Actin Isoforms in Neuronal Development and Function - International Review of Cell and Molecular Biology - page 201

8. CONCLUDING REMARKS
In this chapter, we have presented evidence that distinct functions of
actin isoforms likely comprise a previously unappreciated mechanism to
regulate actin dynamics in neuronal development and function. While the
localization and local translation of β-actin specifically has been the most
investigated area of actin isoforms in neurons, the functional relevance of
this phenomenon in vivo is unclear. Recent studies have revealed, however,
that β- and γ-actin bound to Ca 2+ exhibit significantly different polymer-
ization kinetics. We propose that given the pervasiveness of Ca 2+ signaling
in neuronal function, that the distinct dynamics of Ca 2+ -β-actin could be a
critical player in mediating the localized actin polymerization required for
cellular constriction events mediating tissue bending, synaptic plasticity, and
behavior. Interestingly, ablation of β-actin function in the brain results in
surprisingly restricted phenotypes, revealing novel and unanticipated roles
for β-actin in the morphogenesis of select brain regions and regulation of
specific behaviors. The contributions of γ-actin to neuronal development
and function have only just begun to be characterized, with the distinct and
overlapping functions of these isoforms in neurons remaining to be fully
elucidated. Given the significant roles already assigned to actin isoforms in
neuronal development and function, however, it is likely that even more
exciting discoveries remain to be uncovered.
ACKNOWLEDGMENTS
We would like to thank Drs Ben Perrin and Sarah Greising for helpful comments on this
manuscript.We also regret omitting the citation of any studies pertaining to this subject.Work
relating to the focus of this review was conducted in the authors' laboratory with funding
from the National Institutes of Health Training Program in Muscle Research (AR007612)
and a University of Minnesota Doctoral Dissertation Fellowship to T.R.C. and a grant from
the National Institutes of Health (AR049899) to J.M.E.
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