English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
 
 
DownloadE-Mail
  The non-redundant function of cohesin acetyltransferase Esco2: some answers and new questions.

Whelan, G., Kreidl, E., Peters, J. M., & Eichele, G. (2012). The non-redundant function of cohesin acetyltransferase Esco2: some answers and new questions. Nucleus, 3(4), 1-5. doi:10.4161/nucl.20440.

Item is

Basic

show hide
Item Permalink: http://hdl.handle.net/11858/00-001M-0000-000F-9ADA-B Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-42DB-5
Genre: Journal Article

Files

show Files
hide Files
:
1470164.pdf (Publisher version), 4MB
Name:
1470164.pdf
Description:
-
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
License:
-

Locators

show

Creators

show
hide
 Creators:
Whelan, G.1, Author              
Kreidl, E., Author
Peters, J. M., Author
Eichele, G.1, Author              
Affiliations:
1Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society, ou_persistent34              

Content

show
hide
Free keywords: Cohesin, acetyltransferase, Roberts syndrome, Sororin, DSB repair
 Abstract: Cohesin and cohesin regulatory proteins function in an essential pathway enabling proper cohesion and segregation of sister chromatids. Additionally, these proteins are involved in double-strand break (DSB) repair and transcriptional regulation. Mutations in establishment of cohesion 1 homolog 2 (Esco2), an evolutionary conserved cohesin acetyltransferase, are the cause of Roberts syndrome (RBS), a human congenital disorder. To explore the mechanism by which the deficiency in Esco2 affects cohesin’s functions, we generated a mouse harboring a conditional Esco2 allele. To our surprise and in marked contrast to RBS, mouse Esco2 turns out to be a cell viability factor, the absence of which results in severe chromosome segregation defects and apoptosis. We found that the acetylation of the cohesin subunit Smc3 is significantly reduced in Esco2-deficient cells resulting in a marked reduction of Sororin recruitment to several, but not all cohesin bound loci. Here, we provide evidence that Esco2 is also required for DSB repair, which is consistent with previous studies in RBS cells.

Details

show
hide
Language(s): eng - English
 Dates: 2012-072012
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.4161/nucl.20440
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: Nucleus
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 3 (4) Sequence Number: - Start / End Page: 1 - 5 Identifier: -