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Molecular Biology, Pathobiology and Genetics |
1 The Wistar Institute; 2 Program in Cell and Molecular Biology, Biomedical Graduate Studies; 3 Department of Animal Biology, School of Veterinary Medicine; and 4 Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
Requests for reprints: Thanos D. Halazonetis, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104-4268. Phone: 215-898-3789; Fax: 215-573-9271; E-mail: halazonetis{at}wistar.upenn.edu.
The kinase LATS/WARTS is a tumor suppressor protein conserved in evolution, but its function at the molecular level is not well understood. We report here that human LATS1 interacts with MOB1A, a protein whose homologue in budding yeast associates with kinases involved in mitotic exit. This suggested that LATS1 may be a component of the previously uncharacterized mitotic exit network in higher eukaryotes. Indeed, moderate overexpression of human LATS1 in cells exposed to microtubule poisons facilitated mitotic exit, and this activity required MOB1A. Reciprocally, small interfering RNA–mediated suppression of LATS1 or MOB1A prolonged telophase, but had no effect on the length of the earlier phases of mitosis. A role of LATS1 in mitotic exit may explain its previously described abilities to induce G2 arrest and promote cytokinesis.
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