Resistance protein-mediated defense signalling in response to Turnip Crinkle Virus in Arabidopsis: recent advances

作者：Jeong Mi Ae; Jeong Rae Dong

来源：Journal of Plant Diseases and Protection, 2013, 120(3): 97-104.

DOI：10.1007/BF03356460

• HRT
• hypersensitive response
• photoreceptors
• resistance
• salicylic acid
• TCV

The Turnip Crinkle Virus (TCV) Arabidopsis interaction is one of the best-characterized pathosystems, and studies of this system have contributed significantly to the understanding of plant resistance to viral pathogens. Inoculation of TCV on the resistant Arabidopsis ecotype Di-17 elicits the hypersensitive response (HR), and is accompanied by increased expression of defense genes. The HR to TCV infection is conferred by HRT (HR to TCV) gene, which encodes a CC-NBS-LRR class resistance (R) protein. In contrast to the HR, resistance requires the HRT gene and a recessive locus designated rrt. Unlike most CC-NBS-LRR R proteins, HRT-mediated resistance is dependent on EDS1 (enhanced disease susceptibility 1) and is independent of NDR1 (non-race-specific disease resistance). Resistance is also independent of RAR1 (required for Mla12 resistance), SGT1 (suppressor of the G2 allele of SKP1), and TCV-interacting protein (TIP) but is compromised in the salicylic acid (SA) deficient mutants eds5 (enhanced disease susceptibility 5), pad4 (phytoalexin deficient 4), sid2 (salicylic acid induction deficient 2), and sag101 (senescence associated gene 101). EDS1 and SA have redundant functions in the induction of the HR by HRT. SAG101 interacts with PAD4, via EDS1, and EDS1, PAD4, and SAG101 form a ternary complex and perform independent functions in HRT-mediated resistance. HRT interacts with CRT1 (compromised recognition of TCV), an ATPase and resistance to TCV is partially compromised by a mutation in CRT1. HRT-mediated HR and TCV resistance are also dependent on light. A dark treatment, immediately following TCV inoculation, suppresses the HR, TCV resistance, and the activation of a majority of the TCV-induced genes. Interestingly, a mutation in blue-light photoreceptors compromised TCV resistance and led to degradation of HRT via a proteasome-dependent pathway, resulting in susceptibility to TCV, which correlates with its interaction with the E3 ubiquitin ligase, COP1 (constitutively photomorphogenesis 1). This review aims to document the advances in the understanding of the TCV-Arabidopsis pathosystem as a case study and provide a valuable model for dissecting plant resistance to viral pathogens.

• 出版日期2013-6