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Vol. 16, Issue 7, 3425-3437, July 2005
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* Oncology Research Unit, The Children's Hospital at Westmead, Westmead NSW 2145, Australia;
Discipline of Pediatrics and Child Health, University of Sydney, Sydney NSW 4000, Australia;
|| Muscle Development Unit, Children's Medical Research Institute, Westmead NSW 2145, Australia; and
¶ Department of Biological Sciences, The University of Iowa, Iowa City, IA 52242-1324
Submitted November 1, 2004;
Revised March 15, 2005;
Accepted April 27, 2005
Monitoring Editor: Marianne Bronner-Fraser
Spatially distinct populations of microfilaments, characterized by different tropomyosin (Tm) isoforms, are present within a neuron. To investigate the impact of altered tropomyosin isoform expression on neuronal morphogenesis, embryonic cortical neurons from transgenic mice expressing the isoforms Tm3 and Tm5NM1, under the control of the 
-actin promoter, were cultured in vitro. Exogenously expressed Tm isoforms sorted to different subcellular compartments with Tm5NM1 enriched in filopodia and growth cones, whereas the Tm3 was more broadly localized. The Tm5NM1 neurons displayed significantly enlarged growth cones accompanied by an increase in the number of dendrites and axonal branching. In contrast, Tm3 neurons displayed inhibition of neurite outgrowth. Recruitment of Tm5a and myosin IIB was observed in the peripheral region of a significant number of Tm5NM1 growth cones. We propose that enrichment of myosin IIB increases filament stability, leading to the enlarged growth cones. Our observations support a role for different tropomyosin isoforms in regulating interactions with myosin and thereby regulating morphology in specific intracellular compartments.
Abbreviations used: Tm, tropomyosin.
Present address: Department of Cancer Biology, Vanderbilt University, Nashville, TN 37235
Present address: Imclone System,180 Varick St., 6th Floor, New York, NY 10014.
Address correspondence to: Peter Gunning (peterg3{at}chw.edu.au).
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