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Molecular biology

The Bloom's complex mousetrap

Nature volume 456, pages 453–454 (2008)Cite this article

Genomic instability often underlies cancer. Analyses of proteins implicated in a cancer-predisposing condition called Bloom's syndrome illustrate the intricacies of protein interactions that ensure genomic stability.

Bloom's syndrome, which is characterized by severe growth retardation, immunodeficiency, anaemia, reduced fertility and predisposition to cancer1, is caused by mutations in the gene BLM. At the cellular level, the hallmark of this genetic disorder is a high rate of sister-chromatid exchange — the swapping of homologous stretches of DNA between a chromosome and its identical copy generated during DNA replication2. Understanding how mutations in BLM lead to this chromosomal abnormality has been of considerable interest to both scientists and clinicians. So the latest clue to solving the mystery of Bloom's syndrome, which Xu et al.3 and Singh et al.4 report in Genes & Development, is a welcome advance.

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Figure 1: Double Holliday junctions caught in the mousetrap.

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Authors and Affiliations

  1. Robert M. Brosh Jr is in the Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, Baltimore, Maryland 21224, USA. broshr@mail.nih.gov ,

    Robert M. Brosh Jr

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  1. Robert M. Brosh Jr
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Brosh, R. The Bloom's complex mousetrap. Nature 456, 453–454 (2008). https://doi.org/10.1038/456453a

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