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Expression of the nerve growth factor gene is controlled by the microtubule network
Author(s) -
Baudet C.,
Naveilhan P.,
Jehan F.,
Brachet P.,
Wion D.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490410405
Subject(s) - nerve growth factor , microtubule , colchicine , biology , microbiology and biotechnology , tubulin , nocodazole , microfilament , gene expression , cytoskeleton , biochemistry , gene , cell , genetics , receptor
Colchicine, nocodazol, and vinblastine, three microtubule‐disrupting drugs were shown to increase the levels of both nerve growth factor (NGF) mRNA and cell‐secreted NGF protein in L929 cells, with levels of glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) or amyloid precursor protein (APP) mRNAs remaining unaffected. Northern blot analysis demonstrated that colchicine also increased NGF mRNA levels in rat primary astrocytes and mouse skin fibroblasts. The specificity of the effects observed was assessed by the fact that the microtubulestabilizing agent Taxotere®, a semisynthetic compound structurally related to taxol, suppressed the effects of colchicine, whereas lumicolchicine, a colchicine derivative that has no action on the microtubule network, had no influence on NGF expression. Likewise, the disruption of the microfilament network by cytochalasin B did not increase NGF mRNA levels in L929 cells. Furthermore, the increase in NGF gene expression observed following microtubule disruption depended on a cascade of events involving at least one protein kinase, which is not down‐regulated by phorbol ester, and on a pertussis toxin sensitive step. These results support the concept that tubulin and/or the microtubule cytoskeleton play an active role in the regulation of the NGF gene. © 1995 Wiley‐Liss, Inc.