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OsACL-A2 negatively regulates cell death and disease resistance in rice

January 9th, 2019


Plants have developed hypersensitive responses (HR), which are characterized by programmed cell death (PCD) of cells around the infection site, to protect them from pathogen attack. To better understand the roles of cell death in immune responses, many lesion mimic mutants (LMMs) with spontaneously induced cell death phenotypes have been investigated in rice. ATP-citrate lyase (ACL) is mainly a cytosolic enzyme that catalyses citrate to generate oxaloacetate and acetyl-CoA. ACL plays critical roles in tumour cell propagation, foetal development and growth, and histone acetylation in human and animals. However, neither phenotypes caused by mutations in ACL gene have been reported in plants nor the gene for ACL has been isolated in rice so far.

In order to study molecular mechanisms underlying cell death and disease resistance in rice, researchers from China National Rice Research Institute (CNRRI) at Chinese Academy of Agricultural Sciences (CAAS) and Department of Environmental and Plant Biology at Ohio University isolated a new LMM mutant, designated spotted leaf 30-1 (spl30-1) from EMS treated O. sativa japonica cv. Nipponbare. To identify the gene responsible for the phenotype, they cloned it by map-based cloning strategy. It encodes the subunit A of the heteromeric ACL (OsACL-A2), and mutation of OsACL-A2 caused a decrease in ACL amount via the ubiquitin-26S proteasome system (UPS)-dependent degradation and its total activity, triggered an accumulation of reactive oxygen species (ROS) and enhanced a resistance to bacterial blight, implying a novel role of OsACL in innate immunity response.

This study was supported by the National Key Research and Development Program of China (2016YFD0100406) and the National Natural Science Foundation of China (Grant Nos 31521064 and 91535205). The research findings have been published online in Plant Biotechnology Journal on December 24th (DOI: 10.1111/pbi. 13058). More details are available on the link below:

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