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Overexpressing a NPR1-like gene from Citrus paradisi enhanced Huanglongbing resistance in C. sinensis

Peng, Aihong, Zou, Xiuping, He, Yongrui, Chen, Shanchun, Liu, Xiaofeng, Zhang, Jingyun, Zhang, Qingwen, Xie, Zhu, Long, Junhong, Zhao, Xiaochun
Plant cell reports 2021 v.40 no.3 pp. 529-541
Candidatus Liberibacter asiaticus, Citrus paradisi, Citrus sinensis, genes, grapefruits, greening disease, host-pathogen relationships, immunity, jasmonic acid, pathogenesis-related proteins, phloem, quantitative polymerase chain reaction, salicylic acid, starch, transcription (genetics), transcriptome
KEY MESSAGE: Overexpression of CiNPR4 enhanced resistance of transgenic citrus plants to Huanglongbing by perceiving the salicylic acid and jasmonic acid signals and up-regulating the transcriptional activities of plant–pathogen interaction genes. Developing transgenic citrus plants with enhanced immunity is an efficient strategy to control citrus Huanglongbing (HLB). Here, a nonexpressor of pathogenesis-related gene 1 (NPR1) like gene from HLB-tolerant ‘Jackson’ grapefruit (Citrus paradisi Macf.), CiNPR4, was introduced into ‘Wanjincheng’ orange (Citrus sinensis Obseck). CiNPR4 expression was determined in transgenic citrus plants using quantitative real-time PCR analyses. The Candidatus Liberibacter asiaticus (CLas) pathogen of HLB was successfully transmitted to transgenic citrus plants by grafting infected buds. HLB symptoms developed in transgenic and wild-type (WT) plants by 9 months after inoculation. A CLas population analysis showed that 26.9% of transgenic lines exhibited significantly lower CLas titer levels compared with the CLas-infected WT plants at 21 months after inoculation. Lower starch contents and anatomical aberration levels in the phloem were observed in transgenic lines having enhanced resistance compared with CLas-infected WT plants. CiNPR4 overexpression changed the jasmonic acid, but not salicylic acid, level. Additionally, the jasmonic acid and salicylic acid levels increased after CLas infection. Transcriptome analyses revealed that the enhanced resistance of transgenic plants to HLB resulted from the up-regulated transcriptional activities of plant–pathogen interaction-related genes.