SPL36 Encodes a Receptor-like Protein Kinase that Regulates Programmed Cell Death and Defense Responses in Rice

• Main Authors: R. A. O. Yuchun, J. I. A. O. Ran, W. A. N. G. Sheng, W. U. Xianmei, Y. E. Hanfei, P. A. N. Chenyang, L. I. Sanfeng, Xin Dedong, Z. H. O. U. Weiyong, D. A. I. Gaoxing, H. U. Juan, R. E. N. Deyong, W. A. N. G. Yuexing
• Format: Article
• Language: English
• Published: SpringerOpen 2021-04-01
• Series: Rice
• Subjects: Defense response; Receptor-like protein kinase; Lesion mimic mutant; Rice; Salt resistance; SPL36
• Online Access: https://doi.org/10.1186/s12284-021-00475-y

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.