Abstract
BackgroundIn 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.ResultsSAM-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.ConclusionsThe 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-015-0556-8) contains supplementary material, which is available to authorized users.
Highlights
In dicot Arabidopsis thaliana embryos two cotyledons develop largely autonomously from the shoot apical meristem (SAM)
As typical representatives of dicot angiosperms, Arabidopsis thaliana seedlings display a body plan beginning with an epicotyl region harbouring the shoot apical meristem (SAM), flanked by two cotyledons and followed by the hypocotyl, which ends in a root tip carrying the root apical meristem (RAM) [1]
Strong rpk1 alleles generate SAM-less monocot seedlings The allele rpk1-7 was induced in a gl1 Columbia background and generates ca. 10 % seedlings with cotyledon abnormalities most of them lacking one cotyledon [22]
Summary
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. As typical representatives of dicot angiosperms, Arabidopsis thaliana seedlings display a body plan beginning with an epicotyl region harbouring the shoot apical meristem (SAM), flanked by two cotyledons and followed by the hypocotyl, which ends in a root tip carrying the root apical meristem (RAM) [1]. The initiation of cotyledons vs. SAM is largely independent, as evidenced by mutations that delete the SAM but not the cotyledons [2, 3] and vice versa [4, 5]. The mechanisms of “counting“and arranging these organs together with the SAM in order to establish the apical region are poorly understood.
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