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三种ERECTA家族类受体激酶的协同相互作用通过促进细胞增殖来控制拟南芥器官生长和花发育。

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

作者信息

Shpak Elena D, Berthiaume Chris T, Hill Emi J, Torii Keiko U

机构信息

Department of Biology, University of Washington, Seattle, WA 98195, USA.

出版信息

Development. 2004 Apr;131(7):1491-501. doi: 10.1242/dev.01028. Epub 2004 Feb 25.

Abstract

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 ERL1 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.

摘要

植物器官的生长依赖于细胞增殖的协调进行,随后是细胞生长,但决定器官大小的细胞间信号的本质仍然难以捉摸。拟南芥类受体激酶(RLK)ERECTA调控花序结构。我们之前使用ERECTA的显性负性片段进行的研究揭示了ERECTA介导的信号转导途径中存在冗余。在此,我们报告拟南芥ERL1和ERL2这两个ERECTA的功能旁系同源物在ERECTA信号通路的一部分中发挥冗余但独特的作用,并且三个ERECTA家族RLK的协同相互作用决定地上器官的大小。尽管erl1和erl2突变未产生可检测到的表型,但它们以独特的方式增强了erecta的缺陷。ERL1和ERL2重叠但不同的作用很大程度上可归因于它们复杂的表达模式,而非其作为受体激酶的功能。整个ERECTA家族基因的缺失导致显著矮化、侧器官大小减小和花发育异常,包括花瓣极性扩展、心皮伸长以及花药和胚珠分化缺陷。这些缺陷是由于细胞增殖严重减少所致。我们的研究结果表明,ERECTA家族RLK作为冗余受体,将细胞增殖与器官生长和模式形成联系起来。

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