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

Stefan Stamm; Diana Casper; Veneta Hanson; David M. Helfman

doi:10.1016/S0169-328X(98)00313-1

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

Stefan Stamm, Diana Casper, Veneta Hanson, David M. Helfman

Research output: Contribution to journal › Article › peer-review

33 Scopus citations

Abstract

Clathrin light chain B (LCB) is a major component of clathrin coated vesicles, which are structures involved in intracellular transport. A neuron- specific isoform of LCB is generated by incorporation of a single exon (EN) using an alternative splicing mechanism that reflects the special demands of neurons, such as axonal transport and synaptic neurotransmission. Here, we demonstrate that this neuron-specific exon is developmentally regulated and is excluded in non-neuronal cells because its 5' and 3' splice sites deviate from the mammalian consensus sequences. A gel retardation assay indicated the presence of a developmentally regulated factor in brain that binds to the neuronal exon. In addition, EN usage is repressed by increasing the concentration of htra2-beta1, a splice factor whose isoform expression is influenced by neuronal activity. We propose that a brain-specific factor is involved in EN recognition during development and adulthood. In addition, ubiquitously expressed splicing factors such as htra2-beta1 are involved in regulating EN expression in the adult brain.

Original language	English
Pages (from-to)	108-118
Number of pages	11
Journal	Molecular Brain Research
Volume	64
Issue number	1
DOIs	https://doi.org/10.1016/S0169-328X(98)00313-1
State	Published - Jan 22 1999

Bibliographical note

Funding Information:
This work was supported by the Gottlieb Daimler und Carl Benz Stiftung, the Deutsche Forschungsgemeinschaft (Sta399 1/1) and in part by the Human Frontier Science Program (RG 562/96) (SS). DMH is supported by a NIH grant GM43049 and is an Established Investigator of the American Heart Association. We thank Oliver Nayler, Jim Chalcroft, Hiro Nawa, Adrian Krainer, Jürgen Brosius and David Horowitz for discussion and Frank Pessler for the tar RNA constructs.

Keywords

Alternative splicing
Clathrin light chain B
Transformer-2

ASJC Scopus subject areas

Molecular Biology
Cellular and Molecular Neuroscience

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10.1016/S0169-328X(98)00313-1

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title = "Regulation of the neuron-specific exon of clathrin light chain B",

abstract = "Clathrin light chain B (LCB) is a major component of clathrin coated vesicles, which are structures involved in intracellular transport. A neuron- specific isoform of LCB is generated by incorporation of a single exon (EN) using an alternative splicing mechanism that reflects the special demands of neurons, such as axonal transport and synaptic neurotransmission. Here, we demonstrate that this neuron-specific exon is developmentally regulated and is excluded in non-neuronal cells because its 5' and 3' splice sites deviate from the mammalian consensus sequences. A gel retardation assay indicated the presence of a developmentally regulated factor in brain that binds to the neuronal exon. In addition, EN usage is repressed by increasing the concentration of htra2-beta1, a splice factor whose isoform expression is influenced by neuronal activity. We propose that a brain-specific factor is involved in EN recognition during development and adulthood. In addition, ubiquitously expressed splicing factors such as htra2-beta1 are involved in regulating EN expression in the adult brain.",

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note = "Funding Information: This work was supported by the Gottlieb Daimler und Carl Benz Stiftung, the Deutsche Forschungsgemeinschaft (Sta399 1/1) and in part by the Human Frontier Science Program (RG 562/96) (SS). DMH is supported by a NIH grant GM43049 and is an Established Investigator of the American Heart Association. We thank Oliver Nayler, Jim Chalcroft, Hiro Nawa, Adrian Krainer, J{\"u}rgen Brosius and David Horowitz for discussion and Frank Pessler for the tar RNA constructs.",

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PY - 1999/1/22

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N2 - Clathrin light chain B (LCB) is a major component of clathrin coated vesicles, which are structures involved in intracellular transport. A neuron- specific isoform of LCB is generated by incorporation of a single exon (EN) using an alternative splicing mechanism that reflects the special demands of neurons, such as axonal transport and synaptic neurotransmission. Here, we demonstrate that this neuron-specific exon is developmentally regulated and is excluded in non-neuronal cells because its 5' and 3' splice sites deviate from the mammalian consensus sequences. A gel retardation assay indicated the presence of a developmentally regulated factor in brain that binds to the neuronal exon. In addition, EN usage is repressed by increasing the concentration of htra2-beta1, a splice factor whose isoform expression is influenced by neuronal activity. We propose that a brain-specific factor is involved in EN recognition during development and adulthood. In addition, ubiquitously expressed splicing factors such as htra2-beta1 are involved in regulating EN expression in the adult brain.

AB - Clathrin light chain B (LCB) is a major component of clathrin coated vesicles, which are structures involved in intracellular transport. A neuron- specific isoform of LCB is generated by incorporation of a single exon (EN) using an alternative splicing mechanism that reflects the special demands of neurons, such as axonal transport and synaptic neurotransmission. Here, we demonstrate that this neuron-specific exon is developmentally regulated and is excluded in non-neuronal cells because its 5' and 3' splice sites deviate from the mammalian consensus sequences. A gel retardation assay indicated the presence of a developmentally regulated factor in brain that binds to the neuronal exon. In addition, EN usage is repressed by increasing the concentration of htra2-beta1, a splice factor whose isoform expression is influenced by neuronal activity. We propose that a brain-specific factor is involved in EN recognition during development and adulthood. In addition, ubiquitously expressed splicing factors such as htra2-beta1 are involved in regulating EN expression in the adult brain.

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

Abstract

Bibliographical note

Keywords

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