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CGGBP1 is a nuclear and midbody protein regulating abscission
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
2011 (English)In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 317, no 2, 143-150 p.Article in journal (Refereed) Published
Abstract [en]

Abscission marks the completion of cell division and its failure is associated with delayed cytokinesis and even tetraploidization. Aberrant abscission and consequential ploidy changes can underlie various diseases including cancer. Midbody, a transient structure formed in the intercellular bridge during telophase, contains several proteins including Aurora kinase B (AURKB), which participate in abscission. We report here an unexpected expression pattern and function of the transcription repressor protein CGG triplet repeat-binding protein 1 (CGGBP1), in normal human fibroblasts. We show that CGGBP1, a chromatin-associated protein, trans-localizes to spindle midzone and midbodies in a manner similar to that of AURKB. CGGBP1 depletion resulted in a cell cycle block at G2, characterized by failure of cells to undergo mitosis and also reduced entry into S phase. Consistent with its presence in the midbodies, live microscopy showed that CGGBP1 deficiency caused mitotic failure at abscission resulting in tetraploidy, which could be rescued by CGGBP1 overexpression. These results show that CGGBP1 is a bona fide midbody protein required for normal abscission and mitosis in general.

Place, publisher, year, edition, pages
2011. Vol. 317, no 2, 143-150 p.
Keyword [en]
Abscission, CGGBP1, Midbody, Tetraploidy
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:uu:diva-139866DOI: 10.1016/j.yexcr.2010.08.019ISI: 000285218200002PubMedID: 20832400OAI: oai:DiVA.org:uu-139866DiVA: diva2:382319
Available from: 2010-12-30 Created: 2010-12-30 Last updated: 2017-12-11Bibliographically approved

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Westermark, Bengt

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