PEAPOD regulates lamina size and curvature in Arabidopsis
PEAPOD regulates lamina size and curvature in Arabidopsis
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DOI：
10.1073/pnas.0604349103
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发表时间：
2006-08-29
影响因子：
11.1
通讯作者：
White, Derek W. R.
中科院分区：
文献类型：
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作者：
White, Derek W. R.
尽管已知在真双子叶植物叶片发育期间发生了复杂的散布细胞增殖和细胞分化模式，但协调这种生长的遗传机制尚不清楚。在拟南芥中，PEAPOD（PPD）基因座的缺失增加叶片大小，并导致圆顶形，而不是扁平的叶子。由于额外的叶片生长，Siliques的形状也发生了变化。三角形ppd叶片的曲率反映了叶片的过度生长与其周边延伸能力的限制之间的差异。Delta ppd植物中的过量叶片生长是由于叶片发育期间分散的分生组织细胞（DMC）增殖（例如，分别形成气孔干细胞和维管细胞的分生组织样细胞和原形成层细胞）的延长阶段。PPD基因座由两个同源基因PPD 1和PPD 2组成，它们编码植物特异性推定的DNA结合蛋白。PPD的过表达通过促进叶片和角果发育过程中DMC增殖的早期停滞来降低叶片大小。因此，通过调节DMC增殖的停滞，PPD基因协调组织生长，调节叶片大小，并限制叶片的曲率。我提出了一个修订后的模型，叶发育与两个细胞周期逮捕前线进展从尖端到基地：已知的主要前线，这决定逮捕一般细胞增殖，其次是二级前线，涉及PPD和逮捕DMC司。
Although a complex pattern of interspersed cell proliferation and cell differentiation is known to occur during leaf blade development in eudicot plants, the genetic mechanisms coordinating this growth are unclear. In Arabidopsis, deletion of the PEAPOD (PPD) locus increases leaf lamina size and results in dome-shaped rather than flat leaves. Siliques are also altered in shape because of extra lamina growth. The curvature of a Delta ppd leaf reflects the difference between excess growth of the lamina and a limitation to the extension capacity of its perimeter. Excess lamina growth in Delta ppd plants is due to a prolonged phase of dispersed meristematic cell (DMC) proliferation (for example, the meristemoid and procambium cells that form stomatal stem cells and vascular cells, respectively) during blade development. The PPD locus is composed of two homologous genes, PPD1 and PPD2, which encode plant-specific putative DNA-binding proteins. Overexpression of PPD reduces lamina size by promoting the early arrest of DMC proliferation during leaf and silique development. Therefore, by regulating the arrest of DMC proliferation, the PPD genes coordinate tissue growth, modulate lamina size, and limit curvature of the leaf blade. I propose a revised model of leaf development with two cell-cycle arrest fronts progressing from the tip to the base: the known primary front, which determines arrest of general cell proliferation, followed by a secondary front that involves PPD and arrests DMC division.