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莱茵衣藻鞭毛的伸长与基因表达

Flagellar elongation and gene expression in Chlamydomonas reinhardtii.

作者信息

Periz Goran, Dharia Darshita, Miller Steven H, Keller Laura R

机构信息

Department of Biological Science, Florida State University, Tallahassee, FL 32306-4370, USA.

出版信息

Eukaryot Cell. 2007 Aug;6(8):1411-20. doi: 10.1128/EC.00167-07. Epub 2007 Jun 15.

DOI:10.1128/EC.00167-07
PMID:17573545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1951131/
Abstract

Lithium (Li(+)) affects the physiology of cells from a broad range of organisms including plants and both vertebrate and invertebrate animals. Although its effects result presumably from changes in gene expression elicited by its interaction with intracellular signal transduction pathways, the molecular mechanisms of Li(+) action are not well understood. The biflagellate green alga Chlamydomonas reinhardtii is an ideal genetic model for the integration of the effects on Li(+) on signal transduction, gene expression, and aspects of flagellar biogenesis. Li(+) causes C. reinhardtii flagella to elongate to approximately 1.4 times their normal length and blocks flagellar motility (S. Nakamura, H. Tabino, and M. K. Kojima, Cell Struct. Funct. 12:369-374, 1987). We report here that Li(+) treatment increases the abundance of several flagellar mRNAs, including alpha- and beta-tubulin and pcf3-21. Li(+)-induced flagellar gene expression occurs in cells pretreated with cycloheximide, suggesting that the abundance change is a response that does not require new protein synthesis. Deletion analysis of the flagellar alpha1-tubulin gene promoter showed that sequences necessary for Li(+)-induced expression differed from those for acid shock induction and contain a consensus binding site for CREB/ATF and AP-1 transcription factors. These studies suggest potential promoter elements, candidate factors, and signal transduction pathways that may coordinate the C. reinhardtii cellular response to Li(+).

摘要

锂(Li(+))会影响包括植物以及脊椎动物和无脊椎动物在内的多种生物体细胞的生理功能。尽管其作用可能是通过与细胞内信号转导途径相互作用引发基因表达变化而产生的,但Li(+)作用的分子机制尚未完全明确。双鞭毛绿藻莱茵衣藻是研究Li(+)对信号转导、基因表达以及鞭毛生物发生方面影响整合的理想遗传模型。Li(+)会使莱茵衣藻的鞭毛伸长至正常长度的约1.4倍,并阻断鞭毛运动(S. 中村、H. 田尾野和M. K. 小岛,《细胞结构与功能》12:369 - 374,1987年)。我们在此报告,Li(+)处理会增加几种鞭毛mRNA的丰度,包括α - 和β - 微管蛋白以及pcf3 - 21。Li(+)诱导的鞭毛基因表达发生在用环己酰亚胺预处理的细胞中,这表明丰度变化是一种不需要新蛋白质合成的反应。对鞭毛α1 - 微管蛋白基因启动子的缺失分析表明,Li(+)诱导表达所需的序列与酸休克诱导所需的序列不同,并且包含CREB/ATF和AP - 1转录因子的共有结合位点。这些研究揭示了可能协调莱茵衣藻细胞对Li(+)反应的潜在启动子元件、候选因子和信号转导途径。

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