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首页> 外文期刊>Plant physiology >ALTEREDMERISTEM PROGRAM1 Suppresses Ectopic Stem Cell Niche Formation in the Shoot Apical Meristem in a Largely Cytokinin-Independent Manner
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ALTEREDMERISTEM PROGRAM1 Suppresses Ectopic Stem Cell Niche Formation in the Shoot Apical Meristem in a Largely Cytokinin-Independent Manner

机译:ALTEREDMERISTEM PROGRAM1在很大程度上独立于细胞分裂素的方式抑制芽顶分生组织中异位干细胞小生境的形成。

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摘要

Plants are able to reiteratively form new organs in an environmentally adaptive manner during postembryonic development. Organ formation in plants is dependent on stem cell niches (SCNs), which are located in the so-called meristems. Meristems show a functional zonation along the apical-basal axis and the radial axis. Shoot apical meristems of higher plants are dome-like structures, which contain a central SCN that consists of an apical stem cell pool and an underlying organizing center. Organ primordia are formed in the circular peripheral zone (PZ) from stem cell descendants in which differentiation programs are activated. One mechanism to keep this radial symmetry integrated is that the existing SCN actively suppresses stem cell identity in the PZ. However, how this lateral inhibition system works at the molecular level is far from understood. Here, we show that a defect in the putative carboxypeptidase ALTERED MERISTEM PROGRAM1 (AMP1) causes the formation of extra SCNs in the presence of an intact primary shoot apical meristem, which at least partially contributes to the enhanced shoot meristem size and leaf initiation rate found in the mutant. This defect appears to be neither a specific consequence of the altered cytokinin levels in amp1 nor directly mediated by the WUSCHEL/CLAVATA feedback loop. De novo formation of supernumerary stem cell pools was further enhanced in plants mutated in both AMP1 and its paralog LIKE AMP1, indicating that they exhibit partially overlapping roles to suppress SCN respecification in the PZ.
机译:在胚后发育过程中,植物能够以适应环境的方式反复形成新器官。植物中的器官形成取决于位于所谓的分生组织中的干细胞壁ches(SCN)。分生组织沿顶基轴和the轴显示功能区带。高等植物的茎尖分生组织是圆顶状结构,其包含由茎干细胞池和下面的组织中心组成的中央SCN。器官原基形成于干细胞后代的圆形外围区域(PZ)中,在该区域中分化程序被激活。保持这种径向对称性整合的一种机制是,现有的SCN会主动抑制PZ中的干细胞身份。但是,这种侧向抑制系统如何在分子水平上发挥作用还远未弄清楚。在这里,我们表明推定的羧肽酶ALTERED MERISTEM PROFRAM1(AMP1)中的缺陷会导致完整的初级芽顶端分生组织的存在,形成额外的SCN,这至少部分地有助于提高芽分生组织的大小和叶片的起始速率在突变体中。该缺陷似乎既不是amp1中细胞分裂素水平改变的特定结果,也不是由WUSCHEL / CLAVATA反馈回路直接介导的。在AMP1及其旁系类似AMP1中都发生突变的植物中,多余的干细胞池的从头形成进一步增强,这表明它们在抑制PZ中的SCN重新指定方面表现出部分重叠的作用。

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