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盘基网柄菌前孢子细胞中一种信号转导及转录激活蛋白的诱导性核转位:对形态发生和细胞类型调控的意义

Inducible nuclear translocation of a STAT protein in Dictyostelium prespore cells: implications for morphogenesis and cell-type regulation.

作者信息

Dormann D, Abe T, Weijer C J, Williams J

机构信息

School of Life Sciences, University of Dundee, Wellcome Trust Biocentre, Dow Street, Dundee DD1 5EH, UK.

出版信息

Development. 2001 Apr;128(7):1081-8. doi: 10.1242/dev.128.7.1081.

DOI:10.1242/dev.128.7.1081
PMID:11245573
Abstract

Dd-STATa, the Dictyostelium STAT (signal transducer and activator of transcription) protein, is selectively localised in the nuclei of a small subset of prestalk cells located in the slug tip. Injection of cAMP into the extracellular spaces in the rear of the slug induces rapid nuclear translocation of a Dd-GFP:STATa fusion protein in prespore cells surrounding the site of injection. This suggests that cAMP signals that emanate from the tip direct the localised nuclear accumulation of Dd-STATa. It also shows that prespore cells are competent to respond to cAMP, by Dd-STATa activation, and it implies that cAMP signalling is in some way limiting in the rear of the slug. Co-injection of a specific inhibitor of the cAR1 serpentine cAMP receptor almost completely prevents the cAMP-induced nuclear translocation, showing that most or all of the cAMP signal is transduced by cAR1. Dd-GFP:STATa also rapidly translocates into the nuclei of cells adjoining the front and back cut edges when a slug is bisected. Less severe mechanical disturbances, such as pricking the rear of a slug with an unfilled micropipette, also cause a more limited nuclear translocation of Dd-GFP:STATa. We propose that these signalling events form part of a repair mechanism that is activated when the migrating slug suffers mechanical damage.

摘要

盘基网柄菌信号转导与转录激活因子(Dd - STATa)是盘基网柄菌中的一种STAT(信号转导与转录激活因子)蛋白,它选择性地定位于蛞蝓状幼体顶端一小部分前柄细胞的细胞核中。向蛞蝓状幼体后部的细胞外空间注射环磷酸腺苷(cAMP),会诱导注射部位周围的前孢子细胞中Dd - GFP:STATa融合蛋白迅速发生核转位。这表明从顶端发出的cAMP信号引导了Dd - STATa的局部核积累。这还表明前孢子细胞能够通过激活Dd - STATa对cAMP作出反应,并且这意味着cAMP信号在蛞蝓状幼体后部以某种方式受到限制。共同注射cAR1蛇形cAMP受体的特异性抑制剂几乎完全阻止了cAMP诱导的核转位,表明大部分或所有的cAMP信号是由cAR1转导的。当蛞蝓状幼体被一分为二时,Dd - GFP:STATa也会迅速转位到前后切割边缘相邻细胞的细胞核中。不太严重的机械干扰,如用未装液体的微量移液器刺蛞蝓状幼体的后部,也会导致Dd - GFP:STATa发生更有限的核转位。我们提出,这些信号事件构成了一种修复机制的一部分,当迁移的蛞蝓状幼体受到机械损伤时,该机制被激活。

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