Transcriptome profiling in Eid1-KO mice brain shows that Eid1 links cell proliferation in the brain.
CBP/P300
Differentiation
Histone acetyltransferase
Neural inflammation
Neural stem cells
Journal
Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761
Informations de publication
Date de publication:
30 Oct 2019
30 Oct 2019
Historique:
received:
15
02
2019
revised:
19
07
2019
accepted:
22
07
2019
pubmed:
6
8
2019
medline:
10
9
2019
entrez:
6
8
2019
Statut:
ppublish
Résumé
Eid1 is a member of the EID protein family, which regulates differentiation, transcription and acetyltransferase activity. Accumulating evidence suggests that Eid1 is relevant to neurological disorder, but the main function of Eid1 is still unclear, especially in the brain. To better understand this issue, we generated Eid1-knockout (Eid1-KO) mice and profiled its gene expression changes in the brain by RNA sequencing. This study identified 2531 genes differentially expressed in Eid1-KO mice compared with the wild-type, then qRT-PCR verification demonstrated that the transcriptomic data are reliable. By protein-protein interaction cluster analysis, 'regulation of cell proliferation' were unexpectedly discovered as important Eid1 functions. We then isolated neural progenitor cells (NPCs) and showed that the number of neurospheres and the proliferation rate of Eid1-KO NPCs were obviously lower than that in the control group, furthermore, CCK-8 and immunofluorescence assay clearly demonstrated that the Eid1-KO NPCs showed significantly less cell proliferation than the control group. To the best of our knowledge, this is the first comprehensive report of the Eid1-KO transcriptome of mice brain. Our analysis and experimental data provide a foundation for further studies on understanding function of Eid1 in the brain.
Identifiants
pubmed: 31381951
pii: S0378-1119(19)30657-2
doi: 10.1016/j.gene.2019.143998
pii:
doi:
Substances chimiques
EID1 protein, mouse
0
Nuclear Proteins
0
Repressor Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
143998Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.