The TMK subfamily of receptor-like kinases in Arabidopsis display an essential role in growth and a reduced sensitivity to auxin.

The TMK subfamily of receptor-like kinases in Arabidopsis display an essential role in growth and a reduced sensitivity to auxin.
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DOI:
10.1371/journal.pone.0060990
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Bleecker AB
Bleecker AB
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Dai N;Wang W;Patterson SE;Bleecker AB

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控制植物器官大小的机制还不清楚,但据信涉及细胞水平的传感和信号传导。我们已经在拟南芥中分离出了包含跨膜激酶TMK亚家族受体样激酶(RLKs)的四个基因的功能缺失突变。这些TMK具有细胞外富含亮氨酸的重复基序、单个跨膜区和胞质激酶结构域。虽然单突变体不显示可辨别的表型,但独特的双突变体和三突变体组合导致器官尺寸严重减小和生长显著迟缓。四重突变体显示所有表型的更严重性并且是不育的。对根、下胚轴和雄蕊花丝生长的运动学研究表明,TMKs特异性地控制细胞扩张。在叶中,TMKs控制细胞扩增和细胞增殖。此外,在双突变体中,根和下胚轴显示出对施加的生长素、侧根诱导和生长素反应报告基因DR5:GUS的活化的敏感性降低。因此,结合结构和生物化学证据,TMKs似乎通过调节细胞扩增和细胞增殖以及作为生长素信号传导的组分来协调植物生长。
Mechanisms that govern the size of plant organs are not well understood but believed to involve both sensing and signaling at the cellular level. We have isolated loss-of-function mutations in the four genes comprising the transmembrane kinase TMK subfamily of receptor-like kinases (RLKs) in Arabidopsis. These TMKs have an extracellular leucine-rich-repeat motif, a single transmembrane region, and a cytoplasmic kinase domain. While single mutants do not display discernable phenotypes, unique double and triple mutant combinations result in a severe reduction in organ size and a substantial retardation in growth. The quadruple mutant displays even greater severity of all phenotypes and is infertile. The kinematic studies of root, hypocotyl, and stamen filament growth reveal that the TMKs specifically control cell expansion. In leaves, TMKs control both cell expansion and cell proliferation. In addition, in the tmk double mutants, roots and hypocotyls show reduced sensitivity to applied auxin, lateral root induction and activation of the auxin response reporter DR5: GUS. Thus, taken together with the structural and biochemical evidence, TMKs appear to orchestrate plant growth by regulation of both cell expansion and cell proliferation, and as a component of auxin signaling.
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