Entry URI http://metadb.riken.jp/db/SciNetS_ria224i/cria224u4ria224u18305482i
Entry name Negi Juntaro et al. 2008 Mar. Nature 452(7186):483-6.
Title CO2 regulator SLAC1 and its homologues are essential for anion homeostasis in plant cells.
Authors Hashimoto Mimi|Iba Koh|Kawai-Yamada Maki|Matsuda Osamu|Nagasawa Takashi|Negi Juntaro|Oba Yasuhiro|Takahashi Hideyuki|Uchimiya Hirofumi
Abstract The continuing rise in atmospheric [CO2] is predicted to have diverse and dramatic effects on the productivity of agriculture, plant ecosystems and gas exchange. Stomatal pores in the epidermis provide gates for the exchange of CO2 and water between plants and the atmosphere, processes vital to plant life. Increased [CO2] has been shown to enhance anion channel activity proposed to mediate efflux of osmoregulatory anions (Cl- and malate(2-)) from guard cells during stomatal closure. However, the genes encoding anion efflux channels in plant plasma membranes remain unknown. Here we report the isolation of an Arabidopsis gene, SLAC1 (SLOW ANION CHANNEL-ASSOCIATED 1, At1g12480), which mediates CO2 sensitivity in regulation of plant gas exchange. The SLAC1 protein is a distant homologue of bacterial and fungal C4-dicarboxylate transporters, and is localized specifically to the plasma membrane of guard cells. It belongs to a protein family that in Arabidopsis consists of four structurally related members that are common in their plasma membrane localization, but show distinct tissue-specific expression patterns. The loss-of-function mutation in SLAC1 was accompanied by an over-accumulation of the osmoregulatory anions in guard cell protoplasts. Guard-cell-specific expression of SLAC1 or its family members resulted in restoration of the wild-type stomatal responses, including CO2 sensitivity, and also in the dissipation of the over-accumulated anions. These results suggest that SLAC1-family proteins have an evolutionarily conserved function that is required for the maintenance of organic/inorganic anion homeostasis on the cellular level.
Pubmed ID 18305482
Journal Nature
Volume 452
Issue 7186
Pages 483-6
Publication date 2008 Mar
Num of phenotype gene 0