State Key Laboratory of Agro-Biotechnology, College of Biological Sciences, China Agricultural University, Beijing, China.
College of Plant Protection, China Agricultural University, Beijing, China.
EMBO J. 2021 Aug 2;40(15):e108050. doi: 10.15252/embj.2021108050. Epub 2021 Jun 22.
Selective autophagy mediates specific degradation of unwanted cytoplasmic components to maintain cellular homeostasis. The suppressor of gene silencing 3 (SGS3) and RNA-dependent RNA polymerase 6 (RDR6)-formed bodies (SGS3/RDR6 bodies) are essential for siRNA amplification in planta. However, whether autophagy receptors regulate selective turnover of SGS3/RDR6 bodies is unknown. By analyzing the transcriptomic response to virus infection in Arabidopsis, we identified a virus-induced small peptide 1 (VISP1) composed of 71 amino acids, which harbor a ubiquitin-interacting motif that mediates interaction with autophagy-related protein 8. Overexpression of VISP1 induced selective autophagy and compromised antiviral immunity by inhibiting SGS3/RDR6-dependent viral siRNA amplification, whereas visp1 mutants exhibited opposite effects. Biochemistry assays demonstrate that VISP1 interacted with SGS3 and mediated autophagic degradation of SGS3/RDR6 bodies. Further analyses revealed that overexpression of VISP1, mimicking the sgs3 mutant, impaired biogenesis of endogenous trans-acting siRNAs and up-regulated their targets. Collectively, we propose that VISP1 is a small peptide receptor functioning in the crosstalk between selective autophagy and RNA silencing.
选择性自噬介导对细胞质内不需要的成分进行特异性降解，以维持细胞内稳态。基因沉默抑制子 3（SGS3）和 RNA 依赖性 RNA 聚合酶 6（RDR6）形成的小体（SGS3/RDR6 小体）对于植物体内 siRNA 的扩增是必需的。然而，自噬受体是否调节 SGS3/RDR6 小体的选择性周转尚不清楚。通过分析拟南芥对病毒感染的转录组响应，我们鉴定了一种由 71 个氨基酸组成的病毒诱导小肽 1（VISP1），其含有一个泛素相互作用基序，介导与自噬相关蛋白 8 的相互作用。VISP1 的过表达诱导了选择性自噬，并通过抑制 SGS3/RDR6 依赖性病毒 siRNA 扩增来破坏抗病毒免疫，而 visp1 突变体则表现出相反的效果。生化分析表明，VISP1 与 SGS3 相互作用，并介导 SGS3/RDR6 小体的自噬降解。进一步的分析表明，过表达 VISP1，模拟 sgs3 突变体，损害了内源性反式作用 siRNA 的生物发生，并上调了它们的靶标。总的来说，我们提出 VISP1 是一种小肽受体，在选择性自噬和 RNA 沉默的串扰中发挥作用。
