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Cell Research (2006)16: 394-400
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Primary evidence for involvement of IP3 in heat-shock signal transduction in Arabidopsis

Hong Tao Liu, Fei Gao, Shu Juan Cui, Jin Long Han, Da Ye Sun, Ren Gang Zhou

Institute of Genetics and Physiology, Hebei Academy of Agricultural Sciences, Shijiazhuang 050051, China;
Institute of Molecular Cell Biology, Hebei Normal University, Shijiazhuang 050016, China

Correspondence: Ren Gang Zhou1, Da Ye Sun2 Tel: 86-311-87652127; Fax: 86-311-87652335; E-mail: zhourengang@163.com Tel: 86-311-86269397; Fax: 86-311-85894242; E-mail: dysun@heinfo.net Received 10 Jul 2005; revised 2 Nov 2005; accepted 7 Dec 2005, published  online 13 Apr 2006

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The role of inositol 1,4,5-trisphosphate (IP3) in transducing heat-shock (HS) signals was examined in Arabidopsis. The whole-plant IP3 level increased within 1 min of HS at 37 oC. After 3 min of HS, the IP3 level reached a maximum 2.5 fold increase. Using the transgenic Arabidopsis plants that have AtHsp18.2 promoter-b-glucuronidase (GUS) fusion gene, it was found that the level of GUS activity was up-regulated by the addition of caged IP3 at both non-HS and HS temperatures and was down-regulated by the phospholipase C (PLC) inhibitors {1-[6-((17b-3-Methoxyestra-1,3,5(10)- trien-17-yl)amino)hexyl]-2,5-pyrrolidinedione}(U-73122). The intracellular-free calcium ion concentration ([Ca2+]i) increased during HS at 37 oC in suspension-cultured Arabidopsis cells expressing apoaequorin. Treatment with U-73122 prevented the increase of [Ca2+]i to some extent. Above results provided primary evidence for the possible involvement of IP3 in HS signal transduction in higher plants.

Cell Research (2006) 16:400-406. doi:10.1038/sj.cr.7310051; published online 13 April 2006

Keywords: heat shock, signal transduction, IP3, PLC, [Ca2+]i, Arabidopsis