Turnip crinkle virus Isolate Lacking the CP Counter‐Defence Protein Gene Providing Protection Against the Wild‐Type Strain is Associated with Highly Localized RNA Silencing

• Published in: Journal of phytopathology Vol. 162; no. 11-12; pp. 758 - 769
• Main Authors: Chen, Ying‐Juan, Zhu, Feng, Liu, Jian, Deng, Xing‐Guang, Pu, Xiao‐Jun, Chen, Li‐Juan, Sun, Tian‐Lin, Bao, Wei‐Kai, Xi, De‐Hui, Lin, Hong‐Hui
• Format: Journal Article
• Language: English
• Published: Berlin Parey 01.12.2014; Blackwell Publishing Ltd; Wiley Subscription Services, Inc
• Subjects: Arabidopsis; China; cross-protection; Cucumber mosaic virus; genes; highly localized RNA silencing; mutants; Nicotiana benthamiana; plant viruses; RNA interference; Turnip crinkle virus; viruses
• ISSN: 0931-1785; 1439-0434
• DOI: 10.1111/jph.12258

Cross‐protection has been used successfully and commercially to control a range of virus diseases for which the selection of suitable mild strains of plant viruses is necessary. Turnip crinkle virus (TCV) is highly pathogenic on Arabidopsis plants and its silencing suppressor‐defective mutant, TCVΔCP, can induce highly localized RNA silencing which is differs from that of other protective strains. We found that TCVΔCP provides some protection against wild‐type TCV but lacks complete protection, and the relative locations of the protective virus and challenge virus affect the degree of cross‐protection. However, similar cross‐protection afforded by TCVΔCP is not observed in Nicotiana benthamiana plants. As expected, TCVΔCP pre‐infected Arabidopsis plants fail to protect against infection with the unrelated Cucumber mosaic virus, strain Fhy. It appears that cross‐protection afforded by TCVΔCP requires that the challenge virus be very similar in sequence, which is a characteristic of RNA silencing. In order to investigate whether the protection is associated with the highly localized RNA silencing, mutant plants involved in key silencing pathway genes of RNA silencing machinery, including dcl2, dcl4 and triple dcl2/dcl3/dcl4 mutants were used. The results demonstrate that cross‐protection afforded by TCVΔCP is dependent on host RNA silencing, and both DCL2 and DCL4 play important roles in this process.