The hnRNP and cytoskeletal protein raver1 contributes to synaptic plasticity.
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The hnRNP and cytoskeletal protein raver1 contributes to synaptic plasticity. / Lahmann, Ines; Fabienke, Manuela; Henneberg, Berenike; Pabst, Oliver; Vauti, Franz; Minge, Daniel; Illenberger, Susanne; Jockusch, Brigitte M; Korte, Martin; Arnold, Hans-Henning.
In: EXP CELL RES, Vol. 314, No. 5, 5, 2008, p. 1048-1060.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - The hnRNP and cytoskeletal protein raver1 contributes to synaptic plasticity.
AU - Lahmann, Ines
AU - Fabienke, Manuela
AU - Henneberg, Berenike
AU - Pabst, Oliver
AU - Vauti, Franz
AU - Minge, Daniel
AU - Illenberger, Susanne
AU - Jockusch, Brigitte M
AU - Korte, Martin
AU - Arnold, Hans-Henning
PY - 2008
Y1 - 2008
N2 - Raver1 is an hnRNP protein that interacts with the ubiquitous splicing regulator PTB and binds to cytoskeletal components like alpha-actinin and vinculin/metavinculin. Cell culture experiments suggested that raver1 functions as corepressor in PTB-regulated splicing reactions and may thereby increase proteome complexity. To determine the role of raver1 in vivo, we inactivated the gene by targeted disruption in the mouse. Here we report that raver1-deficient mice develop regularly to adulthood and show no obvious anatomical or behavioral defects. In keeping with this notion, cells from raver1-null mice were indistinguishable from wild type cells and displayed normal growth, motility, and cytoskeletal architecture in culture. Moreover, alternative splicing of exons, including the model exon 3 of alpha-tropomyosin, was not markedly changed in mutant mice, suggesting that the role of raver1 for PTB-mediated exon repression is not absolutely required to generate splice variants during mouse development. Interestingly however, loss of raver1 caused significantly reduced plasticity of synapses on acute hippocampal slices, as elicited by electrophysiological measurements of markedly lower LTP and LTD in mutant neurons. Our results provide evidence that raver1 may play an important role for the regulation of neuronal synaptic plasticity, possibly by controlling especially the late LTP via posttranscriptional mechanisms.
AB - Raver1 is an hnRNP protein that interacts with the ubiquitous splicing regulator PTB and binds to cytoskeletal components like alpha-actinin and vinculin/metavinculin. Cell culture experiments suggested that raver1 functions as corepressor in PTB-regulated splicing reactions and may thereby increase proteome complexity. To determine the role of raver1 in vivo, we inactivated the gene by targeted disruption in the mouse. Here we report that raver1-deficient mice develop regularly to adulthood and show no obvious anatomical or behavioral defects. In keeping with this notion, cells from raver1-null mice were indistinguishable from wild type cells and displayed normal growth, motility, and cytoskeletal architecture in culture. Moreover, alternative splicing of exons, including the model exon 3 of alpha-tropomyosin, was not markedly changed in mutant mice, suggesting that the role of raver1 for PTB-mediated exon repression is not absolutely required to generate splice variants during mouse development. Interestingly however, loss of raver1 caused significantly reduced plasticity of synapses on acute hippocampal slices, as elicited by electrophysiological measurements of markedly lower LTP and LTD in mutant neurons. Our results provide evidence that raver1 may play an important role for the regulation of neuronal synaptic plasticity, possibly by controlling especially the late LTP via posttranscriptional mechanisms.
M3 - SCORING: Zeitschriftenaufsatz
VL - 314
SP - 1048
EP - 1060
JO - EXP CELL RES
JF - EXP CELL RES
SN - 0014-4827
IS - 5
M1 - 5
ER -
