Summary
ATP
‐citrate lyases (
ACL
) play critical roles in tumour cell propagation, foetal development and growth, and histone acetylation in human and animals. Here, we report a novel function of
ACL
in cell death‐mediated pathogen defence responses in rice. Using ethyl methanesulphonate (
EMS
) mutagenesis and map‐based cloning, we identified an
Oryza sativa
ACL
‐A2
mutant allele, termed
spotted leaf 30‐1
(
spl30‐1
), in which an A‐to‐T transversion converts an Asn at position 343 to a Tyr (N343Y), causing a recessive mutation that led to a lesion mimic phenotype. Compared to wild‐type plants,
spl30‐1
significantly reduces
ACL
enzymatic activity, accumulates high reactive oxygen species and increases degradation rate of nuclear deoxyribonucleic acids.
CRISPR
/Cas9‐mediated insertion/deletion mutation analysis and complementation assay confirmed that the phenotype of
spl30‐1
resulted from the defective function of Os
ACL
‐A2 protein. We further biochemically identified that the N343Y mutation caused a significant degradation of
SPL
30
N343Y
in a ubiquitin‐26S proteasome system (
UPS
)‐dependent manner without alteration in transcripts of
Os
ACL
‐A2
in
spl30‐1
. Transcriptome analysis identified a number of up‐regulated genes associated with pathogen defence responses in recessive mutants of
Os
ACL
‐A2,
implying its role in innate immunity. Suppressor mutant screen suggested that
Os
SL
, which encodes a P450 monooxygenase protein, acted as a downstream key regulator in
spl30‐1
‐mediated pathogen defence responses. Taken together, our study discovered a novel role of Os
ACL
‐A2 in negatively regulating innate immune responses in rice.