DOI: 10.1242/dev.124.20.4133. Involvement of RBP-J in biological functions of mouse Notch1 and its derivatives

Involvement of RBP-J in biological functions of mouse Notch1 and its derivatives

10.1242/dev.124.20.4133

Crossref journal-article

The Company of Biologists

Development (237)

Abstract

ABSTRACT Notch is involved in the cell fate determination of many cell lineages. The intracellular region (RAMIC) of Notch1 trans-activates genes by interaction with a DNA binding protein RBP-J. We have compared the activities of mouse RAMIC and its derivatives in transactivation and differentiation sup-pression of myogenic precursor cells. RAMIC comprises two separate domains, IC for transactivation and RAM for RBP-J binding. Although the physical interaction of IC with RBP-J was much weaker than with RAM, transactivation activity of IC was shown to involve RBP-J by using an RBP-J null mutant cell line. IC showed differentiation suppression activity that was generally comparable to its transactivation activity. The RBP-J-VP16 fusion protein, which has strong transactivation activity, also suppressed myogenesis of C2C12. The RAM domain, which has no other activities than binding to RBP-J, synergistically stimulated transactivation activity of IC to the level of RAMIC. The RAM domain was proposed to compete with a putative co-repressor for binding to RBP-J because the RAM domain can also stimulate the activity of RBP-J-VP16. These results taken together, indicate that differentiation suppression of myogenic precursor cells by Notch signalling is due to transactivation of genes carrying RBP-J binding motifs.

Bibliography

Kato, H., Taniguchi, Y., Kurooka, H., Minoguchi, S., Sakai, T., Nomura-Okazaki, S., Tamura, K., & Honjo, T. (1997). Involvement of RBP-J in biological functions of mouse Notch1 and its derivatives. Development, 124(20), 4133â4141.

Authors 8

Hisamune Kato (first)
Yoshihito Taniguchi (additional)
Hisanori Kurooka (additional)
Shigeru Minoguchi (additional)
Takashi Sakai (additional)
Saeko Nomura-Okazaki (additional)
Kumiko Tamura (additional)
Tasuku Honjo (additional)

References 33 Referenced 243

10.1126/science.7716513 / Science / Notch signaling by Artavanis-Tsakonas (1995)
10.1074/jbc.272.17.11336 / J. Biol. Chem / Oncogenic forms of NOTCH1 lacking either the primary binding site for RBP-J kappa or nuclear localization sequences retain the ability to associate with RBP-J kappa and activate transcription by Aster (1997)
10.1093/nar/22.15.2938 / Nucl. Acids Res / Site-directed mutagenesis study on DNA binding regions of the mouse homologue of Suppressor of Hairless, RBP-J kappa by Chung (1994)
10.1242/dev.121.5.1533 / Development / Notch 1 is required for the coordinate segmentation of somites by Conlon (1995)
10.1242/dev.124.6.1139 / Development / Conservation of Notch signalling pathway in mammalian neurogenesis by Pompa (1997)
10.1016/0092-8674(91)90111-B / Cell / TAN-1, the human homolog of the Drosophila Notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms by Ellisen (1991)
10.1016/0092-8674(94)90196-1 / Cell / The Suppressor of Hairless protein participates in Notch receptor signaling by Fortini (1994)
10.1266/jjg.70.505 / Japan. J. Genet / Suppressor of Hairless, the Drosophila homologue of RBP-Jĸ, transactivates the neurogenic gene E(spl)m8 by Furukawa (1995)
10.1128/MCB.16.3.952 / Mol. Cell. Biol / Truncated mammalian Notch1 activates CBF1/RBPJĸ-repressed genes by a mechanism resembling that of Epstein-Barr virus EBNA2 by Hsieh (1996)
10.1038/377355a0 / Nature / Signalling downstream of activated mammalian Notch [see comments] by Jarriault (1995)
10.1073/pnas.88.12.5096 / Proc. Nat. Acad. Sci. USA / Direct derivation of conditionally immortal cell lines from an H-2Kb-tsA58 transgenic mouse by Jat (1991)
10.1016/S0021-9258(18)98396-1 / J. Biol. Chem / Wild type GAL4 binds cooperatively to the GAL1-10 UASG in vitro by Kang (1993)
10.1016/0014-5793(96)01046-0 / FEBS Lett / Functional conservation of mouse Notch receptor family members by Kato (1996)
10.1242/dev.120.9.2385 / Development / The intracellular domain of mouse Notch: a constitutively activated repressor of myogenesis directed at the basic helix-loop-helix region of MyoD by Kopan (1994)
10.1101/gad.9.21.2598 / Genes Dev / The neurogenic suppressor of hairless DNA-binding protein mediates the transcriptional activation of the enhancer of split complex genes triggered by Notch signaling by Lecourtois (1995)
10.1101/gad.7.10.1949 / Genes Dev / Antineurogenic phenotypes induced by truncated Notch proteins indicate a role in signal transduction and may point to a novel function for Notch in nuclei by Lieber (1993)
{'key': '2025021405103172600_DEVELOP_124_20_4133C17', 'article-title': 'RBP-L, a transcription factor related to RBP-J kappa', 'volume-title': 'Mol. Cell. Biol., in press', 'author': 'Minoguchi', 'year': '1997'} / Mol. Cell. Biol., in press / RBP-L, a transcription factor related to RBP-J kappa by Minoguchi (1997)
10.1093/nar/18.17.5322 / Nucl. Acids Res / pEF-BOS, a powerful mammalian expression vector by Mizushima (1990)
10.1006/dbio.1994.1326 / Dev. Biol / Delta-notch signaling and Drosophila cell fate choice by Muskavitch (1994)
10.1242/dev.120.9.2421 / Development / An activated Notch suppresses neurogenesis and myogenesis but not gliogenesis in mammalian cells by Nye (1994)
10.1242/dev.121.10.3291 / Development / Disruption of the mouse RBP-J kappa gene results in early embryonic death by Oka (1995)
10.1084/jem.183.5.2283 / J. Exp. Med / Exclusive development of T cell neoplasms in mice transplanted with bone marrow expressing activated Notch alleles by Pear (1996)
10.1016/0092-8674(91)90064-6 / Cell / Specific EGF repeats of Notch mediate interactions with Delta and Serrate: implications for Notch as a multifunctional receptor by Rebay (1991)
10.1038/364632a0 / Nature / Control of cell fate in C. elegans by a GLP-1 peptide consisting primarily of ankyrin repeats by Roehl (1993)
10.1093/oxfordjournals.jbchem.a124955 / J. Biochem / Loss of immunostaining of the RBP-J kappa transcription factor upon F9 cell differentiation induced by retinoic acid by Sakai (1995)
10.1242/dev.122.12.3765 / Development / Notch signaling inhibits muscle cell differentiation through a CBF1-independent pathway by Shawber (1996)
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10.1242/dev.124.3.693 / Development / The Xenopus homolog of Drosophila Suppressor of Hairless mediates Notch signaling during primary neurogenesis by Wettstein (1997)

Dates

Type	When
Created	4 years, 3 months ago (April 25, 2021, 11:01 p.m.)
Deposited	6 months, 1 week ago (Feb. 14, 2025, 12:10 a.m.)
Indexed	3 weeks, 6 days ago (July 28, 2025, 5:13 p.m.)
Issued	27 years, 10 months ago (Oct. 15, 1997)
Published	27 years, 10 months ago (Oct. 15, 1997)
Published Online	27 years, 10 months ago (Oct. 15, 1997)
Published Print	27 years, 10 months ago (Oct. 15, 1997)

Funders 0

None

BibTeX

@article{Kato_1997, title={Involvement of RBP-J in biological functions of mouse Notch1 and its derivatives}, volume={124}, ISSN={1477-9129}, url={http://dx.doi.org/10.1242/dev.124.20.4133}, DOI={10.1242/dev.124.20.4133}, number={20}, journal={Development}, publisher={The Company of Biologists}, author={Kato, Hisamune and Taniguchi, Yoshihito and Kurooka, Hisanori and Minoguchi, Shigeru and Sakai, Takashi and Nomura-Okazaki, Saeko and Tamura, Kumiko and Honjo, Tasuku}, year={1997}, month=oct, pages={4133–4141} }

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  "abstract": "<jats:title>ABSTRACT</jats:title>\n               <jats:p>Notch is involved in the cell fate determination of many cell lineages. The intracellular region (RAMIC) of Notch1 trans-activates genes by interaction with a DNA binding protein RBP-J. We have compared the activities of mouse RAMIC and its derivatives in transactivation and differentiation sup-pression of myogenic precursor cells. RAMIC comprises two separate domains, IC for transactivation and RAM for RBP-J binding. Although the physical interaction of IC with RBP-J was much weaker than with RAM, transactivation activity of IC was shown to involve RBP-J by using an RBP-J null mutant cell line. IC showed differentiation suppression activity that was generally comparable to its transactivation activity. The RBP-J-VP16 fusion protein, which has strong transactivation activity, also suppressed myogenesis of C2C12. The RAM domain, which has no other activities than binding to RBP-J, synergistically stimulated transactivation activity of IC to the level of RAMIC. The RAM domain was proposed to compete with a putative co-repressor for binding to RBP-J because the RAM domain can also stimulate the activity of RBP-J-VP16. These results taken together, indicate that differentiation suppression of myogenic precursor cells by Notch signalling is due to transactivation of genes carrying RBP-J binding motifs.</jats:p>",
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