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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.

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

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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