The nucleosome remodeling factor (NURF) regulates genes involved in Drosophila innate immunity

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The nucleosome remodeling factor (NURF) regulates genes involved in Drosophila innate immunity. / Kwon, So Yeon; Xiao, H; Glover, BP; Tjian, R; Wu, C; Badenhorst, Paul.

In: Developmental Biology, Vol. 316, 15.04.2008, p. 538-47.

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@article{fe7f8ae352d1412faad94822d6dc0f59,
title = "The nucleosome remodeling factor (NURF) regulates genes involved in Drosophila innate immunity",
abstract = "The Drosophila nucleosome remodeling factor (NURF) is an ISWI-containing chromatin remodeling complex that catalyzes ATP-dependent nucleosome sliding. By sliding nucleosomes, NURF has the ability to alter chromatin structure and regulate transcription. Previous studies have shown that mutation of Drosophila NURF induces melanotic tumors, implicating NURF in innate immune function. Here, we show that NURF mutants exhibit identical innate immune responses to gain-of-function mutants in the Drosophila JAK/STAT pathway. Using microarrays, we identify a common set of target genes that are activated in both mutants. In silico analysis of promoter sequences of these defines a consensus regulatory element comprising a STAT-binding sequence overlapped by a binding-site for the transcriptional repressor Ken. NURF interacts physically and genetically with Ken. Chromatin immunoprecipitation (ChIP) localizes NURF to Ken-binding sites in hemocytes, suggesting that Ken recruits NURF to repress STAT responders. Loss of NURF leads to precocious activation of STAT target genes.",
keywords = "chromatin remodeling, JAK/STAT pathway, innate immunity, ISWI, NURF, Drosophila",
author = "Kwon, {So Yeon} and H Xiao and BP Glover and R Tjian and C Wu and Paul Badenhorst",
year = "2008",
month = apr,
day = "15",
doi = "10.1016/j.ydbio.2008.01.033",
language = "English",
volume = "316",
pages = "538--47",
journal = "Developmental Biology",
issn = "0012-1606",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - The nucleosome remodeling factor (NURF) regulates genes involved in Drosophila innate immunity

AU - Kwon, So Yeon

AU - Xiao, H

AU - Glover, BP

AU - Tjian, R

AU - Wu, C

AU - Badenhorst, Paul

PY - 2008/4/15

Y1 - 2008/4/15

N2 - The Drosophila nucleosome remodeling factor (NURF) is an ISWI-containing chromatin remodeling complex that catalyzes ATP-dependent nucleosome sliding. By sliding nucleosomes, NURF has the ability to alter chromatin structure and regulate transcription. Previous studies have shown that mutation of Drosophila NURF induces melanotic tumors, implicating NURF in innate immune function. Here, we show that NURF mutants exhibit identical innate immune responses to gain-of-function mutants in the Drosophila JAK/STAT pathway. Using microarrays, we identify a common set of target genes that are activated in both mutants. In silico analysis of promoter sequences of these defines a consensus regulatory element comprising a STAT-binding sequence overlapped by a binding-site for the transcriptional repressor Ken. NURF interacts physically and genetically with Ken. Chromatin immunoprecipitation (ChIP) localizes NURF to Ken-binding sites in hemocytes, suggesting that Ken recruits NURF to repress STAT responders. Loss of NURF leads to precocious activation of STAT target genes.

AB - The Drosophila nucleosome remodeling factor (NURF) is an ISWI-containing chromatin remodeling complex that catalyzes ATP-dependent nucleosome sliding. By sliding nucleosomes, NURF has the ability to alter chromatin structure and regulate transcription. Previous studies have shown that mutation of Drosophila NURF induces melanotic tumors, implicating NURF in innate immune function. Here, we show that NURF mutants exhibit identical innate immune responses to gain-of-function mutants in the Drosophila JAK/STAT pathway. Using microarrays, we identify a common set of target genes that are activated in both mutants. In silico analysis of promoter sequences of these defines a consensus regulatory element comprising a STAT-binding sequence overlapped by a binding-site for the transcriptional repressor Ken. NURF interacts physically and genetically with Ken. Chromatin immunoprecipitation (ChIP) localizes NURF to Ken-binding sites in hemocytes, suggesting that Ken recruits NURF to repress STAT responders. Loss of NURF leads to precocious activation of STAT target genes.

KW - chromatin remodeling

KW - JAK/STAT pathway

KW - innate immunity

KW - ISWI

KW - NURF

KW - Drosophila

U2 - 10.1016/j.ydbio.2008.01.033

DO - 10.1016/j.ydbio.2008.01.033

M3 - Article

C2 - 18334252

VL - 316

SP - 538

EP - 547

JO - Developmental Biology

JF - Developmental Biology

SN - 0012-1606

ER -