ESCRT-I mediates FLS2 endosomal sorting and plant immunity.
ESCRT-I mediates FLS2 endosomal sorting and plant immunity.
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DOI：
10.1371/journal.pgen.1004035
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发表时间：
2013
期刊：
影响因子：
4.5
通讯作者：
Robatzek S
中科院分区：
文献类型：
--
作者：
Spallek T;Beck M;Ben Khaled S;Salomon S;Bourdais G;Schellmann S;Robatzek S
植物免疫受体鞭毛蛋白传感2（FLS 2）存在于质膜上，并在其配体鞭毛蛋白（flg 22）活化后内化。我们发现，ESCRT-I亚基在拟南芥FLS 2的内吞作用中发挥作用。VPS 37 -1与FLS 2共定位于内体，并在flg 22引发后与受体免疫沉淀。Vps 37 -1突变体在flg 22诱导的FLS 2内体中减少，但在Rab 5 GTP酶标记的内体中不减少，表明FLS 2运输缺陷而不是内体形成。FLS 2定位于多泡体的内腔，但这在vps 37 -1突变体中改变，表明ESCRT-I功能丧失导致FLS 2的内体分选受损。VPS 37 -1和VPS 28 -2通过在气孔关闭中的作用而对于针对细菌感染的免疫是关键的。我们的研究结果表明，VPS 37 -1，同样VPS 28 -2，调节晚期FLS 2内体分选，并揭示ESCRT-I是关键的flg 22激活气孔防御参与植物免疫。植物利用质膜免疫受体来调查其环境中的潜在威胁。这些受体之一，鞭毛蛋白传感2（FLS 2）识别细菌鞭毛蛋白（flg 22），从而触发多种防御反应，增强对感染性病原体的免疫力。因此，调节FLS 2的亚细胞定位是植物抗病性的一个重要方面。已知FLS 2在质膜和内体区室之间穿梭，但在配体依赖性活化后进入晚期内体运输途径。一个关键问题是激活的FLS 2在晚期内体运输中的调节。在这里，我们表明，FLS 2被内化到管腔的多泡体和发现的遗传抑制，这一步是由组分的内体分选复合物所需的运输-I（ESCRT-I）。此外，我们揭示了这些ESCRT-I组分在植物免疫中起着至关重要的作用，影响flg 22触发的气孔关闭，病原菌的突出入口点，这发生在已知的flg 22响应的下游。这些发现强调了内体运输在调节FLS 2亚细胞定位和植物免疫中的作用。
The plant immune receptor FLAGELLIN SENSING 2 (FLS2) is present at the plasma membrane and is internalized following activation of its ligand flagellin (flg22). We show that ENDOSOMAL SORTING COMPLEX REQUIRED FOR TRANSPORT (ESCRT)-I subunits play roles in FLS2 endocytosis in Arabidopsis. VPS37-1 co-localizes with FLS2 at endosomes and immunoprecipitates with the receptor upon flg22 elicitation. Vps37-1 mutants are reduced in flg22-induced FLS2 endosomes but not in endosomes labeled by Rab5 GTPases suggesting a defect in FLS2 trafficking rather than formation of endosomes. FLS2 localizes to the lumen of multivesicular bodies, but this is altered in vps37-1 mutants indicating compromised endosomal sorting of FLS2 by ESCRT-I loss-of-function. VPS37-1 and VPS28-2 are critical for immunity against bacterial infection through a role in stomatal closure. Our findings identify that VPS37-1, and likewise VPS28-2, regulate late FLS2 endosomal sorting and reveals that ESCRT-I is critical for flg22-activated stomatal defenses involved in plant immunity. Plants deploy plasma membrane immune receptors to survey their environment for potential threats. One of these receptors, FLAGELIN SENSING 2 (FLS2) recognizes bacterial flagellin (flg22) and thereby triggers a multitude of defense responses, enhancing immunity against infectious pathogens. Regulation of the subcellular localization of FLS2 is therefore an important aspect in plant disease resistance. FLS2 is known to shuttle between the plasma membrane and endosomal compartments but enters the late endosomal trafficking pathway upon ligand-dependent activation. A key question is the regulation of activated FLS2 in late endosomal trafficking. Here, we show that FLS2 is internalized into the lumen of multivesicular bodies and discovered by genetic inhibition that this step is regulated by components of the ENDOSOMAL SORTING COMPLEXES REQUIRED FOR TRANSPORT-I (ESCRT-I). Furthermore, we reveal that these ESCRT-I components play crucial roles in plant immunity impacting the flg22-triggered closure of stomata, prominent entry points of pathogenic bacteria, which occurred downstream of the known flg22 responses. These findings highlight the roles of endosomal trafficking in regulating FLS2 subcellular localization and plant immunity.
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