Rapid de-localization of actin leading edge components with BDM treatment.

Published online

Journal Article

BACKGROUND: 2,3-butanedione monoxime (BDM) has been widely used as a non-muscle myosin inhibitor to investigate the role of non-muscle myosinII in the process of actin retrograde flow and other actin cytoskeletal processes. Recent reports show that BDM does not inhibit any non-muscle myosins so far tested, including nm-myosinII, prompting the question, how were these process affected in BDM studies? RESULTS: We have found that treatment of mammalian cells with BDM for only 1 min blocks actin incorporation at the leading edge in a permeabilized cell system. We show that inhibition of actin incorporation occurs through de-localization of leading edge proteins involved in actin polymerization--the Arp2/3 complex, WAVE, and VASP--that de-localize concomitantly with the leading edge actin network. CONCLUSION: De-localization of actin leading edge components by BDM treatment is a newly described effect of this compound. It may explain many of the results previously ascribed to inhibition of non-muscle myosinII by BDM, particularly in studies of leading edge dynamics. Though this effect of BDM is intriguing, future studies probing actin dynamics at the leading edge should use more potent and specific inhibitors.

Full Text

Duke Authors

Cited Authors

  • Yarrow, JC; Lechler, T; Li, R; Mitchison, TJ

Published Date

  • June 3, 2003

Published In

Volume / Issue

  • 4 /

Start / End Page

  • 5 -

PubMed ID

  • 12783627

Pubmed Central ID

  • 12783627

Electronic International Standard Serial Number (EISSN)

  • 1471-2121

Digital Object Identifier (DOI)

  • 10.1186/1471-2121-4-5

Language

  • eng

Conference Location

  • England