Sclerenchyma cell thickening through enhanced lignification induced by <i>OsMYB30</i> prevents fungal penetration of rice leaves
Weitao Li, Kang Wang, Mawsheng Chern, Yuchen Liu, Ziwei Zhu, Jiang Liu, Xiaobo Zhu, Junjie Yin, Ran Li, Jun Xiong, Kaiwei He, Liting Xu, Min He, Jing Wang, Jiali Liu, Yu Bi, Hai Qing, Mingwu Li, Kun Hu, Li Song, Long Wang, Tuo Qi, Qingqing Hou, Weilan Chen, Yan Li, Wenming Wang, Xuewei Chen
Abstract
Summary Broad‐spectrum resistance is highly preferred in crop breeding programmes. Previously, we have reported the identification of the broad‐spectrum resistance‐Digu 1 ( bsr‐d1 ) allele from rice Digu. The bsr‐d1 allele prevents activation of Bsr‐d1 expression by Magnaporthe oryzae infection and degradation of H 2 O 2 by peroxidases, leading to resistance to M. oryzae . However, it remains unknown whether defence pathways other than H 2 O 2 burst and peroxidases contribute to the bsr‐d1 ‐mediated immunity. Blast resistance was determined in rice leaves by spray and punch inoculations. Target genes of OsMYB30 were identified by one‐hybrid assays in yeast and electrophoretic mobility shift assay. Lignin content was measured by phloroglucinol–HCl staining, and acetyl bromide and thioacidolysis methods. Here, we report the involvement of the OsMYB30 gene in bsr‐d1 ‐mediated blast resistance. Expression of OsMYB30 was induced during M. oryzae infection or when Bsr‐d1 was knocked out or downregulated, as occurs in bsr‐d1 plants upon infection. We further found that OsMYB30 bound to and activated the promoters of 4‐coumarate:coenzyme A ligase genes ( Os4CL3 and Os4CL5 ) resulting in accumulation of lignin subunits G and S. This action led to obvious thickening of sclerenchyma cells near the epidermis, inhibiting M. oryzae penetration at the early stage of infection. Our study revealed novel components required for bsr‐d1 ‐mediated resistance and penetration‐dependent immunity, and advanced our understanding of broad‐spectrum disease resistance.