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细胞分裂素途径介导 APETALA1 功能在拟南芥决定花分生组织的建立中。

Cytokinin pathway mediates APETALA1 function in the establishment of determinate floral meristems in Arabidopsis.

机构信息

State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.

出版信息

Proc Natl Acad Sci U S A. 2014 May 6;111(18):6840-5. doi: 10.1073/pnas.1318532111. Epub 2014 Apr 21.

Abstract

In angiosperms, after the floral transition, the inflorescence meristem produces floral meristems (FMs). Determinate growth of FMs produces flowers of a particular size and form. This determinate growth requires specification of floral organs and termination of stem-cell divisions. Establishment of the FM and specification of outer whorl organs (sepals and petals) requires the floral homeotic gene APETALA1 (AP1). To determine FM identity, AP1 also prevents the formation of flowers in the axils of sepals. The mechanisms underlying AP1 function in the floral transition and in floral organ patterning have been studied extensively, but how AP1 terminates sepal axil stem-cell activities to suppress axillary secondary flower formation remains unclear. Here we show that AP1 regulates cytokinin levels by directly suppressing the cytokinin biosynthetic gene LONELY GUY1 and activating the cytokinin degradation gene CYTOKININ OXIDASE/DEHYDROGENASE3. Restoring the expression of these genes to wild-type levels in AP1-expressing cells or suppressing cytokinin signaling inhibits indeterminate inflorescence meristem activity caused by ap1 mutation. We conclude that suppression of cytokinin biosynthesis and activation of cytokinin degradation mediates AP1 function in establishing determinate FM. A deeper understanding of axil-lateral meristem activity provides crucial information for enhancing yield by engineering crops that produce more elaborated racemes.

摘要

在被子植物中,花分生组织在花转变后产生花分生组织(FM)。FM 的有丝分裂生长产生特定大小和形状的花。这种有丝分裂生长需要指定花器官并终止茎细胞分裂。FM 的建立和外部轮生器官(萼片和花瓣)的指定需要花同源基因 APETALA1(AP1)。为了确定 FM 的身份,AP1 还防止在萼片腋处形成花。AP1 在花转变和花器官模式形成中的功能机制已被广泛研究,但 AP1 如何终止萼片腋干细胞活动以抑制腋生次生花的形成仍不清楚。在这里,我们表明 AP1 通过直接抑制细胞分裂素生物合成基因 LONELY GUY1 和激活细胞分裂素降解基因 CYTOKININ OXIDASE/DEHYDROGENASE3 来调节细胞分裂素水平。在 AP1 表达细胞中恢复这些基因的表达水平或抑制细胞分裂素信号,可抑制因 ap1 突变引起的不定丛生分生组织活性。我们得出结论,抑制细胞分裂素生物合成和激活细胞分裂素降解介导了 AP1 在建立确定的 FM 中的功能。对腋侧分生组织活性的更深入了解为通过工程作物产生更复杂的总状花序来提高产量提供了关键信息。

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