On April 8, 2021, the functional genomics research and innovation team of crop pests published an online publication titled”The C4 protein encoded by Tomato leaf curl Yunnan virus interferes with MAPK cascade-related defense responses through inhibiting the dissociation of the ERECTA/BKI1 complex” research paper reveals a new mechanism by which the geminivirus C4 protein escapes the host defense response by inhibiting the plant MAPK pathway.
Geminiviruses are a type of plant single-stranded DNA virus that is mainly spread by whitefly and has a widespread outbreak worldwide, causing devastating damage to global economic and food crops such as tomato, tobacco, cotton, corn, and cassava. Approximately 40%of the geminiviruses circulating in my country are accompanied by satellite DNA. The team found in previous studies that the bC1 protein encoded by the satellite molecule accompanying the geminivirus is the determinant of viral symptoms. At the same time, bC1 can also inhibit the host plant’s MAPK pathway to counteract the host defense response. However, about 60%of the geminiviruses in my country are not accompanied by satellite DNA. How does the infection of these viruses escape the host defense response mediated by the MAPK pathway?
Yunnan Tomato Leaf Curl Virus (TLCYnV) is not accompanied by satellite DNA. Early studies have found that the C4 protein encoded by the virus is a symptom determinant. The C4 protein interacts with NbSKη to change the subcellular location of NbSKη to induce viral symptoms; at the same time, As a multifunctional protein encoded by the virus, C4 protein can also inhibit the defense response of host plants such as hypersensitivity and transcription-level gene silencing. After in-depth research on TLCYnV, it is found that TLCYnV infection can up-regulate the expression of plant EPFs genes. EPFs genes can encode a type of exocrine protein EPFs. After EPFs are secreted to the outside of the cell, they can act as ligands to activate the receptor kinase ERECTA, which is located on the cell membrane. Activate the MAPK signaling pathway downstream of ERECTA. The C4 protein encoded by TLCYnV can interact with the negative regulator BKI1 of ERECTA. Since the N-terminus of C4 protein can be modified by myristoylation to make C4 localize on the cell membrane, C4 protein interacts with BKI1 to anchor BKI1 on the cell membrane, enhancing the inhibitory effect of BKI1 on ERECTA and preventing the ERECTA/BKI1 complex The depolymerization of ERECTA inhibits the activation of the MAPK signaling pathway downstream of ERECTA, thereby creating a cellular environment conducive to virus infection. This study revealed a new mechanism for the defense response of geminivirus escape hosts, and the results provided a theoretical basis for the breeding of geminivirus-resistant varieties.
This research was funded by the National Natural Science Foundation of China’s Key International (Regional) Cooperative Research Project (31720103914).
link to the original text:https://nph.onlinelibrary.wiley.com/doi/abs/10.1111/nph.17387