Abstract
Lesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants’ sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to encode a receptor-like protein kinase containing leucine-rich domains that may be involved in stress responses in rice. spl36 was more sensitive to salt stress than the wild type, suggesting that SPL36 also negatively regulates the salt-stress response. These findings suggest that SPL36 regulates the disease resistance response in rice by affecting the expression of defense- and stress-related genes.
Highlights
The lesion mimic phenotype is characterized by the spontaneous production of disease spots of various sizes and shapes on the leaves and leaf sheaths in the absence of abiotic or biotic stress
We demonstrate that the loss of function of SPL36 is responsible for the cell death, premature senescence, and activation of the defense response in this mutant
No spread of lesion mimics had occurred in the covered areas of leaves, whereas lesion mimics appeared on uncovered control leaves (Fig. 1c)
Summary
The lesion mimic phenotype is characterized by the spontaneous production of disease spots of various sizes and shapes on the leaves and leaf sheaths (and even stalks and seeds) in the absence of abiotic or biotic stress. Lesion mimics are the result of apoptosis caused by the hypersensitive response (HR) (Petrov et al, 2015). Lesion mimic mutants in rice can be divided into the initial (local) type and the spreading type based on phenotype and whether a dominant or recessive mutation is present. The first lesion mimic mutant in plants was reported in maize by the American scientist R. Sekiguchi Lesion (sl), the first lesion mimic mutant identified in rice, was discovered by the Japanese scientist Sekiguchi in the mid-1960s as a naturally occurring mutant (Liu et al, 2004)
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