uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
NF-Y regulates the antisense promoter, bidirectional silencing, and differential epigenetic marks of the Kcnq1 imprinting control region.
Uppsala University, Teknisk-naturvetenskapliga vetenskapsområdet, Faculty of Science and Technology, Biology, Department of Physiology and Developmental Biology. Uppsala University, Teknisk-naturvetenskapliga vetenskapsområdet, Faculty of Science and Technology, Biology, Department of Physiology and Developmental Biology, Animal Development and Genetics. zoologisk utvecklingsbiologi.
Uppsala University, Teknisk-naturvetenskapliga vetenskapsområdet, Faculty of Science and Technology, Biology, Department of Physiology and Developmental Biology, Animal Development and Genetics. Ludwiginstitutet för Cancerforskning.
Show others and affiliations
2004 (English)In: J Biol Chem, ISSN 0021-9258, Vol. 279, no 50, 52685-93 p.Article in journal (Refereed) Published
Abstract [en]

Antisense transcription has been shown to be one of the hierarchies that control gene expression in eukaryotes. Recently, we have documented that the mouse Kcnq1 imprinting control region (ICR) harbors bidirectional silencing property, and this feature is linked to an antisense RNA, Kcnq1ot1. In this investigation, using genomic footprinting, we have identified three NF-Y transcription factor binding sites appearing in a methylation-sensitive manner in the Kcnq1ot1 promoter. By employing a dominant negative mutant to the NF-Y transcription factor, we have shown that the NF-Y transcription factor positively regulates antisense transcription. Selective mutation of the conserved nucleotides in the NF-Y binding sites resulted in the loss of antisense transcription. The loss of antisense transcription from the Kcnq1ot1 promoter coincides with an enrichment in the levels of deacetylation and methylation at the lysine 9 residue of histone H3 and DNA methylation at the CpG residues, implying a crucial role for the NF-Y transcription factor in organizing the parent of origin-specific chromatin conformation in the Kcnq1 ICR. Parallel to the loss of antisense transcription, the loss of silencing of the flanking reporter genes was observed, suggesting that NF-Y-mediated Kcnq1ot1 transcription is critical in the bidirectional silencing process of the Kcnq1 ICR. These data highlight the NF-Y transcription factor as a crucial regulator of antisense promoter-mediated bidirectional silencing and the parent of origin-specific epigenetic marks at the Kcnq1 ICR. More importantly, for the first time, we document that NF-Y is involved in maintaining the antisense promoter activity against strong silencing conditions.

Place, publisher, year, edition, pages
2004. Vol. 279, no 50, 52685-93 p.
Keyword [en]
Animals, Antisense Elements (Genetics), Base Sequence, Binding Sites/genetics, CCAAT-Binding Factor/chemistry/genetics/*metabolism, Cell Line, DNA/genetics, Epigenesis; Genetic, Gene Expression Regulation, Gene Silencing, Genomic Imprinting, Humans, Membrane Proteins/chemistry/genetics/metabolism, Mice, Potassium Channels; Voltage-Gated/chemistry/*genetics/metabolism, Promoter Regions (Genetics), Recombinant Proteins/chemistry/genetics/metabolism, Research Support; Non-U.S. Gov't, Sequence Deletion
Identifiers
URN: urn:nbn:se:uu:diva-73003PubMedID: 15459184OAI: oai:DiVA.org:uu-73003DiVA: diva2:100914
Available from: 2007-02-08 Created: 2007-02-08 Last updated: 2011-01-12

Open Access in DiVA

No full text

Other links

PubMedhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=15459184&dopt=Citation

Authority records BETA

Pandey, Radha RamanEricsson, JohanKanduri, Chandrasekhar

Search in DiVA

By author/editor
Pandey, Radha RamanEricsson, JohanKanduri, Chandrasekhar
By organisation
Department of Physiology and Developmental BiologyAnimal Development and Genetics

Search outside of DiVA

GoogleGoogle Scholar

pubmed
urn-nbn

Altmetric score

pubmed
urn-nbn
Total: 608 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf