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Function of the Neuron-specific Alternatively Spliced Isoforms of Nonmuscle Myosin II-B during Mouse (2005)
BibTeX
@MISC{Development05functionof,
author = {Brain Development and Xuefei Ma and Sachiyo Kawamoto and Jorge Uribe and Robert S. Adelstein},
title = {Function of the Neuron-specific Alternatively Spliced Isoforms of Nonmuscle Myosin II-B during Mouse},
year = {2005}
}
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Abstract
We report that the alternatively spliced isoforms of nonmuscle myosin heavy chain II-B (NHMC II-B) play distinct roles during mouse brain development. The B1-inserted isoform of NMHC II-B, which contains an insert of 10 amino acids near the ATP-binding region (loop 1) of the myosin heavy chain, is involved in normal migration of facial neurons. In contrast, the B2-inserted isoform, which contains an insert of 21 amino acids near the actin-binding region (loop 2), is important for postnatal development of cerebellar Purkinje cells. Deletion of the B1 alternative exon, together with reduced expression of myosin II-B, results in abnormal migration and consequent protrusion of facial neurons into the fourth ventricle. This protrusion is associated with the development of hydrocephalus. Restoring the amount of myosin II-B expression to wild-type levels prevents these defects, showing the importance of total myosin activity in facial neuron migration. In contrast, deletion of the B2 alternative exon results in abnormal development of cerebellar Purkinje cells. Cells lacking the B2-inserted isoform show reduced numbers of dendritic spines and branches. Some of the B2-ablated Purkinje cells are misplaced in the cerebellar molecular layer. All of the B2-ablated mice demonstrated impaired motor coordination.
Keyphrases
nonmuscle myosin ii-b neuron-specific alternatively spliced isoforms amino acid facial neuron cerebellar purkinje cell atp-binding region consequent protrusion b1 alternative exon b2 alternative exon result b2-ablated mouse myosin heavy chain b1-inserted isoform b2-inserted isoform spliced isoforms normal migration reduced expression abnormal development wild-type level prevents impaired motor coordination mouse brain development myosin ii-b dendritic spine postnatal development b2-inserted isoform show nonmuscle myosin heavy chain ii-b myosin ii-b expression facial neuron migration nhmc ii-b cerebellar molecular layer nmhc ii-b fourth ventricle b2-ablated purkinje cell play distinct role actin-binding region abnormal migration total myosin activity
