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Plant defence suppression is mediated by a fungal sirtuin during rice infection by M agnaporthe oryzae
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 sirtui...
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Published in: | Molecular microbiology 2014-10, Vol.94 (1), p.70-88 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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. |
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ISSN: | 0950-382X 1365-2958 |
DOI: | 10.1111/mmi.12743 |