Regulation of the neuron-specific exon of clathrin light chain B

Citation
S. Stamm et al., Regulation of the neuron-specific exon of clathrin light chain B, MOL BRAIN R, 64(1), 1999, pp. 108-118
Citations number
68
Categorie Soggetti
Neurosciences & Behavoir
Journal title
MOLECULAR BRAIN RESEARCH
ISSN journal
0169328X → ACNP
Volume
64
Issue
1
Year of publication
1999
Pages
108 - 118
Database
ISI
SICI code
0169-328X(19990122)64:1<108:ROTNEO>2.0.ZU;2-F
Abstract
Clathrin light chain B (LCB) is a major component of clathrin coated vesicl es, which are structures involved in intracellular transport. A neuron-spec ific isoform of LCB is generated by incorporation of a single exon (EN) usi ng an alternative splicing mechanism that reflects the special demands of n eurons, such as axonal transport and synaptic neurotransmission. Here, we d emonstrate that this 1 neuron-specific exon is developmentally regulated an d is excluded in non-neuronal cells because its 5' and 3' splice sites devi ate from the mammalian consensus sequences. A gel retardation assay indicat ed the presence of a developmentally regulated factor in brain that binds t o the neuronal exon. In addition, EN usage is repressed by increasing the c oncentration of htra2-betal, a splice factor whose isoform expression is in fluenced by neuronal activity. We propose that a brain-specific factor is i nvolved in EN recognition during development and adulthood. In addition, ub iquitously expressed splicing factors such as htra2-betal are involved in r egulating EN expression in the adult brain. (C) 1999 Elsevier Science B.V. All rights reserved.