Aurora B kinase activity is regulated by SET/TAF1 on Sgo2 at the inner centromere.

Journal: Journal of Cell Biology

Published: 2019-09-16

DOI: 10.1083/jcb.201811060

Affiliations: 4

Authors: 12

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Research Highlight

Tension sensor needed for proper chromosome partitioning

© CHRISTOPH BURGSTEDT/SCIENCE PHOTO LIBRARY/Getty

© CHRISTOPH BURGSTEDT/SCIENCE PHOTO LIBRARY/Getty

The molecular mechanism by which a specific cancer-causing oncogene may trigger the onset of acute myeloid leukemia has been uncovered.

Acute myeloid leukemia originates in bone marrow but rapidly affects blood as a result of the rapid proliferation of leukemia cells. Its symptoms include fatigue, bleeding gums, and shortness of breath

A fusion protein called SET normally helps ensure proper tension is applied onto duplicated chromosomes as they pull apart during cell division.

Now, a Waseda University–led team has found that when overactive, SET causes chromosome misalignment that can trigger cancer progression.

The team showed that SET localizes to the central region of dividing chromosome pairs and detects whether the molecular machine responsible for separating the chromosomes is applying the right amount of tension.

Drugs that target SET or its signalling pathway could therefore help blunt cancer growth by maintaining the fidelity of chromosome distribution in replicating cells.

Supported content

  1. Journal of Cell Biology 218, 3223–3236 (2019). doi: 10.1083/jcb.201811060
Institutions Share
Department of Chemistry and Biochemistry, Waseda University, Japan 0.75
Veritas Corporation, Japan 0.08
Faculty of Medicine, University of Tsukuba, Japan 0.08
Cell Cycle Laboratory, The Francis Crick Institute, United Kingdom (UK) 0.08

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