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CohesinMolMech SIGNED

Molecular mechanisms of cohesin-mediated sister chromatid cohesion and chromatin organization

Total Cost €

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EC-Contrib. €

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Partnership

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 CohesinMolMech project word cloud

Explore the words cloud of the CohesinMolMech project. It provides you a very rough idea of what is the project "CohesinMolMech" about.

ring    cells    cohesin    forces    acetylated    ctcf    tirf    onto    molecules    release    localizes    mitosis    syndrome    post    synthesized    found    thought    likewise    mammalian    division    proliferating    latter    disorders    performs    again    establishes    genetic    structure    cancers    biological    dna    spindle    sites    sister    dysfunction    newly    resists    least    locked    scc4    shaped    single    biochemical    poorly    organizing    physically    mediates    frequently    structures    regulation    becomes    complexes    caused    bi    during    cohesion    segregation    mitotic    roles    orientation    genome    molecule    binding    genomic    cohesinopathies    subsequent    chromosomes    inhibited    functions    cooperates    thereby    scc2    mediated    mediating    stabilizes    chromatid    loaded    topologically    pulling    connected    perform    co    otherwise    g2    etiology    sequence    microscopy    wapl    reconstitution    mutations    inhibiting    entrap    symmetrical    gene    sororin    replication    released    protein    chromatin    positioned    questions    cell    combining    organize    stably   

Project "CohesinMolMech" data sheet

The following table provides information about the project.

Coordinator
FORSCHUNGSINSTITUT FUR MOLEKULARE PATHOLOGIE GESELLSCHAFT MBH 

Organization address
address: CAMPUS-VIENNA-BIOCENTER 1
city: WIEN
postcode: 1030
website: www.imp.ac.at

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Austria [AT]
 Project website https://www.imp.ac.at/groups/jan-michael-peters/
 Total cost 2˙500˙000 €
 EC max contribution 2˙500˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-AdG
 Funding Scheme ERC-ADG
 Starting year 2016
 Duration (year-month-day) from 2016-10-01   to  2021-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FORSCHUNGSINSTITUT FUR MOLEKULARE PATHOLOGIE GESELLSCHAFT MBH AT (WIEN) coordinator 2˙500˙000.00

Map

 Project objective

During S-phase newly synthesized “sister” DNA molecules become physically connected. This sister chromatid cohesion resists the pulling forces of the mitotic spindle and thereby enables the bi-orientation and subsequent symmetrical segregation of chromosomes. Cohesion is mediated by ring-shaped cohesin complexes, which are thought to entrap sister DNA molecules topologically. In mammalian cells, cohesin is loaded onto DNA at the end of mitosis by the Scc2-Scc4 complex, becomes acetylated during S-phase, and is stably “locked” on DNA during S- and G2-phase by sororin. Sororin stabilizes cohesin on DNA by inhibiting Wapl, which can otherwise release cohesin from DNA again. In addition to mediating cohesion, cohesin also has important roles in organizing higher-order chromatin structures and in gene regulation. Cohesin performs the latter functions in both proliferating and post-mitotic cells and mediates at least some of these together with the sequence-specific DNA-binding protein CTCF, which co-localizes with cohesin at many genomic sites. Although cohesin and CTCF perform essential functions in mammalian cells, it is poorly understood how cohesin is loaded onto DNA by Scc2-Scc4, how cohesin is positioned in the genome, how cohesin is released from DNA again by Wapl, and how Wapl is inhibited by sororin. Likewise, it is not known how cohesin establishes cohesion during DNA replication and how cohesin cooperates with CTCF to organize chromatin structure. Here we propose to address these questions by combining biochemical reconstitution, single-molecule TIRF microscopy, genetic and cell biological approaches. We expect that the results of these studies will advance our understanding of cell division, chromatin structure and gene regulation, and may also provide insight into the etiology of disorders that are caused by cohesin dysfunction, such as Down syndrome and “cohesinopathies” or cancers, in which cohesin mutations have been found to occur frequently.

 Publications

year authors and title journal last update
List of publications.
2018 Yin Cai, M. Julius Hossain, Jean-Karim Hériché, Antonio Z. Politi, Nike Walther, Birgit Koch, Malte Wachsmuth, Bianca Nijmeijer, Moritz Kueblbeck, Marina Martinic-Kavur, Rene Ladurner, Stephanie Alexander, Jan-Michael Peters, Jan Ellenberg
Experimental and computational framework for a dynamic protein atlas of human cell division
published pages: 411-415, ISSN: 0028-0836, DOI: 10.1038/s41586-018-0518-z
Nature 561/7723 2019-05-27
2018 Miroslav P Ivanov, Rene Ladurner, Ina Poser, Rebecca Beveridge, Evelyn Rampler, Otto Hudecz, Maria Novatchkova, Jean‐Karim Hériché, Gordana Wutz, Petra van der Lelij, Emanuel Kreidl, James RA Hutchins, Heinz Axelsson‐Ekker, Jan Ellenberg, Anthony A Hyman, Karl Mechtler, Jan‐Michael Peters
The replicative helicase MCM recruits cohesin acetyltransferase ESCO2 to mediate centromeric sister chromatid cohesion
published pages: e97150, ISSN: 0261-4189, DOI: 10.15252/embj.201797150
The EMBO Journal 37/15 2019-05-27
2018 Rugile Stanyte, Johannes Nuebler, Claudia Blaukopf, Rudolf Hoefler, Roman Stocsits, Jan-Michael Peters, Daniel W. Gerlich
Dynamics of sister chromatid resolution during cell cycle progression
published pages: 1985-2004, ISSN: 0021-9525, DOI: 10.1083/jcb.201801157
The Journal of Cell Biology 217/6 2019-05-27

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