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Plant and Cell Physiology Advance Access originally published online on August 6, 2005
Plant and Cell Physiology 2005 46(10):1674-1681; doi:10.1093/pcp/pci183
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A PIN1 Family Gene, OsPIN1, involved in Auxin-dependent Adventitious Root Emergence and Tillering in Rice

Min Xu, Ling Zhu, Huixia Shou* and Ping Wu*

State Key Laboratory of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Kaixuan Road, Hangzhou, Zhejiang 310029, PR China

* Corresponding author: Huixia Shou, E-mail, huixia{at}zju.edu.cn; Fax, +86-571-86971172; Ping Wu, E-mail, clspwu{at}zju.edu.cn, Fax, +86-571-86971232.

Auxin transport affects a variety of important growth and developmental processes in plants, including the regulation of shoot and root branching. The asymmetrical localization of auxin influx and efflux carriers within the plasma membrane establishes the auxin gradient and facilitates its transport. REH1, a rice EIR1 (Arabidopsis ethylene insensitive root 1)-like gene, is a putative auxin efflux carrier. Phylogenetic analysis of 32 members of the PIN family, taken from across different species, showed that in terms of evolutionary relationship, OsPIN1 is closer to the PIN1 family than to the PIN2 family. It is, therefore, renamed as OsPIN1 in this study. OsPIN1 was expressed in the vascular tissues and root primordial in a manner similar to AtPIN1. Adventitious root emergence and development were significantly inhibited in the OsPIN1 RNA interference (RNAi) transgenic plants, which was similar to the phenotype of NPA (N-1-naphthylphalamic acid, an auxin-transport inhibitor)-treated wild-type plants. {alpha}-naphthylacetic acid ({alpha}-NAA) treatment was able to rescue the mutated phenotypes occurring in the RNAi plants. Overexpression or suppression of the OsPIN1 expression through a transgenic approach resulted in changes of tiller numbers and shoot/root ratio. Taken together, these data suggest that OsPIN1 plays an important role in auxin-dependent adventitious root emergence and tillering.

(Received June 10, 2005; Accepted July 30, 2005)
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