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拟南芥根中SULTR1;1硫酸转运蛋白的诱导涉及转录调控的蛋白质磷酸化/去磷酸化循环。

Induction of SULTR1;1 sulfate transporter in Arabidopsis roots involves protein phosphorylation/dephosphorylation circuit for transcriptional regulation.

作者信息

Maruyama-Nakashita Akiko, Nakamura Yumiko, Watanabe-Takahashi Akiko, Yamaya Tomoyuki, Takahashi Hideki

机构信息

RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, 230-0045 Japan.

出版信息

Plant Cell Physiol. 2004 Mar;45(3):340-5. doi: 10.1093/pcp/pch029.

DOI:10.1093/pcp/pch029
PMID:15047883
Abstract

SULTR1;1 high-affinity sulfate transporter is highly regulated by sulfur deficiency (-S) in the epidermis and cortex of Arabidopsis roots. The regulatory mechanism of SULTR1;1 expression was studied using inhibitors for transcription, translation, protein phosphorylation and dephosphorylation. The induction of SULTR1;1 mRNA during -S was blocked by the addition of actinomycin D in the medium, suggesting that SULTR1;1 is transcriptionally regulated. Cycloheximide repressed the -S induction of SULTR1;1, but enhanced the basal mRNA level of SULTR1;1 under sulfur replete (+S) condition. In addition, the induction of SULTR1;1 by -S was significantly blocked by okadaic acid (OKA) and calyculin A (CalyA). Regulation of SULTR1;1 was further confirmed in transgenic plants expressing green fluorescent protein (GFP) under the control of SULTR1;1 promoter. Accumulation of GFP during -S was dependent to SULTR1;1 promoter, and the effects of OKA and CalyA were reproducible in the SULTR1;1 promoter-GFP plants. These results suggested that the up-regulation of SULTR1;1 by -S requires protein phosphatase as an upstream regulatory factor.

摘要

SULTR1;1高亲和力硫酸盐转运蛋白在拟南芥根的表皮和皮层中受硫缺乏(-S)的高度调控。使用转录、翻译、蛋白质磷酸化和去磷酸化的抑制剂研究了SULTR1;1表达的调控机制。在培养基中添加放线菌素D可阻断-S期间SULTR1;1 mRNA的诱导,这表明SULTR1;1受转录调控。环己酰亚胺抑制了-S对SULTR1;1的诱导,但在硫充足(+S)条件下提高了SULTR1;1的基础mRNA水平。此外,冈田酸(OKA)和花萼海绵诱癌素A(CalyA)显著阻断了-S对SULTR1;1的诱导。在SULTR1;1启动子控制下表达绿色荧光蛋白(GFP)的转基因植物中进一步证实了对SULTR1;1的调控。-S期间GFP的积累依赖于SULTR1;1启动子,并且OKA和CalyA的作用在SULTR1;1启动子-GFP植物中是可重复的。这些结果表明,-S对SULTR1;1的上调需要蛋白磷酸酶作为上游调控因子。

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