Ectopic shoot meristem generation in monocotyledonous rpk1 mutants is linked to SAM loss and altered seedling morphology

BMC Plant Biology

Research Article

Xiaomeng Yang¹  Ottilie Peis¹  Ramon A. Torres-Ruiz¹  Miriam Luichtl¹  Birgit S. Fiesselmann¹  Michaela Matthes² 

[1] Lehrstuhl für Genetik, Technische Universität München, Wissenschaftszentrum Weihenstephan, Emil-Ramann-Str. 8, D-85354, Freising, Germany;Lehrstuhl für Genetik, Technische Universität München, Wissenschaftszentrum Weihenstephan, Emil-Ramann-Str. 8, D-85354, Freising, Germany;Lehrstuhl für Pflanzenzüchtung, Technische Universität München, Wissenschaftszentrum Weihenstephan, Liesel-Beckmann-Str. 2, D-85354, Freising, Germany;

关键词: RPK1;    Arabidopsis;    Shoot meristem;    SAM;    Cotyledon;    Monocot;    Dicot;    Plant embryo;    Angiosperm evolution;   

DOI  :  10.1186/s12870-015-0556-8

 received in 2015-03-18, accepted in 2015-06-16,  发布年份 2015

来源: Springer

【 摘 要 】

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.

【 授权许可】

Unknown   
© Fiesselmann et al. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.