LML1, Encoding a Conserved Eukaryotic Release Factor 1 Protein, Regulates Cell Death and Pathogen Resistance by Forming a Conserved Complex with SPL33 in Rice

Abstract

Lesion mimic mutants are powerful tools for unveiling the molecular connections between cell death and pathogen resistance. Various proteins responsible for lesion mimics have been identified; however, the mechanisms underlying lesion formation and pathogen resistance are still unknown. Here, we identify a lesion mimic mutant in rice, lesion mimic leaf 1 (lml1). The lml1 mutant exhibited abnormal cell death and resistance to both bacterial blight and rice blast. LML1 is expressed in all types of leaf cells, and encodes a novel eukaryotic release factor 1 (eRF1) protein located in the endoplasmic reticulum. Protein sequences of LML1 orthologs are conserved in yeast, animals and plants. LML1 can partially rescue the growth delay phenotype of the LML1 yeast ortholog mutant, dom34. Both lml1 and mutants of AtLML1 (the LML1 Arabidopsis ortholog) exhibited a growth delay phenotype like dom34. This indicates that LML1 and its orthologs are functionally conserved. LML1 forms a functional complex with a eukaryotic elongation factor 1A (eEF1A)-like protein, SPL33/LMM5.1, whose mutant phenotype was similar to the lml1 phenotype. This complex was conserved between rice and yeast. Our work provides new insight into understanding the mechanism of cell death and pathogen resistance, and also lays a good foundation for studying the fundamental molecular function of Pelota/DOM34 and its orthologs in plants.

A Two-Headed Monster to Avert Disaster: HBS1/SKI7 Is Alternatively Spliced to Build Eukaryotic RNA Surveillance Complexes

“…Loss of PELOTA, the decoding factor that recruits HBS1 to stalled ribosomes, confers resistance to TYCLV infection in tomato; with our identification of tomato HBS1 and HBS1/SKI7 genes, it is now possible to test whether loss of HBS1, SKI7, and/or SKI2/SKI3/SKI8 also confer resistance to TYCLV, and how this RNA degradation machinery interacts with other viruses. In rice, a recessive pelota mutant triggers a salicylic acid-associated autoimmune response, including spontaneous lesions and dwarfism, through unclear mechanisms ( Ding et al, 2018 ; Qin et al, 2018 ; Zhang et al, 2018 ). The rice pelota defects could be related to hyperaccumulation of aberrant RNA species, similar to the tricohepatoenteric autoimmune syndrome in skiv2l human cells ( Eckard et al, 2014 ), or due to specific dysregulation of transcripts in rice that regulate immunity.…”

Semi‐dominant mutation in the cysteine‐rich receptor‐like kinase gene, ALS1, conducts constitutive defence response in rice

“…) and lml1 (Qin et al . ); spl33 and lml1 showed similar phenotypes with lesions on the leaf blade only. In addition, SPL33 and LML1 formed a complex to regulate cell death and pathogen resistance in rice.…”

Identification of stress repressive zinc finger gene family and its expression analysis in rice under abiotic constraints

“…Both OsSRZ18 and LML1 are involved in the regulation of programmed cell death and they interact between each other. Their deletion mutation causes dwarfing and premature senescence in rice [23][24]. This suggests a prominent role for the SRZ family in the regulation of growth and development in rice plants [23][24].…”

“…Their deletion mutation causes dwarfing and premature senescence in rice [23][24]. This suggests a prominent role for the SRZ family in the regulation of growth and development in rice plants [23][24]. However, the expression profiles of rice SRZ genes family (OsSRZ) have not yet been previously demonstrated.…”

“…oryzae by up-regulating defense-related genes [23]. A recent study showed that LML1 encodes a conserved eukaryotic release factor 1 protein and regulates cell death and pathogen resistance by forming a conserved complex with OsSRZ18 in rice [24].…”