Literature DB >> 19723591

Expression of cohesin and condensin genes during zebrafish development supports a non-proliferative role for cohesin.

Maren Mönnich1, Stephen Banks, Michael Eccles, Emma Dickinson, Julia Horsfield.   

Abstract

Cohesin and condensin are similar, but distinct multi-subunit protein complexes that have well-described roles in sister chromatid cohesion and chromosome condensation, respectively. Recently it has emerged that cohesin, and proteins that regulate cohesin function have additional developmental roles. To further understand the role of cohesin in development, we analyzed the expression of genes encoding cohesin and condensin subunits in developing zebrafish embryos and juvenile brain. We found that cohesin subunits are expressed in a pattern that is similar (but not quite identical) to the expression of condensin subunits. Cohesin genes smc1a, rad21, pds5b and smc3 were expressed in the forebrain ventricular zone, the tectum, the mid-hindbrain boundary, the fourth ventricle, branchial arches, the otic vesicle, the eye and faintly in the developing pectoral fins. Condensin genes smc2 and smc4 were expressed in the forebrain ventricular zone, the tectum, the mid-hindbrain boundary, the fourth ventricle, branchial arches, eye and pectoral fins. Condensin genes were additionally expressed in the hindbrain proliferative zone, an area in which cohesin genes were not detected. A comparison with pcna expression and BrdU incorporation revealed that the expression of cohesins and condensins closely overlap with zones of proliferation. Interestingly, cohesin genes were expressed in non-proliferating cells flanking rhombomere boundaries in the developing brain. In mature brain and eye, cohesin was expressed in both proliferating cells and in broad zones of post-mitotic cells. The distribution of cohesin and condensin mRNAs supports existing evidence for a non-cell cycle role for cohesin in the developing brain.

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Year:  2009        PMID: 19723591     DOI: 10.1016/j.gep.2009.08.004

Source DB:  PubMed          Journal:  Gene Expr Patterns        ISSN: 1567-133X            Impact factor:   1.224


  11 in total

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Authors:  Amanda S Brooker; Karen M Berkowitz
Journal:  Methods Mol Biol       Date:  2014

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Review 3.  Cohesinopathies, gene expression, and chromatin organization.

Authors:  Tania Bose; Jennifer L Gerton
Journal:  J Cell Biol       Date:  2010-04-19       Impact factor: 10.539

4.  A zebrafish model of Roberts syndrome reveals that Esco2 depletion interferes with development by disrupting the cell cycle.

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5.  Multifactorial origins of heart and gut defects in nipbl-deficient zebrafish, a model of Cornelia de Lange Syndrome.

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6.  Functional Urate-Associated Genetic Variants Influence Expression of lincRNAs LINC01229 and MAFTRR.

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Journal:  Front Genet       Date:  2019-01-21       Impact factor: 4.599

7.  Diverse developmental disorders from the one ring: distinct molecular pathways underlie the cohesinopathies.

Authors:  Julia A Horsfield; Cristin G Print; Maren Mönnich
Journal:  Front Genet       Date:  2012-09-12       Impact factor: 4.599

8.  Cornelia de Lange Syndrome: NIPBL haploinsufficiency downregulates canonical Wnt pathway in zebrafish embryos and patients fibroblasts.

Authors:  A Pistocchi; G Fazio; A Cereda; L Ferrari; L R Bettini; G Messina; F Cotelli; A Biondi; A Selicorni; V Massa
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9.  Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells.

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Journal:  Cell Cycle       Date:  2014-02-07       Impact factor: 4.534

Review 10.  Function Over Form: Modeling Groups of Inherited Neurological Conditions in Zebrafish.

Authors:  Robert A Kozol; Alexander J Abrams; David M James; Elena Buglo; Qing Yan; Julia E Dallman
Journal:  Front Mol Neurosci       Date:  2016-07-07       Impact factor: 5.639

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