Synergistic interaction of three ERECTA-family receptor-like kinases controls Arabidopsis organ growth and flower development by promoting cell proliferation

Synergistic interaction of three ERECTA-family receptor-like kinases controls Arabidopsis organ growth and flower development by promoting cell proliferation
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DOI:
10.1242/dev.01028
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发表时间:
2004-04-01
期刊:
影响因子:
4.6
通讯作者:
Torii, KU
Torii, KU
中科院分区:
生物学2区
文献类型:
--
作者:
Shpak, ED;Berthiaume, CT;Torii, KU

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植物器官的生长依赖于协调的细胞增殖,然后是细胞生长,但指定器官大小的细胞-细胞信号的性质仍然难以捉摸。拟南芥受体样激酶(RLK)ERECTA调节花序结构。我们先前的研究使用ERECTA的显性负性片段揭示了ERECTA介导的信号转导通路中存在冗余。在这里,我们报告说,拟南芥ERL 1和ERL 2,ERECTA的两个功能旁系同源物,发挥冗余,但独特的作用,在ERECTA信号通路的一部分,并协同相互作用的三个ERECTA家族RLK定义气生器官的大小。虽然erl 1和erl 2突变没有可检测的表型,但它们以独特的方式增强了勃起缺陷。ERM和ERL 2的重叠但不同的作用主要归因于它们复杂的表达模式,而不是它们作为受体激酶的功能。整个ERECTA家族基因的丢失导致显著的侏儒症,侧器官大小减少和异常的花发育,包括花瓣极性扩张,心皮伸长,花药和胚珠分化的缺陷。这些缺陷是由于细胞增殖严重减少。我们的发现将ERECTA家族RLK作为将细胞增殖与器官生长和模式化联系起来的冗余受体。
Growth of plant organs relies on coordinated cell proliferation followed by cell growth, but the nature of the cell-cell signal that specifies organ size remains elusive. The Arabidopsis receptor-like kinase (RLK) ERECTA regulates inflorescence architecture. Our previous study using a dominant-negative fragment of ERECTA revealed the presence of redundancy in the ERECTA-mediated signal transduction pathway. Here, we report that Arabidopsis ERL1 and ERL2, two functional paralogs of ERECTA, play redundant but unique roles in a part of the ERECTA signaling pathway, and that synergistic interaction of three ERECTA-family RLKs define aerial organ size. Although erl1 and erl2 mutations conferred no detectable phenotype, they enhanced erecta defects in a unique manner. Overlapping but distinct roles of ERM and ERL2 can be ascribed largely to their intricate expression patterns rather than their functions as receptor kinases. Loss of the entire ERECTA family genes led to striking dwarfism, reduced lateral organ size and abnormal flower development, including defects in petal polar expansion, carpel elongation, and anther and ovule differentiation. These defects are due to severely reduced cell proliferation. Our findings place ERECTA-family RLKs as redundant receptors that link cell proliferation to organ growth and patterning.