野生型和connexin43缺失小鼠脑和心脏中四类细胞-细胞/细胞-基质基因的转录组学特征。

D A Iacobaş, Marcia Urban, Sanda Iacobaş, D C Spray
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引用次数: 0

摘要

我们使用了一种高度可量化的cDNA微阵列方法来确定新生儿小鼠大脑和心脏中涉及细胞-细胞和细胞-基质相互作用的基因家族的稳定性和表达水平。此外,我们还描述了缺口连接蛋白connexin43 (Cx43)的缺失对这些特征的影响程度。我们对个体基因的观察揭示了家族成员之间转录水平的一系列差异和变异;基因组病理学(基因表达改变的全局测量)的计算表明,这些细胞相互作用基因对整体表型的贡献不成比例。我们发现大脑和心脏之间存在显著的转录组差异,Cx43的缺失大大降低了基因表达的可变性,并且在Cx43缺失的小鼠中,编码蛋白参与细胞-细胞或细胞-基质相互作用的基因的平均病理贡献约为其他基因的20倍。这些发现表明,间隙连接基因的表达影响其他参与细胞间和细胞-底物相互作用的基因的表达,这些基因的表达在Cx43缺失的小鼠中受到强大的调控压力,可能代表了对Cx43缺失的代偿反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transcriptomic characterization of four classes of cell-cell/cell-matrix genes in brains and hearts of wild type and connexin43 null mice.

We have used a highly quantifiable cDNA microarray method to determine the stabilities and expression levels within gene families involved in cell-cell and cell-matrix interactions in neonatal mouse brain and heart. In addition, we have characterized the extent to which deletion of the gap junction protein connexin43 (Cx43) affects these characteristics. Our observations for individual genes revealed a range of differences and variabilities in transcription level among family members; calculation of the genomic patholog (a global measure of gene expression alteration) indicates that these cell interaction genes contribute disproportionately to the overall phenotype. We found significant transcriptomic differences between brain and heart, that deletion of Cx43 considerably decreased gene expression variability and that the average contribution to the pathology of the genes whose encoded proteins are involved in cell-cell or cell-matrix interaction in the Cx43-null mice was about twenty times higher than that of other genes. These findings indicate that gap junction gene expression influences the expression of other genes involved in intercellular and cell-substrate interaction and that expression of these genes is under strong regulatory pressure in the Cx43-null mouse, presumably representing a compensatory response to Cx43 deletion.

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