Vinculin-mediated axon growth requires interaction with actin but not talin in mouse neocortical neurons
Cell. Mol. Life Sci.. 2021-06-20; 78(15): 5807-5826
DOI: 10.1007/s00018-021-03879-7
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Mandal P(1), Belapurkar V(1), Nair D(1), Ramanan N(2).
Author information:
(1)Centre for Neuroscience, Indian Institute of Science, Bangalore, 560012,
Karnataka, India.
(2)Centre for Neuroscience, Indian Institute of Science, Bangalore, 560012,
Karnataka, India. .
The actin-binding protein vinculin is a major constituent of focal adhesion, but
its role in neuronal development is poorly understood. We found that vinculin
deletion in mouse neocortical neurons attenuated axon growth both in vitro and in
vivo. Using functional mutants, we found that expression of a constitutively
active vinculin significantly enhanced axon growth while the head-neck domain had
an inhibitory effect. Interestingly, we found that vinculin-talin interaction was
dispensable for axon growth and neuronal migration. Strikingly, expression of the
tail domain delayed migration, increased branching, and stunted axon. Inhibition
of the Arp2/3 complex or abolishing the tail domain interaction with actin
completely reversed the branching phenotype caused by tail domain expression
without affecting axon length. Super-resolution microscopy showed increased
mobility of actin in tail domain expressing neurons. Our results provide novel
insights into the role of vinculin and its functional domains in regulating
neuronal migration and axon growth.
© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.