Shoot apical meristem function in Arabidopsis requires the combined activities of three BEL1-like homeodomain proteins
Shoot apical meristem function in Arabidopsis requires the combined activities of three BEL1-like homeodomain proteins
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DOI：
10.1111/j.1365-313x.2009.03809.x
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发表时间：
2009-05-01
期刊：
影响因子：
7.2
通讯作者：
Proveniers, Marcel
中科院分区：
文献类型：
--
作者：
Rutjens, Bas;Bao, Dongping;Proveniers, Marcel
在植物中，大部分地上体是通过茎顶端分生组织（SAM）的连续器官发生潜力在胚后形成的。SAM的适当功能需要维持干细胞子体消耗成发育中的原基和中央干细胞群增殖之间的微妙平衡。在这里，我们表明，启动和维护拟南芥SAM，包括花分生组织，需要的组合行动的三个成员的贝尔家族的TALE同源结构域蛋白，拟南芥HOMEOBOX 1（ATH 1），PENNYWISE（PNY）和POUND-FOOLISH（PNF）。所有三种蛋白质与KNOX TALE同源结构域蛋白STM相互作用，并且ATH 1、PNY和PNF中的组合病变导致stm突变的表型。因此，我们建议，ath 1 pny pnf分生组织缺陷的损失造成的组合BELL-STM控制。此外，我们表明，异源二聚化控制的细胞定位的贝尔和KNOX蛋白涉及CRM 1/exportin-1介导的核排斥机制，这可能是通用的控制活动的贝尔和KNOX组合。我们的结论是，在动物和植物中，相应的机制通过控制这些蛋白质的核-胞质分布来调节TALE同源结构域蛋白的活性。
In plants, most of the above-ground body is formed post-embryonically by the continuous organogenic potential of the shoot apical meristem (SAM). Proper function of the SAM requires maintenance of a delicate balance between the depletion of stem cell daughters into developing primordia and proliferation of the central stem cell population. Here we show that initiation and maintenance of the Arabidopsis SAM, including that of floral meristems, requires the combinatorial action of three members of the BELL-family of TALE homeodomain proteins, ARABIDOPSIS THALIANA HOMEOBOX 1 (ATH1), PENNYWISE (PNY) and POUND-FOOLISH (PNF). All three proteins interact with the KNOX TALE homeodomain protein STM, and combined lesions in ATH1, PNY and PNF result in a phenocopy of stm mutations. Therefore, we propose that ath1 pny pnf meristem defects result from loss of combinatorial BELL-STM control. Further, we demonstrate that heterodimerization-controlled cellular localization of BELL and KNOX proteins involves a CRM1/exportin-1-mediated nuclear exclusion mechanism that is probably generic to control the activity of BELL and KNOX combinations. We conclude that in animals and plants corresponding mechanisms regulate the activity of TALE homeodomain proteins through controlled nuclear-cytosolic distribution of these proteins.