与BI-1相互作用的PVY的P3/P3N-PIPO抑制ATG6对NIb的降解，以促进病毒在……中的复制。

P3/P3N-PIPO of PVY interacting with BI-1 inhibits the degradation of NIb by ATG6 to facilitate virus replication in .

作者信息

Qing Zhen, Ahmad Shakeel, Chen Yuemeng, Liang Qingmin, Zhang Lijuan, Chen Baoshan, Wen Ronghui

机构信息

State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.

College of Agriculture, Guangxi University, Nanning, China.

出版信息

Front Plant Sci. 2023 Apr 17;14:1183144. doi: 10.3389/fpls.2023.1183144. eCollection 2023.

DOI:10.3389/fpls.2023.1183144

PMID:37139112

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10149851/

Abstract

INTRODUCTION

Autophagy not only plays an antiviral role but also can be utilized by viruses to facilitate virus infection. However, the underlying mechanism of potato virus Y (PVY) infection against plant autophagy remains unclear. BI-1, localizing to the endoplasmic reticulum (ER), is a multifunctional protein and may affect the virus infection.

METHODS

In this study, Y2H, BiFC, qRT-PCR, RNA-Seq, WB and so on were used for research.

RESULTS

P3 and P3N-PIPO of PVY can interact with the Bax inhibitor 1 (BI-1) of . However, BI-1 knockout mutant showed better growth and development ability. In addition, when the BI-1 gene was knocked out or knocked down in , the PVY-infected mutant showed milder symptoms and lower virus accumulation. Analysis of transcriptome data showed that the deletion of NbBI-1 weakened the gene expression regulation induced by PVY infection and NbBI-1 may reduce the mRNA level of NbATG6 by regulated IRE1-dependent decay (RIDD) in PVY-infected . The expression level of the ATG6 gene of PVY-infected WT was significantly down-regulated, relative to the PVY-infected mutant. Further results showed that ATG6 of can degrade NIb, the RNA-dependent RNA polymerase (RdRp) of PVY. NbATG6 has a higher mRNA level in PVY-infected BI-1 knockout mutants than in PVY-infected WT.

CONCLUSSION

The interaction of P3 and/or P3N-PIPO of PVY with BI-1 decrease the expression of the ATG6 gene might be mediated by RIDD, which inhibits the degradation of viral NIb and enhances viral replication.

摘要

引言

自噬不仅发挥抗病毒作用，还可被病毒利用以促进病毒感染。然而，马铃薯Y病毒（PVY）感染植物自噬的潜在机制仍不清楚。定位于内质网（ER）的BI-1是一种多功能蛋白，可能影响病毒感染。

方法

在本研究中，采用酵母双杂交（Y2H）、双分子荧光互补（BiFC）、定量逆转录聚合酶链反应（qRT-PCR）、RNA测序（RNA-Seq）、蛋白质免疫印迹（WB）等方法进行研究。

结果

PVY的P3和P3N-PIPO可与……的Bax抑制剂1（BI-1）相互作用。然而，BI-1基因敲除突变体表现出更好的生长发育能力。此外，当在……中敲除或下调BI-1基因时，感染PVY的突变体症状较轻且病毒积累量较低。转录组数据分析表明，NbBI-1的缺失削弱了PVY感染诱导的基因表达调控，并且在感染PVY的……中，NbBI-1可能通过调控IRE1依赖性衰变（RIDD）降低NbATG6的mRNA水平。相对于感染PVY的突变体，感染PVY的野生型中ATG6基因的表达水平显著下调。进一步结果表明，……的ATG6可降解PVY的RNA依赖性RNA聚合酶（RdRp）NIb。在感染PVY的BI-1基因敲除突变体中，NbATG6的mRNA水平高于感染PVY的野生型。