,
Cornwell Kathryn M.,
Li Gang,
Wilson Richard A.
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12743
Subject(s) - biology , gene , mutant , superoxide dismutase , microbiology and biotechnology , reactive oxygen species , gene expression , genetics , oxidative stress , biochemistry
Summary Crop destruction by the hemibiotrophic rice pathogen M agnaporthe oryzae requires plant defence suppression to facilitate extensive biotrophic growth in host cells before the onset of necrosis. How this is achieved at the genetic level is not well understood. Here, we report that a M . oryzae sirtuin, MoSir2 , plays an essential role in rice defence suppression and colonization by controlling superoxide dismutase ( SOD ) gene expression. Loss of MoSir2 function in Δ sir2 strains did not affect appressorial function, but biotrophic growth in rice cells was attenuated. Compared to wild type, Δ sir2 strains failed to neutralize plant‐derived reactive oxygen species ( ROS ) and elicited robust defence responses in rice epidermal cells that included elevated pathogenesis‐related gene expression and granular depositions. Deletion of a SOD ‐encoding gene under MoSir2 control generated Δ sod1 deletion strains that mimicked Δ sir2 for impaired rice defence suppression, confirming SOD activity as a downstream output of MoSir2 . In addition, comparative protein acetylation studies and forward genetic analyses identified a JmjC domain‐containing protein as a likely target of MoSir2 , and a Δ sir2 Δ jmjc double mutant was restored for MoSOD1 expression and defence suppression in rice epidermal cells. Together, this work reveals MoSir2 and MoJmjC as novel regulators of early rice cell infection.