Mutations of two FERONIA-like receptor genes enhance rice blast resistance without growth penalty

Abstract Genes that provide resistance to fungi and/or bacteria usually reduce plant growth and ultimately affect grain yield. Thus, crop breeding programs need to find genetic resources that balance disease resistance with growth. The receptor kinase FERONIA regulates cell growth and survival in Ar...

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Veröffentlicht in:Journal of experimental botany 2020-03, Vol.71 (6), p.2112-2126
Hauptverfasser: Yang, Zhuhong, Xing, Junjie, Wang, Long, Liu, Yue, Qu, Jianing, Tan, Yang, Fu, Xiqin, Lin, Qinlu, Deng, Huafeng, Yu, Feng
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Sprache:eng
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Zusammenfassung:Abstract Genes that provide resistance to fungi and/or bacteria usually reduce plant growth and ultimately affect grain yield. Thus, crop breeding programs need to find genetic resources that balance disease resistance with growth. The receptor kinase FERONIA regulates cell growth and survival in Arabidopsis. Here, we investigate, in rice, the role of members of the FERONIA-like receptor (FLR) gene family in the balance between growth and the response to the fungal pathogen Magnaporthe oryzae (Pyricularia oryzae), which causes the most devastating disease in rice. We carried out genome-wide gene expression and functional screenings in rice via a gene knockout strategy, and we successfully knocked out 14 FLR genes in rice. Using these genetic resources, we found that mutations in the FLR2 and FLR11 genes provide resistance to rice blast without a profound growth penalty. Detailed analyses revealed that FLR2 mutation increased both defense-related gene expression and M. oryzae-triggered production of reactive oxygen species. Thus, our results highlight novel genetic tools for studying the underlying molecular mechanisms of enhancing disease resistance without growth penalty. The FERONIA-like receptor (FLR) is essential for the response to Magnaporthe oryzae in rice, and mutations in FLR2 and FLR11 enhance resistance in the absence of significantly growth penalty.
ISSN:0022-0957
1460-2431
DOI:10.1093/jxb/erz541