Summary
mi
RNA
s contribute to plant resistance against pathogens. Previously, we found that the function of miR398b in immunity in rice differs from that in Arabidopsis. However, the underlying mechanisms are unclear.
In this study, we characterized the mutants of miR398b target genes and demonstrated that multiple superoxide dismutase genes contribute to miR398b‐regulated rice immunity against the blast fungus
Magnaporthe oryzae
.
Out of the four target genes of miR398b, mutations in
Cu/Zn‐Superoxidase Dismutase1
(
CSD
1
),
CSD
2
and
Os11g09780
(
Superoxide DismutaseX
,
SODX
) led to enhanced resistance to
M. oryzae
and increased hydrogen peroxide (H
2
O
2
) accumulation. By contrast, mutations in
Copper Chaperone for Superoxide Dismutase
(
CCSD
) resulted in enhanced susceptibility. Biochemical studies revealed that
csd1
,
csd2
and
sodx
displayed altered expression of
CSD
s and other superoxide dismutase (
SOD
) family members, leading to increased total
SOD
enzyme activity that positively contributed to higher H
2
O
2
production. By contrast, the
ccsd
mutant showed
CSD
protein deletion, resulting in decreased
CSD
and total
SOD
enzyme activity.
Our results demonstrate the roles of different
SOD
s in miR398b‐regulated resistance to rice blast disease, and uncover an integrative regulatory network in which miR398b boosts total
SOD
activity to upregulate H
2
O
2
concentration and thereby improve disease resistance.
MicroRNAs (miRNAs) are known to fine‐tune growth, development, and stress‐induced responses. Osa‐miR1873 is a rice‐specific miRNA targeting LOC_Os05g01790. Here, we show that Osa‐miR1873 fine‐tunes rice immunity against Magnaporthe oryzae and yield traits via LOC_Os05g01790. Osa‐miR1873 was significantly upregulated in a susceptible accession but downregulated in a resistance accession at 24 h post‐inoculation (hpi) of M. oryzae. Overexpressing Osa‐miR1873 enhanced susceptibility to M. oryzae and compromised induction of defense responses. In contrast, blocking Osa‐miR1873 through target mimicry compromised susceptibility to M. oryzae and enhanced induction of defense responses. Altered expression of Osa‐miR1873 also resulted in some defects in yield traits, including grain numbers and seed setting rate. Moreover, overexpression of the target gene LOC_Os05g01790 increased rice blast disease resistance but severely penalized growth and yield. Taken together, we demonstrate that Osa‐miR1873 fine‐tunes the rice immunity‐growth trade‐off via LOC_Os05g01790, and blocking Osa‐miR1873 could improve blast disease resistance without significant yield penalty. Thus, the Osa‐miR1873‐LOC_Os05g01790 regulatory module is valuable in balancing yield traits and blast resistance.
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