CRE promoter sites modulate alternative splicing via p300-mediated histone acetylation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F14%3A10285589" target="_blank" >RIV/00216208:11310/14:10285589 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/61388971:_____/14:00439939 RIV/68378050:_____/14:00434660

Výsledek na webu

<a href="http://dx.doi.org/10.4161/rna.29441" target="_blank" >http://dx.doi.org/10.4161/rna.29441</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.4161/rna.29441" target="_blank" >10.4161/rna.29441</a>

Jazyk výsledku

angličtina

Název v původním jazyce

CRE promoter sites modulate alternative splicing via p300-mediated histone acetylation

Popis výsledku v původním jazyce

Histone acetylation modulates alternative splicing of several hundred genes. Here, we tested the role of the histone acetyltransferase p300 in alternative splicing and showed that knockdown of p300 promotes inclusion of the fibronectin (FN1) alternativeEDB exon. p300 associates with CRE sites in the promoter via the CREB transcription factor. We created mini-gene reporters driven by an artificial promoter containing CRE sites. Both deletion and mutation of the CRE site affected EDB alternative splicingin the same manner as p300 knockdown. Next we showed that p300 controls histone H4 acetylation along the FN1 gene. Consistently, p300 depletion and CRE deletion/mutation both reduced histone H4 acetylation on mini-gene reporters. Finally, we provide evidence that the effect of CRE inactivation on H4 acetylation and alternative splicing is counteracted by the inhibition of histone deacetylases. Together, these data suggest that histone acetylation could be one of the mechanisms how promo

Název v anglickém jazyce

CRE promoter sites modulate alternative splicing via p300-mediated histone acetylation

Popis výsledku anglicky

Histone acetylation modulates alternative splicing of several hundred genes. Here, we tested the role of the histone acetyltransferase p300 in alternative splicing and showed that knockdown of p300 promotes inclusion of the fibronectin (FN1) alternativeEDB exon. p300 associates with CRE sites in the promoter via the CREB transcription factor. We created mini-gene reporters driven by an artificial promoter containing CRE sites. Both deletion and mutation of the CRE site affected EDB alternative splicingin the same manner as p300 knockdown. Next we showed that p300 controls histone H4 acetylation along the FN1 gene. Consistently, p300 depletion and CRE deletion/mutation both reduced histone H4 acetylation on mini-gene reporters. Finally, we provide evidence that the effect of CRE inactivation on H4 acetylation and alternative splicing is counteracted by the inhibition of histone deacetylases. Together, these data suggest that histone acetylation could be one of the mechanisms how promo

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/GBP305%2F12%2FG034" target="_blank" >GBP305/12/G034: Centrum biologie RNA</a><br>

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

RNA Biology

ISSN

1547-6286

e-ISSN

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Svazek periodika

11

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

865-874

Kód UT WoS článku

000342901600013

EID výsledku v databázi Scopus

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