Association of the bloom syndrome protein with topoisomerase IIIα in somatic and meiotic cells

F. Brad Johnson, David B. Lombard, Norma F. Neff, Mary Ann Mastrangelo, William Dewolf, Nathan A. Ellis, Robert A. Marciniak, Yizhong Yin, Rudolf Jaenisch, Leonard Guarente

Research output: Contribution to journalArticlepeer-review

138 Scopus citations

Abstract

Bloom syndrome (BS) is characterized by genomic instability and cancer susceptibility caused by defects in BLM, a DNA helicase of the RecQ-family (J. German and N.A. Ellis, The Genetic Basis of Human Cancer, pp. 301-316, 1998). RecQ helicases and topoisomerase III proteins interact physically and functionally in yeast (S. Gangloff et al., Mol. Cell. Biol., 14: 8391-8398, 1994) and in Escherichia coli can function together to enable passage of double-stranded DNA (F. G. Harmon et al., Mol. Cell, 3: 611-620, 1999). We demonstrate in somatic and meiotic human cells an association between BLM and topoisomerase IIIα. These proteins colocalize in promyelocytic leukemia protein nuclear bodies, and this localization is disrupted in BS cells. Thus, mechanisms by which RecQ helicases and topoisomerase III proteins cooperate to maintain genomic stability in model organisms likely apply to humans.

Original languageEnglish (US)
Pages (from-to)1162-1167
Number of pages6
JournalCancer Research
Volume60
Issue number5
StatePublished - Mar 1 2000
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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