Topoisomerase 2β and DNA topology during B cell development

Olivier Papapietro; Sergey Nejentsev

doi:https://doi.org/10.3389/fimmu.2022.982870

Topoisomerase 2β and DNA topology during B cell development

Olivier Papapietro, Sergey Nejentsev

Molecular cell biology and Immunology (VUmc)

Research output: Contribution to journal › Article › Academic › peer-review

1 Citation (Scopus)

Abstract

Topoisomerase 2β (TOP2B) introduces transient double strand breaks in the DNA helix to remove supercoiling structures and unwind entangled DNA strains. Advances in genomic technologies have enabled the discovery of novel functions for TOP2B in processes such as releasing of the paused RNA polymerase II and maintaining the genome organization through DNA loop domains. Thus, TOP2B can regulate transcription directly by acting on transcription elongation and indirectly by controlling interactions between enhancer and promoter regions through genome folding. The identification of TOP2B mutations in humans unexpectedly revealed a unique role of TOP2B in B-cell progenitors. Here we discuss the functions of TOP2B and the mechanisms leading to the B-cell development defect in patients with TOP2B deficiency.

Original language	English
Article number	982870
Pages (from-to)	982870
Number of pages	1
Journal	Frontiers in immunology
Volume	13
DOIs	https://doi.org/10.3389/fimmu.2022.982870
Publication status	Published - 15 Aug 2022

Keywords

B cell
genome organization
immunodeficiency
topoisomerase
transcription

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https://doi.org/10.3389/fimmu.2022.982870

Cite this

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title = "Topoisomerase 2β and DNA topology during B cell development",

abstract = "Topoisomerase 2β (TOP2B) introduces transient double strand breaks in the DNA helix to remove supercoiling structures and unwind entangled DNA strains. Advances in genomic technologies have enabled the discovery of novel functions for TOP2B in processes such as releasing of the paused RNA polymerase II and maintaining the genome organization through DNA loop domains. Thus, TOP2B can regulate transcription directly by acting on transcription elongation and indirectly by controlling interactions between enhancer and promoter regions through genome folding. The identification of TOP2B mutations in humans unexpectedly revealed a unique role of TOP2B in B-cell progenitors. Here we discuss the functions of TOP2B and the mechanisms leading to the B-cell development defect in patients with TOP2B deficiency.",

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author = "Olivier Papapietro and Sergey Nejentsev",

note = "Funding Information: SN was supported by the ERC Advanced grant (832721) and the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre. OP was supported by the Marie Sk{\l}odowska-Curie Individual Fellowship (657633). Publisher Copyright: Copyright {\textcopyright} 2022 Papapietro and Nejentsev.",

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AU - Nejentsev, Sergey

N1 - Funding Information: SN was supported by the ERC Advanced grant (832721) and the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre. OP was supported by the Marie Skłodowska-Curie Individual Fellowship (657633). Publisher Copyright: Copyright © 2022 Papapietro and Nejentsev.

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AB - Topoisomerase 2β (TOP2B) introduces transient double strand breaks in the DNA helix to remove supercoiling structures and unwind entangled DNA strains. Advances in genomic technologies have enabled the discovery of novel functions for TOP2B in processes such as releasing of the paused RNA polymerase II and maintaining the genome organization through DNA loop domains. Thus, TOP2B can regulate transcription directly by acting on transcription elongation and indirectly by controlling interactions between enhancer and promoter regions through genome folding. The identification of TOP2B mutations in humans unexpectedly revealed a unique role of TOP2B in B-cell progenitors. Here we discuss the functions of TOP2B and the mechanisms leading to the B-cell development defect in patients with TOP2B deficiency.

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KW - genome organization

KW - immunodeficiency

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Topoisomerase 2β and DNA topology during B cell development

Abstract

Keywords

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