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Overexpression of miR319a Affects the Balance Between Mitosis and Endoreduplication in Arabidopsis Leaves

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Abstract

Endoreduplication, a type of cell cycle in which DNA replication continues without cell division, is deeply involved in plant development and differentiation. Many researches about miR319a influence on plant development have been reported, but there is little information to indicate whether plant cell division and development are the collective effect of miR319a. To examine the effect of miR319a on cell division and development, miR319a was overexpressed in Arabidopsis in this study. miR319a-overexpressing plants exhibited abnormal organ phenotypes such as heavy serrated leaves, crinkled siliques, bushy trichomes, spoon-like sepals, and abnormal floral organs. These phenomena suggested that miR319a played important roles in modulating plant morphogenesis. At the cellular level, overexpression of miR319a decreased the final size of leaf epidermal cell. Furthermore, miR319a overexpression also reduced endoreduplication in leaf cells and upregulated the expression of some members of the cell cycle-related genes. Taken together, miR319a plays a pivotal role in development and cell division in Arabidopsis.

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Acknowledgments

This work was supported by the National Natural Science Foundation of China (No. 31272114, 30771459 and 30430450) and the Natural Science Foundation of Zhejiang Province, China (Y305251 and Y306145). We also thank the Innovation and Improving project of Zhejiang Academy of Agricultural Sciences providing the initiation fund (2014CX016) for our work. Our laboratory was also supported by the Key Laboratory Prospective Study project (2010DS700124KF1402) from Zhejiang Academy of Agricultural Sciences. We show our acknowledgments to all these supports.

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Correspondence to Renhu Liu.

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Wang, F., Zheng, T., Wu, G. et al. Overexpression of miR319a Affects the Balance Between Mitosis and Endoreduplication in Arabidopsis Leaves. Plant Mol Biol Rep 33, 2006–2013 (2015). https://doi.org/10.1007/s11105-015-0893-7

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