<i>putzig</i>Is Required for Cell Proliferation and Regulates Notch Activity in<i>Drosophila</i>

Kugler, Sabrina J.; Nagel, Anja C.

doi:10.1091/mbc.e07-03-0263

Cited by 28 publications

(66 citation statements)

References 43 publications

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“…Despite the relative simplicity of primary Notch signaling, the presence of a large number of fine-tuning regulators at different levels, from the outside of the cell membrane to the nucleus, dramatically increases the complexity of Notch pathway outputs and its cellular responses, thus controlling a wide range of developmental processes (Neumann and Cohen, 1998;Acar et al, 2008;Hautbergue et al, 2009;Kim et al, 2009;Xie et al, 2012). At the nuclear level, recent findings suggest that chromatin-associated regulatory mechanisms are important for proper Notch target gene expression (Bray et al, 2005;Kugler and Nagel, 2007;Moshkin et al, 2009;Duan et al, 2011;Mulligan et al, 2011;Domanitskaya and Schüpbach, 2012;Endo et al, 2012). Transcriptional silencing complexes have been identified by proteomic methods in the absence of Notch activation (Moshkin et al, 2009;Mulligan et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

CAF-1 promotes Notch signaling through epigenetic control of target gene expression during Drosophila development

Chen

et al. 2013

Development

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SUMMARYThe histone chaperone CAF-1 is known for its role in DNA replication-coupled histone deposition. However, loss of function causes lethality only in higher multicellular organisms such as mice and flies, but not in unicellular organisms such as yeasts, suggesting that CAF-1 has other important functions than histone deposition during animal development. Emerging evidence indicates that CAF-1 also has a role in higher order chromatin organization and heterochromatin-mediated gene expression; it remains unclear whether CAF-1 has a role in specific signaling cascades to promote gene expression during development. Here, we report that knockdown of one of the subunits of Drosophila CAF-1, dCAF-1-p105 (Caf1-105), results in phenotypes that resemble those of, and are augmented synergistically by, mutations of Notch positive regulatory pathway components. Depletion of dCAF-1-p105 leads to abrogation of cut expression and to downregulation of other Notch target genes in wing imaginal discs. dCAF-1-p105 is associated with Suppressor of Hairless [Su(H)] and regulates its binding to the enhancer region of E(spl)mβ. The association of dCAF-1-p105 with Su(H) on chromatin establishes an active local chromatin status for transcription by maintaining a high level of histone H4 acetylation. In response to induced Notch activation, dCAF-1 associates with the Notch intracellular domain to activate the expression of Notch target genes in cultured S2 cells, manifesting the role of dCAF-1 in Notch signaling. Together, our results reveal a novel epigenetic function of dCAF-1 in promoting Notch pathway activity that regulates normal Drosophila development.

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Section: Introductionmentioning

confidence: 99%

CAF-1 promotes Notch signaling through epigenetic control of target gene expression during Drosophila development

Chen

et al. 2013

Development

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“…Although numerous Notch target genes have been identified in different tissues or organs during different developmental stages, how the Su(H)-NICD-Mam ternary complex regulates their expression is largely unclear. Recent findings in different systems have suggested that chromatin-associated epigeneticallyregulatory mechanisms are very important for proper expression of Notch target genes (Bray et al, 2005;Domanitskaya and Schüpbach, 2012;Endo et al, 2011;Kugler and Nagel, 2007;Mulligan et al, 2011;Yu et al, 2013;Zeng et al, 2013). In flies, histone chaperones Asf1 and Nap1 are differentially associated with LID-associated factor (LAF) and RPD3-LID-associated factor (RLAF) silencing complexes to mediate epigenetic silencing at the Notch target Enhancer of Split [E(spl)] cluster (Moshkin et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

E(y)1/TAF9 mediates the transcriptional output of Notch signaling in Drosophila

Xie

Jia

et al. 2014

Journal of Cell Science

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Transcriptional activation of Notch signaling targets requires the formation of a ternary complex that involves the intracellular domain of the Notch receptor (NICD), DNA-binding protein Suppressor of Hairless [Su(H), RPBJ in mammals], and coactivator Mastermind (Mam). Here we report that E(y)1/TAF9, a component of the transcription factor TFIID complex, interacts specifically with the NICD/Su(H)/Mam complex to facilitate the transcriptional output of Notch signaling. We identified E(y)1/TAF9 in a large-scale in vivo RNAi screen for genes involved in a Notch-dependent mitotic-to-endocycle transition in Drosophila follicle cells. Knockdown of e(y)1/TAF9 displayed Notch-like phenotypes and defects in target gene and activity reporter expression in both the follicle cells and wing imaginal discs. Epistatic analyses in these two tissues indicate that E(y)1/TAF9 functions downstream of the Notch cleavage. Biochemical studies in S2 cells demonstrated that E(y)1/TAF9 physically interacts with the transcriptional effectors of Notch signaling, Su(H) and NICD. Together, our data suggest that the association of the NICD/Su(H)/Mastermind complex with E(y)1/TAF9 in response to Notch activation recruits the transcription initiation complex to induce Notch target genes, coupling Notch signaling with the transcriptional machinery.

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“…It encodes a zinc finger protein with a molecular weight of about 160 kDa (Eggert et al 2004;Kugler and Nagel 2007). Pzg was identified as p160, being an integral component of the TATA-binding protein-related factor 2 (TRF2)/ DNA replication-related element binding factor (DREF) multiprotein complex (Hochheimer et al 2002).…”

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confidence: 99%

“…The downregulation of pzg gene activity by RNA interference (pzg-RNAi) revealed the fact that Pzg is essential for the function of the TRF2/DREF complex, which regulates cell cycling and growth during Drosophila development (Kugler and Nagel 2007). The ubiquitous induction of pzg-RNAi is associated with a developmental delay and leads to loss of tissue due to reduced proliferation (Kugler and Nagel 2007).…”

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confidence: 99%

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The Putzig-NURF Nucleosome Remodeling Complex Is Required for Ecdysone Receptor Signaling and Innate Immunity in Drosophila melanogaster

Kugler

Gehring²,

Wallkamm³

et al. 2011

Genetics

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Putzig (Pzg) was originally identified as being an integral component of the TRF2/DREF complex in Drosophila melanogaster, thereby regulating the transcriptional activation of replication-related genes. In a DREF-independent manner, Pzg was shown to mediate Notch target gene activation. This function of Pzg entails an association with the nucleosome remodeling factor complex NURF, which directly binds the ecdysone receptor EcR and coregulates targets of the EcR via the NURF-specific subunit Nurf-301. In contrast, Nurf-301 acts as a negative regulator of JAK/STAT signaling. Here, we provide evidence to show that Pzg is fundamental for these functions of NURF, apart from the regulation of Notch signaling activity. A jump-out mutagenesis provided us with a pzg null mutant displaying early larval lethality, defects in growth, and molting accompanied by aberrant feeding behavior. We show that Pzg is associated with EcR in vivo and required for the transcriptional induction of EcR target genes, whereas reduced ecdysteroid levels imply a NURF-independent function of Pzg. Moreover, pzg interferes with JAK/STAT-signaling activity by acting as a corepressor of Ken. Lamellocyte differentiation was consistently affected in a JAK/STAT mutant background and the expression level of defense response genes was elevated in pzg mutants, leading to the formation of melanotic tumors. Our results suggest that Pzg acts as an important partner of NURF in the regulation of EcR and JAK/STAT signaling.

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putzigIs Required for Cell Proliferation and Regulates Notch Activity inDrosophila

Cited by 28 publications

References 43 publications

CAF-1 promotes Notch signaling through epigenetic control of target gene expression during Drosophila development

CAF-1 promotes Notch signaling through epigenetic control of target gene expression during Drosophila development

E(y)1/TAF9 mediates the transcriptional output of Notch signaling in Drosophila

The Putzig-NURF Nucleosome Remodeling Complex Is Required for Ecdysone Receptor Signaling and Innate Immunity in Drosophila melanogaster

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