The silent information regulator 1 (Sirt1) is a positive regulator of the Notch pathway in Drosophila

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F16%3A00465215" target="_blank" >RIV/60077344:_____/16:00465215 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/60076658:12310/16:43891909

Výsledek na webu

<a href="http://dx.doi.org/10.1042/BCJ20160563" target="_blank" >http://dx.doi.org/10.1042/BCJ20160563</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1042/BCJ20160563" target="_blank" >10.1042/BCJ20160563</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The silent information regulator 1 (Sirt1) is a positive regulator of the Notch pathway in Drosophila

Popis výsledku v původním jazyce

The silent information regulator 1 (Sirt1) has previously been shown to have negative effects on the Notch pathway in several contexts. We bring evidence that Sirt1 has a positive effect on Notch activation in Drosophila, in the context of sensory organ precursor specification and during wing development. The phenotype of Sirt1 mutant resembles weak Notch loss of function phenotypes and genetic interactions of Sirt1 with the components of the Notch pathway also suggest a positive role of Sirt1 in Notch signalling. Sirt1 is necessary for the efficient activation of E(spl) genes by Notch in S2N cells. Additionally, the Notch dependent response of several E(spl) genes is sensitive to metabolic stress caused by 2-deoxyglucose treatment, in a Sirt1 dependent manner. We found Sirt1 associated with several proteins involved in Notch repression as well as activation, including the cofactor exchange factor ebi (TBL1), the RLAF/LAF histone chaperon complex and the Tip60 acetylation complex. Moreover, Sirt1 participates in the deacetylation of the CSL transcription factor Su(H). The role of Sirt1 in Notch signalling is therefore more complex than previously recognised and its diverse effects may be explained by a plethora of Sirt1 substrates involved in the regulation of Notch signalling.n

Název v anglickém jazyce

The silent information regulator 1 (Sirt1) is a positive regulator of the Notch pathway in Drosophila

Popis výsledku anglicky

The silent information regulator 1 (Sirt1) has previously been shown to have negative effects on the Notch pathway in several contexts. We bring evidence that Sirt1 has a positive effect on Notch activation in Drosophila, in the context of sensory organ precursor specification and during wing development. The phenotype of Sirt1 mutant resembles weak Notch loss of function phenotypes and genetic interactions of Sirt1 with the components of the Notch pathway also suggest a positive role of Sirt1 in Notch signalling. Sirt1 is necessary for the efficient activation of E(spl) genes by Notch in S2N cells. Additionally, the Notch dependent response of several E(spl) genes is sensitive to metabolic stress caused by 2-deoxyglucose treatment, in a Sirt1 dependent manner. We found Sirt1 associated with several proteins involved in Notch repression as well as activation, including the cofactor exchange factor ebi (TBL1), the RLAF/LAF histone chaperon complex and the Tip60 acetylation complex. Moreover, Sirt1 participates in the deacetylation of the CSL transcription factor Su(H). The role of Sirt1 in Notch signalling is therefore more complex than previously recognised and its diverse effects may be explained by a plethora of Sirt1 substrates involved in the regulation of Notch signalling.n

Druh

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

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

<a href="/cs/project/GA14-08583S" target="_blank" >GA14-08583S: Role sirtuinů v signalizační dráze Notch receptoru a ve vývoji Drosophily</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2016

Kód důvěrnosti údajů

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

Název periodika

Biochemical Journal

ISSN

0264-6021

e-ISSN

—

Svazek periodika

473

Číslo periodika v rámci svazku

22

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

15

Strana od-do

4129-4143

Kód UT WoS článku

000393759300004

EID výsledku v databázi Scopus

2-s2.0-85009516150