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Ratoon rice generated from primed parent plants exhibit enhanced herbivore resistance

Mao Ye, Yuan‐Yuan Song, Scott R. Baerson, Jun Long, Jie Wang, Zhiqiang Pan, Wen‐Xiong Lin, Ren‐Sen Zeng
Plant, cell and environment 2017 v.40 no.5 pp. 779-787
RNA interference, rice, labor, insect larvae, pest resistance, trypsin, hydroperoxide dehydratase, jasmonic acid, parents, ratooning, peroxidase, crop production, catechol oxidase, plant-insect relations, methyl jasmonate, resistance mechanisms, pathogenesis-related proteins, vegetative growth, biosynthesis, phytophagous insects, Cnaphalocrocis medinalis, proteinase inhibitors
Rice ratooning is practiced in many rice‐growing countries for achieving increased rice production with limited labour input. Here, we report that attack by insect herbivores, or treatment with a defense signaling compound in parent plants, can prime anti‐herbivore defense responses in subsequent ratoon plants. We compared the defense responses of rice ratoons generated from parent plants that had been either infested by Cnaphalocrocis medinalis (rice leaffolder, LF) caterpillars or treated with methyl jasmonate (MeJA) during vegetative growth, with ratoons generated from control parent plants. Ratoon plants generated from parents receiving prior LF infestation or MeJA treatment exhibited higher jasmonic acid (JA) levels, as well as elevated levels of transcripts of defense‐related genes associated with JA signaling. In addition, elevated activities of peroxidase, polyphenol oxidase and trypsin protease inhibitor were observed, as well as enhanced resistance towards subsequent LF infestation. Pre‐priming of ratoon defense responses was significantly reduced in plants where expression of OsAOS (allene oxide synthase, involved in JA biosynthesis) or OsCOI1 (CORONATINE INSENSITIVE1, involved in JA perception) was inhibited by RNA interference. Our results indicate that herbivore exposure or MeJA treatment in rice parent plants enhances anti‐herbivore resistance in subsequently generated ratoons through priming of JA‐mediated defenses.