Drosophila Chromosome Condensation Proteins Topoisomerase II and Barren Colocalize with Polycomb and Maintain Fab-7 PRE Silencing

Lupo, Rossella; Breiling, Achim; Bianchi, Marco E.; Orlando, Valerio

doi:10.1016/s1097-2765(01)00161-7

Cited by 109 publications

(89 citation statements)

References 47 publications

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“…Type II DNA topoisomerases of various organisms were reported to physically interact with a diverse collection of proteins (35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50). Several of these proteins are of particular interest.…”

Section: Discussionmentioning

confidence: 99%

Aberrant lamination in the cerebral cortex of mouse embryos lacking DNA topoisomerase IIβ

Lyu

Wang²

2003

Proc. Natl. Acad. Sci. U.S.A.

106

115

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We have examined corticogenesis in mouse embryos lacking DNA topoisomerase II␤ (II␤) in the brain or in all tissues. The absence of II␤, a type II DNA topoisomerase normally expressed in postmitotic cells in the developing cortex, severely affects cerebral stratification: no subplate is discernible, and neurons born at later stages of corticogenesis fail to migrate to the superficial layers. This abnormal pattern of neuron positioning in the cerebral cortex is reminiscent of that observed in mouse mutants defective in the reelin-signaling pathway. Significantly, the level of reelin in the neocortex is much reduced when II␤ is absent. These results implicate a role of II␤ in brain development. The enzyme may be required in implementing particular genetic programs in postmitotic cells, such as reelin expression in Cajal-Retzius cells, perhaps through its action on nucleoprotein structure of particular chromosomal regions.M ammalian DNA topoisomerase II␤ (II␤) is a type II DNA topoisomerase that catalyzes the transport of one DNA double-helix through another (1-3). Unlike the II␣ isozyme, which is specifically expressed in proliferating cells and most likely performs the essential function of resolving intertwined chromosome pairs during mitosis (4-6), II␤ is apparently dispensable in cell growth (reviewed in ref. 7). Targeted disruption of the murine TOP2␤ gene showed; however, that II␤ has a critical role in neural and neuromuscular development (8). Whereas top2␤ ϩ/⌬ mice are phenotypically TOP2␤ ϩ and indistinguishable from their TOP2␤ ϩ/ϩ littermates, top2␤ ⌬/⌬ nullizygotes die of a breathing impairment at birth, most likely owing to neural and neuromuscular defects (8).In mammals, II␣ and II␤ are largely expressed in proliferating cells and nonproliferating cells, respectively (7). In a detailed examination of the expression of the two forms during postnatal development of rat cerebellum, a sharp transition from II␣ to II␤ expression was observed in cell populations that had undergone the final division and committed to differentiate into Purkinje or granule cells (9). The amount of DNA-bound II␤ becomes undetectable, however, when cells reach terminal differentiation (10).To further test the role of II␤ in neural development, we have examined cerebral corticogenesis in embryos of mouse lines lacking II␤ in all tissues or specifically in certain brain structures including the telencephalon. We report here that II␤ has a remarkable role in neurogenesis. The induction of II␤ expression, after the final division of cells committed to a neuronal fate, appears necessary for the developmentally regulated expression of certain specific genes in these cells. The role of II␤ is unlikely to be limited to neuronal development and may also be important in the genetic programming of other postmitotic cells. Materials and MethodsConstruction of the Targeting Vector. The left and right arms of TOP2␤-derived sequences, for targeted insertion of DNA sequences between them into the mouse genome, were obtained by PCR. The right ...

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Section: Discussionmentioning

confidence: 99%

Aberrant lamination in the cerebral cortex of mouse embryos lacking DNA topoisomerase IIβ

Lyu

Wang²

2003

Proc. Natl. Acad. Sci. U.S.A.

106

115

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“…Structural maintenance of chromosome2 and 4 are chromosomal ATPases, whereas the non-SMC proteins likely modulate the activity of the SMC heterodimer or may regulate the spatial and temporal distribution of each complex. [1][2][3] Recent studies have provided evidence that condensin complexes and individual condensin subunits contribute to nonmitotic processes such as X-chromosome dosage compensation in Caenorhabditis elegans 4,5 epigenetic control of homeotic gene expression in Drosophila 6 and DNA repair in Saccharomyces pombe. 7 In addition to mitosis, chromosome condensation is also a common phenomenon during terminal differentiation of many hematopoietic cells, including erythroid cells, megakaryocytes and lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

MTB, the murine homolog of condensin II subunit CAP-G2, represses transcription and promotes erythroid cell differentiation

Leung

Lee

et al. 2006

Leukemia

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Chromosome condensation is essential for proper segregation of duplicated sister chromatids in mitosis. Mammalian erythroid maturation is also associated with gradual nuclear condensation. However, few proteins that are directly involved in chromosome condensation during erythropoiesis have been identified. In this report, we show that MTB (more than blood), which was initially isolated in a yeast two-hybrid screen for proteins that interact with the basic helix-loop-helix (bHLH) protein stem cell leukemia (SCL), and later identified as the murine homolog of the condensin II subunit CAP-G2, participates in erythroid cell development. MTB interacts with SCL and another hematopoietic bHLH protein, E12, and is recruited to the nucleus by SCL and E12. In addition, MTB can repress SCL/E12-mediated transcriptional activation. Consistent with the model that MTB may function together with SCL/E12 heterodimer during erythroid cell development, MTB is highly expressed in the erythroid lineage and is upregulated upon erythroid differentiation. Moreover, overexpression of MTB promotes the terminal differentiation of the murine erythroleukemia erythroid cell line. Together, these findings demonstrate that the condensin II subunit MTB/mCAP-G2 plays a novel function during erythropoiesis and suggest that key hematopoietic transcription factors such as SCL and E12 may regulate the terminal differentiation of hematopoietic cells through the interaction with condensin complexes.

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“…(21) Surprisingly, this mechanism seems also to be involved in gene repression within large regions. (24) In Drosophila, topoisomerase II and a SMC family protein BARR have been found tightly colocalized on many regulatory elements, including enhancers and PREs, over a 340 Kb of the Bx-c locus, and exhibit physical interaction with the chromatin-remodeling PcG proteins, resulting in maintenance of Fab-7 PRE silencing. Both activators trxG and repressors PcG bind to PREs.…”

Section: Chromatin Remodeling and Chromatin Domain Openingmentioning

confidence: 99%

“…For example, topoisomerase II has been identified on many regulatory regions in the Bx-c locus. (24) Furthermore, topoisomerase II-beta inhibitor can inhibit the action of certain developmental specific genes (Ref. 28, and discussed in detail below).…”

Section: Chromatin Remodeling and Chromatin Domain Openingmentioning

confidence: 99%

“…(60) Also as discussed above, topoisomerase combined with mitotic chromosome condensation proteins and chromatin remodeling complex condense targeted chromatin domain and maintain silencing of genes in interphase. (24) So it is possible that, in early G 1 phase, topoisomerase combines with chromatin remodeling complexes and other transcription activators to decondense chromosome and open particular chromatin domains. Recent findings have prompted people to propose unified theories of gene expression control.…”

Section: Further Considerationmentioning

confidence: 99%

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A hypothesis for chromatin domain opening

Liu

Ling

2003

BioEssays

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SummaryThe eukaryotic genome is organized into different domains by cis-acting elements, such as boundaries/ insulators and matrix attachment regions, and is packaged with different degrees of condensation. In the M phase, the chromatin becomes further highly condensed into chromosomes. The first step for transcriptional activation of a given gene, at a particular time during development, in any locus, is the opening of its chromatin domain. This locus needs to be kept in this state in each early G 1 phase during every cell cycle. Certain distal enhance elements, including locus control regions (LCRs) and enhancers, are believed to perform this target chromatin domain opening process and several models have been proposed to explain distal enhance action. But they did not explain precisely how a given chromatin domain is opened. Based on various studies, we propose a hypothesis for the mechanism of opening chromatin on a large scale. One important mechanism may involved breaking one or two DNA strands and reducing the linking numbers within chromatin domain. The topological changes can overpass some complexes formed on DNA strands and can be transmitted from specific localized points over a broad region, until boundary elements or insulators are reached. These may initiate downstream events such as propagation of histone acetylation and the binding of transcription factors to proximal promoters and may further augment the action mediated by distal enhancer elements.

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Drosophila Chromosome Condensation Proteins Topoisomerase II and Barren Colocalize with Polycomb and Maintain Fab-7 PRE Silencing

Cited by 109 publications

References 47 publications

Aberrant lamination in the cerebral cortex of mouse embryos lacking DNA topoisomerase IIβ

Aberrant lamination in the cerebral cortex of mouse embryos lacking DNA topoisomerase IIβ

MTB, the murine homolog of condensin II subunit CAP-G2, represses transcription and promotes erythroid cell differentiation

A hypothesis for chromatin domain opening

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