[Objective]The paper was to obtain a pathogen-inducible responsive gene TcREMORIN from Taxus chinesis.[Method]Total RNA was extracted by Trizol reagent,and cDNA was synthesized using TaKaRa reverse transcription kit a...[Objective]The paper was to obtain a pathogen-inducible responsive gene TcREMORIN from Taxus chinesis.[Method]Total RNA was extracted by Trizol reagent,and cDNA was synthesized using TaKaRa reverse transcription kit and Invitrogen M-MLV Reverse Transcriptase kit.The TcREMORIN gene was amplified by qRT-PCR.[Result]The full length of TcREMORIN was 778 bp with a 501 bp open reading frame(ORF)which encoded 166 amino acids.Bioinformatics analysis indicated that TcREMORIN possessed a conserved domain of remorin family genes and located probably in cell plasma membrane.The results of real-time quantitative PCR assay revealed that the target gene was induced by anthracnose of T.chinesis and its expression level was up-regulated by PEG,NaCl,H2O2 and 4℃stresses.[Conclusion]The TcREMORIN gene may play a critical role in plant-pathogen interaction.展开更多
Remorins are plant-specific membrane-associated proteins and were proposed to play crucial roles in plant-pathogen interactions. However, little is known about how pathogens counter remorin-mediated host responses. In...Remorins are plant-specific membrane-associated proteins and were proposed to play crucial roles in plant-pathogen interactions. However, little is known about how pathogens counter remorin-mediated host responses. In this study, by quantitative whole-proteome analysis we found that the remorin protein （NbREM1） is downregulated early in Rice stripe virus （RSV） infection. We further discovered that the turn- over of NbREM1 is regulated by S-acylation modification and its degradation is mediated mainly through the autophagy pathway. Interestingly, RSV can interfere with the S-acylation of NbREM1, which is required to negatively regulate RSV infection by restricting virus cell-to-cell trafficking. The disruption of NbREM1 S-acylation affects its targeting to the plasma membrane microdomain, and the resulting accumulation of non-targeted NbREM1 is subjected to autophagic degradation, causing downregulation of NbREMI. Moreover, we found that RSV-encoded movement protein, NSvc4, alone can interfere with NbREM1 S-acylation through binding with the C-terminal domain of NbREM1 the S-acylation of OsREM1.4, the homologous remorin of NbREM1, and thus remorin-mediated defense against RSV in rice, the original host of RSV, indicating that downregulation of the remorin protein level by interfering with its S-acylation is a common strategy adopted by RSV to overcome remorin-mediated inhibition of virus movement.展开更多
基金Supported by Science and Technology Project of Henan Province(182102110132).
文摘[Objective]The paper was to obtain a pathogen-inducible responsive gene TcREMORIN from Taxus chinesis.[Method]Total RNA was extracted by Trizol reagent,and cDNA was synthesized using TaKaRa reverse transcription kit and Invitrogen M-MLV Reverse Transcriptase kit.The TcREMORIN gene was amplified by qRT-PCR.[Result]The full length of TcREMORIN was 778 bp with a 501 bp open reading frame(ORF)which encoded 166 amino acids.Bioinformatics analysis indicated that TcREMORIN possessed a conserved domain of remorin family genes and located probably in cell plasma membrane.The results of real-time quantitative PCR assay revealed that the target gene was induced by anthracnose of T.chinesis and its expression level was up-regulated by PEG,NaCl,H2O2 and 4℃stresses.[Conclusion]The TcREMORIN gene may play a critical role in plant-pathogen interaction.
文摘Remorins are plant-specific membrane-associated proteins and were proposed to play crucial roles in plant-pathogen interactions. However, little is known about how pathogens counter remorin-mediated host responses. In this study, by quantitative whole-proteome analysis we found that the remorin protein （NbREM1） is downregulated early in Rice stripe virus （RSV） infection. We further discovered that the turn- over of NbREM1 is regulated by S-acylation modification and its degradation is mediated mainly through the autophagy pathway. Interestingly, RSV can interfere with the S-acylation of NbREM1, which is required to negatively regulate RSV infection by restricting virus cell-to-cell trafficking. The disruption of NbREM1 S-acylation affects its targeting to the plasma membrane microdomain, and the resulting accumulation of non-targeted NbREM1 is subjected to autophagic degradation, causing downregulation of NbREMI. Moreover, we found that RSV-encoded movement protein, NSvc4, alone can interfere with NbREM1 S-acylation through binding with the C-terminal domain of NbREM1 the S-acylation of OsREM1.4, the homologous remorin of NbREM1, and thus remorin-mediated defense against RSV in rice, the original host of RSV, indicating that downregulation of the remorin protein level by interfering with its S-acylation is a common strategy adopted by RSV to overcome remorin-mediated inhibition of virus movement.
