PHOSPHA TIDYLSERINE SYNTHASE1 is Required for Inflorescence Meristem and Organ Development in Arabidopsis

Phosphatidylserine （PS）, a quantitatively minor membrane phospholipid, is involved in many biological processes besides its role in membrane structure. One PS synthesis gene, PHOSPHATIDYLSERINE SYNTHASE1 （PSSl）, has been discovered to be required for microspore development in Arabidopsis thaliana L....

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Bibliographic Details
Published in:植物学报：英文版 2013 (8), p.682-695
Main Author: Chengwu Liu Hengfu Yin Peng Gao Xiaohe Hu Jun Yang Zhongchi Liu Xiangdong Fu Da Luo
Format: Article
Language:English
Subjects:
RNA原位杂交
分生组织
器官
拟南芥属
磷脂酰丝氨酸
胚后发育
膜磷脂
花序
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Summary:Phosphatidylserine （PS）, a quantitatively minor membrane phospholipid, is involved in many biological processes besides its role in membrane structure. One PS synthesis gene, PHOSPHATIDYLSERINE SYNTHASE1 （PSSl）, has been discovered to be required for microspore development in Arabidopsis thaliana L. but how PSS1 affects postembryonic development is still largely unknown. Here, we show that PSSl is also required for inflorescence meristem and organ development in Arabidopsis. Disruption of PSSI causes severe dwarfism, smaller lateral organs and reduced size of inflorescence meristem. Morphological and molecular studies suggest that both cell division and cell elongation are affected in the pssl-1 mutant. RNA in situ hybridization and promoter GUS analysis show that expression of both WUSCHEL （WUS） and CLA VA TA3 （CL V3） depend on PSS1. Moreover, the defect in meristem maintenance is recovered and the expression of WUS and CLV3 are restored in the pssl-1 clvl-1 double mutant. Both SHOOTSTEMLESS （STM） and BREVIPEDICELLUS （BP） are upregulated, and auxin distribution is disrupted in rosette leaves of pssl-1. However, expression of BP, which is also a regulator of internode development, is lost in the pssl-1 inflorescence stem. Our data suggest that PSS1 plays essential roles in inflorescence meristem maintenance through the WUS-CLV pathway, and in leaf and internode development by differentially regulating the class I KNOX genes.
ISSN:1672-9072
1744-7909