Journal
MOLECULAR MICROBIOLOGY
Volume 94, Issue 1, Pages 70-88Publisher
WILEY
DOI: 10.1111/mmi.12743
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Funding
- National Science Foundation [IOS-1145347]
- USDA-NIFA [2014-67013-21559]
- Hardin Fellowship
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [1145347] Funding Source: National Science Foundation
- NIFA [2014-67013-21559, 688531] Funding Source: Federal RePORTER
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Crop destruction by the hemibiotrophic rice pathogen Magnaporthe 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 Delta sir2 strains did not affect appressorial function, but biotrophic growth in rice cells was attenuated. Compared to wild type, Delta 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 Delta sod1 deletion strains that mimicked Delta 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 Delta sir2 Delta 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.
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