Myosin X is a downstream effector of PI(3)K during phagocytosis

Dianne Cox, Jonathan S. Berg, Michael Cammer, John O. Chinegwundoh, Benjamin M. Dale, Richard E. Cheney, Steven Greenberg

Research output: Contribution to journalArticlepeer-review

181 Scopus citations


Phagocytosis is a phosphatidylinositol-3-OH-kinase (PI(3)K)-dependent process in macrophages. We identified Myo10 (Myosin-X), an unconventional myosin with pleckstrin homology (PH) domains, as a potential downstream target of PI(3)K. Myo10 was recruited to phagocytic cups in a wortmannin-sensitive manner. Expression of a truncation construct of Myo10 (Myo10 tail) in a macrophage cell line or cytosolic loading of anti-Myo10 antibodies in bovine alveolar macrophages inhibited phagocytosis. In contrast, expression of a Myo10 tail construct containing a point mutation in one of its PH domains failed to inhibit phagocytosis. Expression of Myo10 tail inhibited spreading, but not adhesion, on IgG-coated substrates, consistent with a function for Myo10 in pseudopod extension. We propose that Myo10 provides a molecular link between PI(3)K and pseudopod extension during phagocytosis.

Original languageEnglish (US)
Pages (from-to)469-477
Number of pages9
JournalNature Cell Biology
Issue number7
StatePublished - 2002
Externally publishedYes

ASJC Scopus subject areas

  • Cell Biology


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