Somatic embryogenesis receptor-like kinase 5 in the ecotype Landsberg erecta of Arabidopsis is a functional RD LRR-RLK in regulating brassinosteroid signaling and cell death control.
Somatic embryogenesis receptor-like kinase 5 in the ecotype Landsberg erecta of Arabidopsis is a functional RD LRR-RLK in regulating brassinosteroid signaling and cell death control.
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拟南芥兰兹伯格直立生态型中的体细胞胚胎发生受体样激酶 5 是调节油菜素类固醇信号传导和细胞死亡控制的功能性 RD LRR-RLK
DOI：
10.3389/fpls.2015.00852
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发表时间：
2015
影响因子：
5.6
通讯作者：
He K
中科院分区：
文献类型：
--
作者：
Wu W;Wu Y;Gao Y;Li M;Yin H;Lv M;Zhao J;Li J;He K
在植物中，LRR-RLKs在调节细胞外信号的感知和各种环境挑战下的细胞反应的启动中发挥核心作用。拟南芥SERK基因包括SERK 1至SERK 5，构成LRR-RLK亚家族。SERK 1、SERK 2、SERK 3/BAK 1和SERK 4/BKK 1在油菜素类固醇信号传导、细胞死亡控制、发病机制和花粉发育等多个生理过程中起着重要的调节作用。尽管与BKK 1具有极高的序列同一性，但据报道SERK 5与BKK 1没有功能重叠，BKK 1先前被鉴定为调节BR和细胞死亡控制途径，这可能是由于Col-0生态型中SERK 5激酶结构域中高度保守的RD基序中的天然突变。通过对几个拟南芥种质的基因测序分析，我们能够在兰茨贝格直立（Ler）基因组中鉴定出编码具有完整RD基序的LRR-RLK的SERK 5。SERK 5-Ler的过表达部分抑制了BR缺陷型bri 1 -5和bak 1 -3 bkk 1 -1的表型，表明SERK 5-Ler在BR信号传导中起正调节剂的作用。此外，通过酵母双杂交和BiFC测定证实了SERK 5-Ler和BRI 1之间的相互作用，并且遗传结果显示SERK 5-Ler的激酶死亡形式的表达升高导致bri 1 -5中的显性阴性表型。此外，SERK 5-Ler的过表达能够延迟而不是完全抑制bak 1 -3 bkk 1 -1的细胞死亡表型。在这项研究中，我们首次揭示了SERK 5-Ler是介导多种信号通路的生物功能组分。
In plants, LRR-RLKs play central roles in regulating perception of extracellular signals and initiation of cellular responses under various environmental challenges. Arabidopsis SERK genes, including SERK1 to SERK5, constitute a LRR-RLK sub-family. SERK1, SERK2, SERK3/BAK1, and SERK4/BKK1 have been well characterized to function as crucial regulators in multiple physiological processes such as brassinosteroid signaling, cell death control, pathogenesis, and pollen development. Despite extremely high sequence identity with BKK1, SERK5 is reported to have no functional overlapping with BKK1, which is previously identified to regulate BR and cell death control pathways, probably due to a natural mutation in a highly conserved RD motif in the kinase domain of SERK5 in Col-0 ecotype. Through a gene sequencing analysis in several Arabidopsis accessions, we are able to identify SERK5 in Landsberg erecta (Ler) genome encoding a LRR-RLK with an intact RD motif. Overexpression of SERK5-Ler partially suppresses the BR defective phenotypes of bri1-5 and bak1-3 bkk1-1, indicating SERK5-Ler functions as a positive regulator in BR signaling. Furthermore, the interaction between SERK5-Ler and BRI1 is confirmed by yeast two-hybrid and BiFC assays, and the genetic result showing that elevated expression of a kinase-dead form of SERK5-Ler causes a dominant-negative phenotype in bri1-5. In addition, overexpression of SERK5-Ler is capable of delaying, not completely suppressing, the cell death phenotype of bak1-3 bkk1-1. In this study, we first reveal that SERK5-Ler is a biologically functional component in mediating multiple signaling pathways.