约5亿年前，植物登陆。环境稳态的消失促使植物不断在生长与抗逆间切换。在细胞水平上，盐胁迫等较强逆境往往引发分泌等合成通路的下调与自噬等降解通路的上调。同时，促进生长的信号通路关闭，而抗逆通路打开。找到植物用来做决定的关键蛋白及其介导的胞内运输通路切换，是理解植物生存策略的前提。我们鉴定了陆生植物特有的抗逆蛋白NRP介导的两条生长-抗逆通路。二者的共性为，早期内体（EE）定位的NRP招募生长信号蛋白，将它们定位到早期内体，并共同进入液泡降解。此过程符合自噬的定义。的确，NRP具有进化保守的、可被磷酸化的ATG8互作基序LIR。盐胁迫下可观察到ATG8被NRP大量招募。推测NRP是植物特有的、抗逆专用的自噬受体，在逆境下其LIR被FyPP3去磷酸化，由此招募ATG8并介导早期内体与分离膜/自噬体的互作，在早期内体处将生长状态下的胞吐、受体蛋白回收等合成通路切换到自噬，帮助植物从生长转向抗逆。

The first land plants appeared during the Ordovician Period. The lack of environmental homeostasis forced the sessile plants to gain the ability to constantly shuttle between growth and stress adaptation. At the cellular level, severe stress conditions such as salinity can trigger the rapid down-regulation of biosynthetic pathways such as secretory pathway, and the equally rapid induction of degradation pathways such as autophagy. In the meantime, signaling pathways that lead to growth and development are tuned down; whereas the stress signaling pathways take over. The identification of essential elements in such changes and the elucidation of their molecular functions are the key to understanding the survival strategy of plants. We have previously characterized the stress-responsive protein NRP as such an element. NRP play roles in two distinct stress responsive pathways, turning plant growth to abiotic or biotic stress adaptation. When examining the two pathways, we noticed that they have something in common: the early endosome (EE)-localized NRP recruits positive regulators of growth and development by protein-protein interaction, bringing them to EE. Then NRP and its interacting partners are destined for vacuolar degradation. By definition, this process qualifies for macroautophagy. Sequence analysis showed that NRP has three evolutionarily conserved ATG8-interacting motifs (AIM/LIR), and the first LIR can be phosphorylated. We observed that salt stress induced a re-location of ATG8 to NRP-residing structures. We hypothesized that NRP can be a plant-specific and stress-inducible autophagic receptor, and that stress induces its de-phosphorylation by FyPP3, thus facilitates its interaction with ATG8. In this way can NRP mediate the interaction between a certain population of EE and isolation membrane/autophagosome, leading to the shuttle from exocytosis and secretory pathway to autophagy and promoting stress adaptation in plants.