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Entry URI http://metadb.riken.jp/db/SciNetS_ria224i/cria224u4ria224u17360695i
Entry name Nakagawa Yuko et al. 2007 Feb. Proc. Natl. Acad. Sci. U.S.A. 104(9):3639-44.
Title Arabidopsis plasma membrane protein crucial for Ca2+ influx and touch sensing in roots.
Authors Furuichi Takuya|Iida Hidetoshi|Iida Kazuko|Ikeda Mitsunobu|Katagiri Takeshi|Kato Tomohiko|Kishigami Akio|Kojima Itaru|Nakagawa Yuko|Nakano Masataka|Qi Zhi|Sato Shusei|Shinozaki Kazuo|Sokabe Masahiro|Tabata Satoshi|Tatsumi Hitoshi|Terashima Asuka|Yamanaka Takuya
Abstract Plants can sense and respond to mechanical stimuli, like animals. An early mechanism of mechanosensing and response is speculated to be governed by as-yet-unidentified sensory complexes containing a Ca(2+)-permeable, stretch-activated (SA) channel. However, the components or regulators of such complexes are poorly understood at the molecular level in plants. Here, we report the molecular identification of a plasma membrane protein (designated Mca1) that correlates Ca(2+) influx with mechanosensing in Arabidopsis thaliana. MCA1 cDNA was cloned by the functional complementation of lethality of a yeast mid1 mutant lacking a putative Ca(2+)-permeable SA channel component. Mca1 was localized to the yeast plasma membrane as an integral membrane protein and mediated Ca(2+) influx. Mca1 also increased [Ca(2+)](cyt) upon plasma membrane distortion in Arabidopsis. The growth of MCA1-overexpressing plants was impaired in a high-calcium but not a low-calcium medium. The primary roots of mca1-null plants failed to penetrate a harder agar medium from a softer one. These observations demonstrate that Mca1 plays a crucial role in a Ca(2+)-permeable SA channel system that leads to mechanosensing in Arabidopsis. We anticipate our findings to be a starting point for a deeper understanding of the molecular mechanisms of mechanotransduction in plants.
Pubmed ID 17360695
Journal Proceedings of the National Academy of Sciences of the United States of America
Volume 104
Issue 9
Pages 3639-44
Publication date 2007 Feb
Num of phenotype gene 0