4.4 Article

Dictyostelium huntingtin controls chemotaxis and cytokinesis through the regulation of myosin II phosphorylation

Journal

MOLECULAR BIOLOGY OF THE CELL
Volume 22, Issue 13, Pages 2270-2281

Publisher

AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E10-11-0926

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Funding

  1. American Heart Association [0765345U, 0730247N]
  2. National Institutes of Health [GM-084015, GM089853, GM066817, GM50009, 2R15GM066789]
  3. Muscular Dystrophy grant [69361]

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Abnormalities in the huntingtin protein (Htt) are associated with Huntington's disease. Despite its importance, the function of Htt is largely unknown. We show that Htt is required for normal chemotaxis and cytokinesis in Dictyostelium discoideum. Cells lacking Htt showed slower migration toward the chemoattractant cAMP and contained lower levels of cortical myosin II, which is likely due to defects in dephosphorylation of myosin II mediated by protein phosphatase 2A (PP2A). htt(-) cells also failed to maintain myosin II in the cortex of the cleavage furrow, generating unseparated daughter cells connected through a thin cytoplasmic bridge. Furthermore, similar to Dictyostelium htt(-) cells, siRNA-mediated knockdown of human HTT also decreased the PP2A activity in HeLa cells. Our data indicate that Htt regulates the phosphorylation status of myosin II during chemotaxis and cytokinesis through PP2A.

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