Asset Details
Do you wish to reserve the book?
CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing
Do you wish to request the book?
CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing
2011
Overview
Alternative splicing of pre-messenger RNA is a key feature of transcriptome expansion in eukaryotic cells, yet its regulation is poorly understood. Spliceosome assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence alternative splicing. Supporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at exons relative to introns. Moreover, the rate of transcription elongation has been linked to alternative splicing. Here we provide the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide. We further show that CTCF binding to
CD45
exon 5 is inhibited by DNA methylation, leading to reciprocal effects on exon 5 inclusion. These findings provide a mechanistic basis for developmental regulation of splicing outcome through heritable epigenetic marks.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Biological and medical sciences
/ DNA
/ Fundamental and applied biological sciences. Psychology
/ Genetics
/ Humanities and Social Sciences
/ Humans
/ Leukocyte Common Antigens - genetics
/ Mice
/ Molecular and cellular biology
/ Repressor Proteins - metabolism
/ RNA Polymerase II - metabolism
/ Saccharomyces cerevisiae - enzymology
/ Science
/ Transcription, Genetic - genetics
/ Transcription. Transcription factor. Splicing. Rna processing
