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两个富含亮氨酸重复序列的受体激酶介导信号传导,将拟南芥中的细胞壁生物合成与乙烯合成酶联系起来。

Two leucine-rich repeat receptor kinases mediate signaling, linking cell wall biosynthesis and ACC synthase in Arabidopsis.

作者信息

Xu Shou-Ling, Rahman Abidur, Baskin Tobias I, Kieber Joseph J

机构信息

Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599-3280, USA.

出版信息

Plant Cell. 2008 Nov;20(11):3065-79. doi: 10.1105/tpc.108.063354. Epub 2008 Nov 18.

Abstract

The plant cell wall is a dynamic structure that changes in response to developmental and environmental cues through poorly understood signaling pathways. We identified two Leu-rich repeat receptor-like kinases in Arabidopsis thaliana that play a role in regulating cell wall function. Mutations in these FEI1 and FEI2 genes (named for the Chinese word for fat) disrupt anisotropic expansion and the synthesis of cell wall polymers and act additively with inhibitors or mutations disrupting cellulose biosynthesis. While FEI1 is an active protein kinase, a kinase-inactive version of FEI1 was able to fully complement the fei1 fei2 mutant. The expansion defect in fei1 fei2 roots was suppressed by inhibition of 1-aminocyclopropane-1-carboxylic acid (ACC) synthase, an enzyme that converts Ado-Met to ACC in ethylene biosynthesis, but not by disruption of the ethylene response pathway. Furthermore, the FEI proteins interact directly with ACC synthase. These results suggest that the FEI proteins define a novel signaling pathway that regulates cell wall function, likely via an ACC-mediated signal.

摘要

植物细胞壁是一种动态结构,通过尚不清楚的信号通路响应发育和环境信号而发生变化。我们在拟南芥中鉴定出两种富含亮氨酸重复序列的类受体激酶,它们在调节细胞壁功能中发挥作用。这些FEI1和FEI2基因(以中文“肥”字命名)的突变会破坏各向异性扩展和细胞壁聚合物的合成,并与破坏纤维素生物合成的抑制剂或突变产生累加效应。虽然FEI1是一种活性蛋白激酶,但FEI1的激酶失活版本能够完全互补fei1 fei2突变体。通过抑制1-氨基环丙烷-1-羧酸(ACC)合酶可抑制fei1 fei2根中的扩展缺陷,ACC合酶是一种在乙烯生物合成中将腺苷甲硫氨酸转化为ACC的酶,但破坏乙烯反应途径则不能抑制。此外,FEI蛋白直接与ACC合酶相互作用。这些结果表明,FEI蛋白定义了一种新的信号通路,可能通过ACC介导的信号调节细胞壁功能。

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