Autophagy plays an important role in plant–pathogen interactions. Several pathogens including viruses induce autophagy in plants, but the underpinning mechanism remains largely unclear. Furthermore, in virus–plant interactions, viral factor(s) that induce autophagy have yet to be identified. Here, we report that the βC1 protein of Cotton leaf curl Multan betasatellite (CLCuMuB) interacts with cytosolic glyceraldehyde-3-phosphate dehydrogenase (GAPC), a negative autophagic regulator, to induce autophagy in Nicotiana benthamiana. CLCuMuB βC1 bound to GAPCs and disrupted the interaction between GAPCs and autophagy-related protein 3 (ATG3). A mutant βC1 protein (βC1^3A) in which I45, Y48, and I53 were all substituted with Ala (A), had a dramatically reduced binding capacity with GAPCs, failed to disrupt the GAPCs-ATG3 interactions and failed to induce autophagy. Furthermore, mutant virus carrying βC1^3A 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。几种病原体（包括病毒）在植物中诱导自噬，但其基本机制仍不清楚。此外，在病毒与植物的相互作用中，诱导自噬的病毒因子尚未确定。在这里，我们报告说棉叶卷曲的木尔坦β卫星（CLCuMuB）的βC1蛋白与细胞质中的自噬负调节剂甘油醛3磷酸脱氢酶（GAPC）相互作用，从而诱导本生烟草的自噬。CLCuMuBβC1与GAPC结合，破坏了GAPC与自噬相关蛋白3（ATG3）之间的相互作用。一种突变βC1蛋白（βC1 ^3A），其中I45，Y48和I53都被Ala（A）取代，与GAPC的结合能力大大降低，未能破坏GAPC-ATG3相互作用，也无法诱导自噬。此外，突变体病毒携带βC1 ^3A表明增加的症状和与用于在植物自噬降低相关病毒DNA积累。这些结果表明，CLCuMuBβC1通过破坏GAPCs-ATG3相互作用来激活自噬。