![]() vesicatoria ( Xcv) suppresses host autophagy and promotes infection by utilizing type-III effector XopL, which interacts with and degrades host autophagy component SH3P2 via its E3 ligase activity to promote infection 16. The other Pto DC3000 secretory effectors, HrpZ1 and HopF3, enhance or suppress autophagy to promote infection by interacting with ATG4 or ATG8, while AvrPtoB affects ATG1 kinase activity to enhance bacterial virulence 15. tomato ( Pto) DC3000 utilizes type-III effector HopM1 to stimulate autophagy for proteasome degradation and the benefit of infection in Arabidopsis 14. On the other hand, some phytopathogens directly interfere with ATGs and manipulate autophagy to promote their proliferation and virulence in plant cells 13, 14, 15, 16. Selective autophagy limits cauliflower mosaic virus (CaMV) infection through the removal of viral capsid protein and particles by autophagy cargo receptor NEIGHBOR OF BRCA1 (NBR1) 12. Geminivirus Cotton leaf curl Multan virus (CLCuMuV) infection activates autophagy, and that autophagy targets the virulence factor βC1 for degradation through its interaction with the key autophagy-related protein 8 (ATG8) and improves host immunity 11. On the one hand, a large number of studies have shown that autophagy eliminates and inhibits pathogen and virus infection by direct identification and degradation of microbe components so as to achieve the purpose of disease resistance 11, 12. In general, it is widely believed that autophagy plays dual and pleiotropic roles in plant immune response 9, 10. Subsequently, autophagy was increasingly demonstrated to be involved in plant defense and disease resistance responses to viral, bacterial and fungal pathogens 6, 7, 8. were the first to discover that autophagy positively regulates plant immunity during N protein-mediated defense against tobacco mosaic virus (TMV) 5. Autophagy also plays a crucial role in plant nutrient deficiencies and abiotic stress responses, including heat, salt, drought and darkness 2, 3, 4. In plant cells, autophagy maintains homeostasis under normal conditions and is a survival mechanism under external stress 1. Therefore, autophagy promotes JA-mediated defense against RKNs via forming a positive feedback circuit in the degradation of JAMs and transcriptional activation by ERF1.Īutophagy is a highly conserved self-degrading process that breaks down unnecessary damaged components in eukaryotes and recycles cellular nutrients. Furthermore, ERF1 acts in a positive feedback loop and regulates autophagy activity by transcriptionally activating ATG expression in response to RKN infection. JAM1 impairs the formation of a transcriptional activation complex between ETHYLENE RESPONSE FACTOR 1 (ERF1) and MEDIATOR 25 (MED25) and interferes with transcriptional regulation of JA-mediated defense-related genes by ERF1. The jasmonate (JA) signaling negative regulators JASMONATE-ASSOCIATED MYC2-LIKE 1 (JAM1), JAM2 and JAM3 interact with ATG8s via an ATG8-interacting motif (AIM), and JAM1 is degraded by autophagy during RKN infection. ![]() Here, we show that root-knot nematode (RKN Meloidogyne incognita) infection induces autophagy in tomato ( Solanum lycopersicum) and different atg mutants exhibit high sensitivity to RKNs. However, the involvement of autophagy in the plant immune system and its function in plant nematode resistance are largely unknown. ![]() Autophagy, as an intracellular degradation system, plays a critical role in plant immunity. ![]()
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