Abstract:

【Objective】The objective of this study is to isolate rice WRKY30 and provide not only a foundation for elucidating the roles of WRKY transcription factors in the regulation of defense responses in rice, but also gene sources for reasonable utilization of pathogen-resistance and genetic modification in rice breeding. 【Method】RT-PCR was used to amplify the full cDNA length of WRKY30 including its largest open reading frame (ORF). Bioinformatical tools were employed to analyze its sequence and coding protein. Copies of WRKY30 in the rice genome were determined by Southern hybridization, and the organ-specific expression characteristics and induced expression profiles under pathogen challenges, hormone treatments and abiotic stresses were investigated by Northern blot or RT-PCR. 【Result】The WRKY30 contained an entire ORF in length of 2 022 bp and was predicted to encode a protein of 674 amino acid residues consisting of two WRKY domains each with a zinc finger motif of C2H2 and a nuclear localization signal, belonging to the WRKY subgroup I. WRKY30 shared high amino acid sequence identity with those from monocots such as wheat (Hordeum vulgare), Sorghum bicolor and Brachypodium sylvaticum. WRKY30 exists as a single copy in the rice genome. The transcript levels of WRKY30 were relatively high in stem, leaf and grain, next were root and panicle, and the least was flower. WRKY30 was rapidly induced in response to challenges with Magnaporthe grisea and Rhizoctonia solani, and also induced by exogenous salicylic acid (SA) and methyl jasmonate (MeJA), two important defense-related hormones. However,ethephon (ET) exerted no obvious effects on its expression. By contrast, abscisic acid inhibited the transcription of WRKY30. On the hand, wounding lead to upregulation of WRKY30 transcription, whereas there were no significant effects on its expression subjected to other abiotic stresses such as cold, high salt and dehydration. 【Conclusion】WRKY30 may be involved in the regulation of rice defense responses to blast and sheath blight fungi through SAand JA, but not ET-dependent signaling pathways.