Autophagy is known to play an important role in plant-pathogen interactions. Several pathogens including viruses are reported to induce autophagy in plants, but the underpinning mechanism remains largely unclear. Further, in virus-plant interplay it is yet to identify any viral factor(s) responsible for induction of autophagy. Here, we report that βC1 protein of Cotton leaf curl Multan betasatellite (CLCuMuB) interacts with cytosolic glyceraldehyde-3-phosphate dehydrogenases (GAPCs), a negative autophagic regulator, to induce autophagy in plants. CLCuMuB βC1 bound to GAPCs and disrupted the interaction between GAPCs and ATG3. A mutant βC1 protein (βC13A) in which I45, Y48, and I53 were all substituted with alanine (A), dramatically reduced its binding capacity with GAPCs, failed to disrupt the GAPCs-ATG3 interactions and failed to induce autophagy. Furthermore, mutant virus carrying βC13A showed increased symptoms and viral DNA accumulation associated with decreased autophagy in plants. These results suggest that CLCuMuB βC1 activates autophagy by disrupting GAPCs-ATG3 interactions.

自噬在植物与病原体的相互作用中起着重要作用。据报道，包括病毒在内的几种病原体可诱导植物自噬，但其基本机制仍不清楚。此外，在病毒-植物相互作用中，尚未鉴定出引起自噬的任何病毒因子。在这里，我们报告棉叶卷曲的木尔坦β卫星（CLCuMuB）的βC1蛋白与细胞质中的自噬负调控物甘油醛3磷酸脱氢酶（GAPC）相互作用，以诱导植物自噬。CLCuMuBβC1与GAPC结合并破坏GAPC与ATG3之间的相互作用。I45，Y48和I53均被丙氨酸（A）取代的突变型βC1蛋白（βC13A），大大降低了其与GAPC的结合能力，未能破坏GAPCs-ATG3的相互作用，也无法诱导自噬。此外，携带βC13A的突变病毒显示出症状增加和病毒DNA积累与植物自噬减少有关。这些结果表明，CLCuMuBβC1通过破坏GAPCs-ATG3相互作用来激活自噬。