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J. Biol. Chem., Vol. 277, Issue 43, 40633-40639, October 25, 2002
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From the Activation of protein kinase C (PKC) increases
microtubule (MT) growth lifetimes, resulting in extension of a
nocodazole-sensitive population of MTs in Aplysia growth
cones. We examined whether the two phorbol ester-activated PKCs in
Aplysia, the Ca2+-activated PKC Apl I and the
Ca2+-independent PKC Apl II, are associated with these MTs.
Phorbol esters translocated PKC to the Triton X-100-insoluble fraction, and a significant portion of this translocated pool was sensitive to
low concentrations of nocodazole. Low doses of nocodazole had no effect
on the amount of PKC in the Triton X-100-insoluble fraction in the
absence of phorbol esters, whereas higher doses of nocodazole reduced
basal levels of PKC Apl II. The F-actin cytoskeletal disrupter, latrunculin A, removed both PKCs from the Triton X-100-insoluble fraction in both control and phorbol ester-treated nervous systems. PKC
Apl II also directly interacted with purified MTs. In
detergent-extracted cells, both PKCs immunolocalized predominantly with
MTs. PKCs were associated with newly formed MTs invading the actin-rich peripheral growth cone domain after PKC activation. Our results are
consistent with a central role for PKCs in regulating MT extension.
Protein Kinase C Isoforms Are Translocated to
Microtubules in Neurons*
§,
Department of Neurology and Neurosurgery,
Montreal Neurological Institute, McGill University,
Montreal, Quebec H3A 2B4, Canada and ¶ Yale University,
New Haven, Connecticut 06520-8103
*
This work was supported in part by National Institutes of
Health Grant RO1-NS28695 (to P. F.) and by Canadian Institutes of Health Research Grant MT-12046 and National Science and Engineering Research Council Grant 187018 (to W. S. S.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a Canadian Institutes of Health Research
scientist award. To whom correspondence should be addressed: Dept. of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, Rm. 776, 3801 rue University, Montreal, Quebec H3A 2B4,
Canada. Tel.: 514-398-1486; Fax: 514-398-8106; E-mail: wayne.sossin@ mcgill.ca.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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