Ectopic shoot meristem generation in monocotyledonous rpk1 mutants is linked to SAM loss and altered seedling morphology
Ectopic shoot meristem generation in monocotyledonous rpk1 mutants is linked to SAM loss and altered seedling morphology
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DOI：
10.1186/s12870-015-0556-8
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发表时间：
2015-07-07
影响因子：
5.3
通讯作者：
Torres-Ruiz, Ramon A.
中科院分区：
文献类型：
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作者：
Fiesselmann, Birgit S.;Luichtl, Miriam;Torres-Ruiz, Ramon A.
背景：在双子叶拟南芥胚胎中，两个子叶在很大程度上是从顶端分生组织(SAM)自主发育而来的。拟南芥受体样激酶RPK1的隐性突变导致单子叶幼苗，由于复杂的功能冗余，外显率低(10%)。在强rpk1等位基因中，约有10%(即占所有纯合子的1%)没有发生SAM。我们想知道RPK1除了对细胞分裂和PINFORMED1(Pin1)极性的随机影响外，是否还控制SAM基因的表达和SAM的产生。结果：无SAM幼苗的形态简单，下胚轴-子叶结构直而连续，缺乏可识别的上胚轴。根据RPK1‘S生长素相关的Pin1缺陷，幼苗在维管组织中表现出缺陷。令人惊讶的是，没有SAM的幼苗沿着下胚轴-子叶结构向上进入子叶薄片，可变地表达了SAM特有的必需基因。很少有人能够在子叶顶端发育出异位芽分生组织(ESM)。结论：这些结果突出了SAM和子叶发育的自主性，表明rpk1的主要缺陷不在于幼苗表达SAM基因或发育茎分生组织的能力。相反，RPK1的S已知细胞分裂和生长素动态平衡的缺陷，这是由于PIN1极性的紊乱，对腺泡膜和器官生成的影响。在早期胚胎阶段，这种失败产生了简化的单子叶形态。一旦产生，这可能会导致位置信息的损失，进而影响SAM的时空发展。含SAM和不含SAM的单子叶植物表型在形态上与真正的单子叶植物或双子叶植物相似，后者只发育一个子叶。因此，rpk1突变体中特有的子叶缺陷揭示了从两个子叶转变为一个子叶的发育意义。
Background: In dicot Arabidopsis thaliana embryos two cotyledons develop largely autonomously from the shoot apical meristem (SAM). Recessive mutations in the Arabidopsis receptor-like kinase RPK1 lead to monocotyledonous seedlings, with low (10 %) penetrance due to complex functional redundancy. In strong rpk1 alleles, about 10 % of these (i. e. 1 % of all homozygotes) did not develop a SAM. We wondered whether RPK1 might also control SAM gene expression and SAM generation in addition to its known stochastic impact on cell division and PINFORMED1 (PIN1) polarity in the epidermis.Results: SAM-less seedlings developed a simple morphology with a straight and continuous hypocotyl-cotyledon structure lacking a recognizable epicotyl. According to rpk1's auxin-related PIN1 defect, the seedlings displayed defects in the vascular tissue. Surprisingly, SAM-less seedlings variably expressed essential SAM specific genes along the hypocotyl-cotyledon structure up into the cotyledon lamina. Few were even capable of developing an ectopic shoot meristem (eSM) on top of the cotyledon.Conclusions: The results highlight the developmental autonomy of the SAM vs. cotyledons and suggest that the primary rpk1 defect does not lie in the seedling's ability to express SAM genes or to develop a shoot meristem. Rather, rpk1's known defects in cell division and auxin homeostasis, by disturbed PIN1 polarity, impact on SAM and organ generation. In early embryo stages this failure generates a simplified monocotyledonous morphology. Once generated, this likely entails a loss of positional information that in turn affects the spatiotemporal development of the SAM. SAM-bearing and SAM-less monocotyledonous phenotypes show morphological similarities either to real monocots or to dicot species, which only develop one cotyledon. The specific cotyledon defect in rpk1 mutants thus sheds light upon the developmental implications of the transition from two cotyledons to one.