SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 2 controls floral organ development and plant fertility by activating ASYMMETRIC LEAVES 2 in Arabidopsis thaliana

SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 2 controls floral organ development and plant fertility by... A network of genes is coordinately expressed to ensure proper development of floral organs and fruits, which are essential for generating new offspring in flowering plants. In Arabidopsis thaliana, microRNA156 (miR156) plays a role in regulating the development of flowers and siliques by targeting members of the SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) gene family. Despite the important roles of the miR156/SPL network, our understanding of its downstream genes that are involved in floral organ and silique growth is still incomplete. Here, we report that the miR156/SPL2 regulatory pathway regulates pollen production, fertility rate, and the elongation of floral organs, including petals, sepals, and siliques in Arabidopsis. Transgenic plants exhibiting both overexpression of miR156 and dominant-negative alleles of SPL2 had reduced ASYMMETRIC LEAVES 2 (AS2) transcript levels in their siliques. Furthermore, their fertility phenotype was similar to that of the AS2 loss-of-function mutant. We also demonstrate that the SPL2 protein binds to the 5′UTR of the AS2 gene in vivo, indicating that AS2 is directly regulated by SPL2. Our results suggest that the miR156/SPL2 pathway affects floral organs, silique development and plant fertility, as well as directly regulates AS2 expression. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 2 controls floral organ development and plant fertility by activating ASYMMETRIC LEAVES 2 in Arabidopsis thaliana

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Publisher
Springer Netherlands
Copyright
Copyright © 2016 by Her Majesty the Queen in Right of Canada
Subject
Life Sciences; Plant Sciences; Biochemistry, general; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1007/s11103-016-0536-x
Publisher site
See Article on Publisher Site

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