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SERK 家族受体样激酶与 PXY 一起作为共受体在植物血管发育中发挥作用。

SERK Family Receptor-like Kinases Function as Co-receptors with PXY for Plant Vascular Development.

机构信息

Ministry of Education Key Laboratory of Protein Science, Center for Structural Biology, School of Life Sciences, Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing 100084, China.

State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking-Tsinghua Joint Center for Life Sciences, Peking University, Beijing 100871, China.

出版信息

Mol Plant. 2016 Oct 10;9(10):1406-1414. doi: 10.1016/j.molp.2016.07.004. Epub 2016 Jul 21.

Abstract

In Arabidopsis, the CLAVATA3/EMBRYO SURROUNDING REGION-RELATED (CLE) peptides play important roles in regulating proliferation and differentiation of plant-specific stem cells. Although receptors of CLEs are reported to be leucine-rich repeat receptor kinases, the mechanisms underlying CLE-induced receptor activation remain largely unknown. Here we show that SOMATIC EMBRYOGENESIS RECEPTOR KINASEs (SERKs) serve as co-receptors in CLE41/TDIF-PXY signaling to regulate plant vascular development. TDIF induces interaction of its receptor PXY with SERKs in vitro and in vivo. Furthermore, the serk1-1 serk2-1 bak1-5 mutant plants are less sensitive to TDIF, phenocopying the pxy mutant with a compromised promotion of procambial cell proliferation. Crystal structure of the PXY-TDIF-SERK2 complex reveals that the last amino acid of TDIF conserved among CLEs and other evolutionary-related peptides is important for the interaction between SERK2 and PXY. Taken together, our current study identifies SERKs as signaling components of the TDIF-PXY pathway and suggests a conserved activation mechanism of CLE receptors.

摘要

在拟南芥中,CLAVATA3/EMBRYO SURROUNDING REGION-RELATED(CLE)肽在调节植物特异性干细胞的增殖和分化中发挥重要作用。尽管已经报道 CLE 的受体是富含亮氨酸重复的受体激酶,但 CLE 诱导的受体激活的机制在很大程度上仍不清楚。在这里,我们表明 SOMATIC EMBRYOGENESIS RECEPTOR KINASEs(SERKs)作为 CLE41/TDIF-PXY 信号传导中的共受体,调节植物血管发育。TDIF 在体外和体内诱导其受体 PXY 与 SERKs 的相互作用。此外,serk1-1 serk2-1 bak1-5 突变体植物对 TDIF 的敏感性降低,与 pxy 突变体一样,促进原形成层细胞增殖的能力受损。PXY-TDIF-SERK2 复合物的晶体结构表明,CLE 中保守的和其他进化相关肽的 TDIF 最后一个氨基酸对于 SERK2 和 PXY 之间的相互作用很重要。总之,我们目前的研究将 SERKs 鉴定为 TDIF-PXY 途径的信号成分,并提出了 CLE 受体的保守激活机制。

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