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一种SET/MYND染色质重塑蛋白调控盘基网柄菌的前孢子模式形成。

A SET/MYND chromatin re-modelling protein regulates Dictyostelium prespore patterning.

作者信息

Nuñez-Corcuera Beatriz, Birch Joanna, Williams Jeffrey G

机构信息

College of Life Sciences, Welcome Trust Building, University of Dundee, Dundee, UK.

出版信息

Int J Dev Biol. 2011;55(2):205-8. doi: 10.1387/ijdb.113309bn.

DOI:10.1387/ijdb.113309bn
PMID:21671223
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3586672/
Abstract

SmdA is a Dictyostelium orthologue of the SET/MYND chromatin re-modelling proteins. In developing structures derived from a null mutant for smdA (a smdA- strain), prestalk patterning is normal, but using a prespore lacZ reporter fusion, there is ectopic accumulation of beta-galactosidase in the prestalk region. As wild type slugs migrate, there is continual forward movement and re-differentiation of prespore cells into prestalk cells. Thus, a potential explanation for the ectopic reporter localization in smdA null prestalk cells is an increased rate of re-differentiation and anterior movement of prespore cells. In support of this notion, analysis of an unstable lacZ reporter, driven by the prespore promoter, reveals a normal staining pattern in the smdA- strain. We suggest that one or more genes regulated by SmdA acts to repress prespore re-specification.

摘要

SmdA是SET/MYND染色质重塑蛋白在盘基网柄菌中的同源物。在由smdA基因敲除突变体(smdA-菌株)发育而来的结构中,前柄细胞的模式形成正常,但使用前孢子lacZ报告基因融合体时,β-半乳糖苷酶在前柄区域出现异位积累。当野生型蛞蝓移动时,前孢子细胞会持续向前移动并重新分化为前柄细胞。因此,smdA基因敲除的前柄细胞中报告基因异位定位的一个可能解释是前孢子细胞重新分化和向前移动的速率增加。支持这一观点的是,对由前孢子启动子驱动的不稳定lacZ报告基因的分析显示,smdA-菌株中的染色模式正常。我们认为,受SmdA调控的一个或多个基因起到抑制前孢子重新特化的作用。

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