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© The Rockefeller University Press, 0021-9525/1997//1279 $5.00
The Journal of Cell Biology, Volume 138, Number 6, , 1997 1279-1287

Article

Delayed Retraction of Filopodia in Gelsolin Null Mice



Mei Lu*, Walter Witke§, David J. Kwiatkowski{ddagger}, and Kenneth S. Kosik*

* Center for Neurologic Diseases, and {ddagger} Division of Experimental Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and § Mouse Biology Programme, European Molecular Biology Laboratory, 00015 Monterotondo/Rome, Italy

Growth cones extend dynamic protrusions called filopodia and lamellipodia as exploratory probes that signal the direction of neurite growth. Gelsolin, as an actin filament-severing protein, may serve an important role in the rapid shape changes associated with growth cone structures. In wild-type (wt) hippocampal neurons, antibodies against gelsolin labeled the neurite shaft and growth cone. The behavior of filopodia in cultured hippocampal neurons from embryonic day 17 wt and gelsolin null (Gsn–) mice (Witke, W., A.H. Sharpe, J.H. Hartwig, T. Azuma, T.P. Stossel, and D.J. Kwiatkowski. 1995. Cell. 81:41–51.) was recorded with time-lapse video microscopy. The number of filopodia along the neurites was significantly greater in Gsn– mice and gave the neurites a studded appearance. Dynamic studies suggested that most of these filopodia were formed from the region of the growth cone and remained as protrusions from the newly consolidated shaft after the growth cone advanced. Histories of individual filopodia in Gsn– mice revealed elongation rates that did not differ from controls but an impaired retraction phase that probably accounted for the increased number of filopodia long the neutrite shaft. Gelsolin appears to function in the initiation of filopodial retraction and in its smooth progression.

Abbreviations used in this paper: ADF, actin depolymerizing factor; DIC, differential interference contrast; PPI, phosphoinositides; VEC, video enhanced contrast; wt, wild type.

Please address all correspondence to Dr. Kenneth S. Kosik, Center for Neurological Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; Tel.: (617) 525-5230; Fax: (617) 525-5252.

M. Lu was supported by National Institutes of Health training grant (NS07009-21) through Dr. G. Strichartz. This work was supported by National Institutes of Health grants NS29031 (K.S. Kosik) and HL54188 and HL48743 (D.J. Kwiatkowski).


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