NDLI: Developmental acquisition of enhancer function requires a unique coactivator activity.

Content Provider	PubMed Central
Author	Majumder, S. Zhao, Z. Kaneko, K. Depamphilis, M. L.
Abstract	Enhancers are believed to stimulate promoters by relieving chromatin-mediated repression. However, injection of plasmid-encoded genes into mouse oocytes and embryos revealed that enhancers failed to stimulate promoters prior to formation of a two-cell embryo, even though the promoter was repressed in the maternal nucleus of both oocytes and one-cell embryos. The absence of enhancer function was not due to the absence of a required sequence-specific enhancer activation protein, because enhancer function was not elicited even when these proteins either were provided by an expression vector (GAL4:VP16) or were present as an endogenous transcription factor (TEF-1) and shown to be active in stimulating promoters. Instead, enhancer function in vivo required a unique coactivator activity in addition to enhancer-specific DNA binding proteins and promoter repression. This coactivator activity first appeared during mouse development in two- to four-cell embryos, concurrent with the major onset of zygotic gene expression. Competition between various enhancers was observed in these embryos, but not competition between enhancers and promoters, and competition between enhancers was absent in one-cell embryos. Moreover, enhancer function in oocytes could be partially restored by pre-injecting mRNA from cells in which enhancers were active, the same mRNA did not affect enhancer function in two- to four-cell embryos.
Related Links	http://dx.doi.org/10.1093/emboj/16.7.1721
Ending Page	1731
Page Count	11
Starting Page	1721
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	7
Volume Number	16
Language	English
Publisher Date	1997-04-01
Access Restriction	Open
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function

A unique right end–enhancer complex precedes synapsis of Mu ends: the enhancer is sequestered within the transpososome throughout transposition

Endosomal transport function in yeast requires a novel AAA-type ATPase, Vps4p.

Recruitment of p300 by C/EBPβ triggers phosphorylation of p300 and modulates coactivator activity

DNA methylation status predicts cell type-specific enhancer activity

MYST protein acetyltransferase activity requires active site lysine autoacetylation

Crif1 is a novel transcriptional coactivator of STAT3

Coactivator MBF1 preserves the redox-dependent AP-1 activity during oxidative stress in Drosophila

Unique anti-apoptotic activity of EAAC1 in injured motor neurons

Developmental acquisition of enhancer function requires a unique coactivator activity.

Similar Documents

Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function

A unique right end–enhancer complex precedes synapsis of Mu ends: the enhancer is sequestered within the transpososome throughout transposition

Endosomal transport function in yeast requires a novel AAA-type ATPase, Vps4p.

Recruitment of p300 by C/EBPβ triggers phosphorylation of p300 and modulates coactivator activity

DNA methylation status predicts cell type-specific enhancer activity

MYST protein acetyltransferase activity requires active site lysine autoacetylation

Crif1 is a novel transcriptional coactivator of STAT3

Coactivator MBF1 preserves the redox-dependent AP-1 activity during oxidative stress in Drosophila

Unique anti-apoptotic activity of EAAC1 in injured motor neurons

Developmental acquisition of enhancer function requires a unique coactivator activity.