期刊
CELL COMMUNICATION AND ADHESION
卷 15, 期 1-2, 页码 195-206出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15419060802014222
关键词
Cx43 knockout; Cx43 siRNA; gene expression coordination; Gene Regulatory Network (GRN); microarray; transcription factors
资金
- NICHD NIH HHS [P01 HD032573, P01 HD032573-05, HD32573] Funding Source: Medline
- NINDS NIH HHS [NS41023, R01 NS041282, R01 NS041023-05, R01 NS041023, NS41282, R01 NS041282-06] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [P01HD032573] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS041023, R01NS041282] Funding Source: NIH RePORTER
Previous findings of widespread transcriptomic alteration in tissues from connexin null mice raise the issue of whether the transcriptomic changes are directly due to connexin down-regulation or to compensatory developmental alterations for the missing gene. To start addressing this question, the authors compared with wild-type control the gene expression profiles of connexin43 (Cx43) knockout and Cx43siRNA knockdown wild-type cortical astrocytes. Array analysis revealed remarkable parallelism of transcriptomic changes in knockout and knockdown astrocytes, with similarly altered genes being located on all chromosomes and encoding proteins involved in a wide diversity of cell functions. Moreover, gene expression variability was analogously higher in Cx43 null and siRNA-treated astrocytes, and expression interlinkages were similarly altered among a selected subset of genes. This highly significant overlap between transcriptomic alterations in Cx43 knockout and knockdown astrocytes suggests that the widespread changes more likely reflect connexin-dependent Gene Regulatory Networks rather than developmental compensation for the missing gene.
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