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Cantil: a previously unreported organ in wild-type Arabidopsis regulated by FT, ERECTA and heterotrimeric G proteins

基本信息

DOI:
10.1242/dev.195545
发表时间:
2021-06-01
期刊:
影响因子:
4.6
通讯作者:
Assmann, Sarah M.
中科院分区:
生物学2区
文献类型:
Article
作者: Gookin, Timothy E.;Assmann, Sarah M.研究方向: -- MeSH主题词: --
关键词: --
来源链接:pubmed详情页地址

文献摘要

We describe a previously unreported macroscopic Arabidopsis organ, the cantil, named for its 'cantilever' function of holding the pedicel at a distance from the stem. Cantil development is strongest at the first nodes after the vegetative to reproductive inflorescence transition; cantil magnitude and frequency decrease acropetally. Cantils develop in wild-type Arabidopsis accessions (e.g. Col-0, Ws and Di-G) as a consequence of delayed flowering in short days; cantil formation is observed in long days when flowering is delayed by null mutation of the floral regulator FLOWERING LOCUS T. The receptor-like kinase ERECTA is a global positive regulator of cantil formation; therefore, cantils never form in the Arabidopsis strain Ler. ERECTA functions genetically upstream of heterotrimeric G proteins. Cantil expressivity is repressed by the specific heterotrimeric complex subunits GPA1, AGB1 and AGG3, which also play independent roles: GPA1 suppresses distal spurs at cantil termini, while AGB1 and AGG3 suppress ectopic epidermal rippling. These G protein mutant traits are recapitulated in long-day flowering gpa1-3 ft-10 plants, demonstrating that cantils, spurs and ectopic rippling occur as a function of delayed phase transition, rather than as a function of photoperiod per se.
我们描述了一种此前未被报道的拟南芥宏观器官——悬臂(cantil),因其具有使花梗与茎保持一定距离的“悬臂”功能而得名。在营养生长向生殖生长的花序转变后的第一节处,悬臂发育最为强烈;悬臂的大小和出现频率向顶逐渐降低。在短日照条件下,由于开花延迟,野生型拟南芥品种(例如Col - 0、Ws和Di - G)会发育出悬臂;当开花因花调控因子FLOWERING LOCUS T的无效突变而延迟时,在长日照条件下也能观察到悬臂的形成。类受体激酶ERECTA是悬臂形成的全局正调控因子;因此,在拟南芥Ler品系中从不形成悬臂。ERECTA在遗传上作用于异源三聚体G蛋白的上游。悬臂的表达受到特定的异源三聚体复合物亚基GPA1、AGB1和AGG3的抑制,它们也各自发挥独立的作用:GPA1抑制悬臂末端的远侧距,而AGB1和AGG3抑制异位的表皮褶皱。这些G蛋白突变体的特征在长日照开花的gpa1 - 3 ft - 10植株中重现,这表明悬臂、距和异位褶皱的出现是相变延迟的结果,而不是光周期本身的作用。
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Assmann, Sarah M.
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