Growth cone collapse through coincident loss of actin bundles and leading edge actin without actin depolymerization.

Growth cone collapse through coincident loss of actin bundles and leading edge actin without actin depolymerization.
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DOI:
10.1083/jcb.153.5.1071
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发表时间:
2001-05-28
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Cohan CS
Cohan CS
中科院分区:
其他
文献类型:
--
作者:
Zhou FQ;Cohan CS

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Repulsive guidance cues can either collapse the whole growth cone to arrest neurite outgrowth or cause asymmetric collapse leading to growth cone turning. How signals from repulsive cues are translated by growth cones into this morphological change through rearranging the cytoskeleton is unclear. We examined three factors that are able to induce the collapse of extending Helisoma growth cones in conditioned medium, including serotonin, myosin light chain kinase inhibitor, and phorbol ester. To study the cytoskeletal events contributing to collapse, we cultured Helisoma growth cones on polylysine in which lamellipodial collapse was prevented by substrate adhesion. We found that all three factors that induced collapse of extending growth cones also caused actin bundle loss in polylysine-attached growth cones without loss of actin meshwork. In addition, actin bundle loss correlated with specific filamentous actin redistribution away from the leading edge that is characteristic of repulsive factors. Finally, we provide direct evidence using time-lapse studies of extending growth cones that actin bundle loss paralleled collapse. Taken together, these results suggest that actin bundles could be a common cytoskeletal target of various collapsing factors, which may use different signaling pathways that converge to induce growth cone collapse.
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