The tissue polarity gene nemo carries out multiple roles in patterning during Drosophila development

Verheyen, Esther M.; Mirkovic, Ivana; MacLean, Sheila J.; Langmann, Caillin; Andrews, Bryan C.; MacKinnon, Christina

doi:10.1016/s0925-4773(00)00574-8

Cited by 43 publications

(58 citation statements)

References 63 publications

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“…The following fly strains were used: nmo DB24 (D. Bessette and E.M.V., unpublished); nmo adk1 and UAS-nmo C5-1e (Verheyen et al, 2001); nmo P (also referred to as nmo-lacZ) (Choi and Benzer, 1994); sd-Gal4 (sd SG29.1 ); UAS-Daxin A2-4 (Willert et al, 1999); UAS-flu∆arm and AyGal4.25-UAS-GFP.S65T (Ito et al, 1997;Zecca et al, 1996);vgGal4, Dll-lacZ, Ubi-GFP FRT 79D, ap-Gal4, dpp-lacZ (Morimura et al, 1996); 71B-Gal4, UAS-lacZ, zw3 m11 and UAS-DFz2N (Zhang and Carthew, 1998) and dsh v26 .…”

Section: Fly Strainsmentioning

confidence: 99%

“…Subsequent analysis has shown that Nemo functions in multiple tissues and has diverse roles in development. In addition to its effect on eye polarity, we have found that disruption of nmo results in changes in wing shape and size, wing vein specification, fertility and viability (Verheyen et al, 2001). nmo is essential for embryonic development as loss of maternal and zygotic nmo results in embryonic lethality characterized by patterning defects in the head and ventral denticle belts as well as disruption of apoptosis (Mirkovic et al, 2002).…”

Section: Introductionmentioning

confidence: 98%

“…In addition to its role in the non-canonical Fz pathway regulating epithelial planar polarity (EPP) in the eye, wing and abdomen (Choi and Benzer, 1994;Strutt et al, 1997;Verheyen et al, 2001), we have previously reported preliminary evidence that modulating levels of nmo results in phenotypes consistent with a role as a Wg-antagonist (Verheyen et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Nemo is an inducible antagonist of Wingless signaling duringDrosophilawing development

Zeng

Verheyen

2004

Development

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is suppressed in wing discs ectopically expressing nmo and enhanced cell autonomously in nmo mutant clones. We find that nmo itself is a target of Wg signaling in the imaginal wing disc. nmo expression is induced upon high levels of Wg signaling and can be inhibited by interfering with Wg signaling. Finally, we observe alterations in Arm stabilization upon modulation of Nemo. These observations suggest that the patterning mechanism governed by Wg involves a negative feedback circuit in which Wg induces expression of its own antagonist Nemo.

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Section: Fly Strainsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Nemo is an inducible antagonist of Wingless signaling duringDrosophilawing development

Zeng

Verheyen

2004

Development

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“…Genetic studies revealed that homologs of NLK function as suppressors of the Wnt signaling pathway in the development of C. elegans and Drosophila. [1][2][3][4] A recent study showed that Wnt5a-Ca 2+ signaling, which is a negative regulator of Wnt, 5) can be an upstream activator of NLK for suppression of canonical Wnt-β-catenin signaling in the Xenopus system. 6) The target molecules of NLK in the Wnt-β-catenin pathway are conserved between worm and mammals.…”

mentioning

confidence: 99%

Nemo‐like kinase suppresses a wide range of transcription factors, including nuclear factor‐kB

et al. 2004

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Nemo-like kinase (NLK) is a serine/threonine kinase that suppresses the transcription activity of the β β β β-catenin-T-cell factor (TCF) complex through phosphorylation of TCF. Our previous study showed that NLK overexpression induces apoptosis in DLD-1 human colon cancer cells and that apoptosis induction presumably requires a mechanism other than the suppression of β β β β-catenin-TCF complex. Luciferase reporter gene assay with pNF-κ κ κ κB-Luc revealed that NLK could suppress transcription activity of NF-κ κ κ κB in a kinase-dependent manner. However, it appeared that transcription co-activators of NF-κ κ κ κB, such as CREB binding protein (CBP)/p300, were likely to be the direct targets of NLK, rather than NF-κ κ κ κB itself. Luciferase reporter gene analysis of GAL4-CBP fusion proteins revealed that the C-terminal region of CBP was critical for transcription suppression by NLK. In vitro kinase assay showed that NLK could phosphorylate the C-terminal domain of CBP. However, HAT activity was not suppressed by the induction of wild-type NLK in DLD-1 cells. Furthermore, we observed that NLK suppressed the transcription activity of AP-1, Smad, and p53, all of which also utilize CBP as a co-activator. The extent of suppression by NLK was similar among the transcription factors tested (50-60% reduction). Our results suggest that NLK may suppress a wide range of gene expression, possibly through CBP. he Nemo-like kinase (NLK) is an evolutionarily conserved serine/threonine kinase that plays an important role in the development of organisms. Genetic studies revealed that homologs of NLK function as suppressors of the Wnt signaling pathway in the development of C. elegans and Drosophila. 1-4)A recent study showed that Wnt5a-Ca 2+ signaling, which is a negative regulator of Wnt,5) can be an upstream activator of NLK for suppression of canonical Wnt-β-catenin signaling in the Xenopus system.6) The target molecules of NLK in the Wnt-β-catenin pathway are conserved between worm and mammals. NLK phosphorylates T-cell factor (TCF) and consequently suppresses the transcription activity of the β-catenin-TCF complex. 3,6,7) In C. elegans, LIT-1, a homolog of NLK, could phosphorylate a TCF related protein, POP-1, in vivo and in vitro and suppress its asymmetric distribution between two daughter cells mediated by the worm Wnt signaling pathway. 1,8) As Wnt-β-catenin signaling is known to be involved in human carcinogenesis, especially in colon and liver, 9, 10) one can speculate that NLK may play a suppressive role in carcinogenesis mediated by the activated Wnt-β-catenin-TCF signaling.We have recently showed that overexpression of NLK could induce growth suppression and apoptosis in a human colon cancer cell line, DLD-1. 11) Although the overall results of our study were consistent with the aforementioned studies, there were minor discrepancies. Two independent studies showed that overexpression of dominant-negative TCF could efficiently suppress the transcription activity of β-catenin-TCF complex, but did not induce apoptos...

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“…The signalling pathway is also regulated by the Nemo-like kinase (Nlk). Nlk is the mammalian homologue the Drosophila Nemo (nmo) Ser/Thr kinase, that is involved in apoptosis [16] and in multiple developmental processes [17] and was initially identified as a protein required for planar cell polarity in the developing Drosophila eye [18]. Nlk can be activated by the upstream MAP kinase kinase kinase (MAPKKK) family member transforming growth factor-␤ activated kinase-1 (Tak1) [19][20][21].…”

Section: ␤-Catenin Activates the Family Of T-cell Factor (Tcf) And Lymentioning

confidence: 99%

The ubiquitin specific protease 4 (USP4) is a new player in the Wnt signalling pathway

Zhao¹,

Schlesiger²,

Masucci³

et al. 2009

Journal of Cellular and Molecular Medicine

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The tissue polarity gene nemo carries out multiple roles in patterning during Drosophila development

Cited by 43 publications

References 63 publications

Nemo is an inducible antagonist of Wingless signaling duringDrosophilawing development

Nemo is an inducible antagonist of Wingless signaling duringDrosophilawing development

Nemo‐like kinase suppresses a wide range of transcription factors, including nuclear factor‐kB

The ubiquitin specific protease 4 (USP4) is a new player in the Wnt signalling pathway

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