A mouse homologue of Strawberry Notch is transcriptionally regulated by Reelin signal

Baba, Kousuke; Dekimoto, Hideyuki; Muraoka, Daisuke; Agata, Kiyokazu; Terashima, Toshio; Katsuyama, Yu

doi:10.1016/j.bbrc.2006.09.135

Cited by 9 publications

(23 citation statements)

References 34 publications

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“…We observed that both the nuclear Notch ICD expression and Notch ICD activity-dependent Rbpj-mediated transcription typical of wild type migrating neurons were significantly reduced in Reeler cortex (Figure 1 and Figure S3). These findings are consistent with a report that the expression of the Notch target gene, Strawberry Notch , is also downregulated in Reeler (Baba et al, 2006). …”

Section: Discussionsupporting

confidence: 93%

“…Although a Reelin homologue has not been identified in invertebrates including Drosophila , it also has been shown that Disabled (a Drosophila homologue of mammalian Dab1) binds Notch in vitro (Giniger, 1998; Le Gall and Giniger, 2004; Le Gall et al, 2008). Furthermore, reduction of a Notch downstream gene has been reported in Reeler mutant mice (Baba et al, 2006). These led us to hypothesize that Notch may play a role in Reelin-regulated lamination of the mammalian neocortex.…”

Section: Introductionmentioning

confidence: 99%

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Interaction between Reelin and Notch Signaling Regulates Neuronal Migration in the Cerebral Cortex

Hashimoto-Torii

Torii

Sarkisian

et al. 2008

Neuron

194

186

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Summary Neuronal migration is a fundamental component of brain development whose failure is associated with various neurological and psychiatric disorders. Reelin is essential for the stereotypical inside-out sequential lamination of the neocortex, but the molecular mechanisms of its action still remain unclear. Here we show that regulation of Notch activity plays an important part in Reelin signal-dependent neuronal migration. We found that Reelin-deficient mice have reduced levels of the cleaved form of Notch intracellular domain (Notch ICD) and that loss of Notch signaling in migrating neurons results in migration and morphology defects. Further, overexpression of Notch ICD mitigates the laminar and morphological abnormalities of migrating neurons in Reeler. Finally, our in vitro biochemical studies show that Reelin signaling inhibits Notch ICD degradation via Dab1. Together, our results indicate that neuronal migration in the developing cerebral cortex requires a Reelin-Notch interaction.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Interaction between Reelin and Notch Signaling Regulates Neuronal Migration in the Cerebral Cortex

Hashimoto-Torii

Torii

Sarkisian

et al. 2008

Neuron

194

186

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“…The N- and C-terminal regions of Sbno/Sno are highly conserved in both vertebrates and invertebrates1213, and these regions contain two characteristic motifs, the DExH box and helicase-c domain, respectively. Based upon these structural features, Sbno/Sno is classified as a helicase-like protein141516 that belongs to the SF2 superfamily. Nonetheless, the molecular functions of Sbno/Sno, especially from a viewpoint of transcriptional control, remain obscure.…”

mentioning

confidence: 99%

Notch and Hippo signaling converge on Strawberry Notch 1 (Sbno1) to synergistically activate Cdx2 during specification of the trophectoderm

Watanabe

Miyasaka

Kubo

et al. 2017

Sci Rep

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The first binary cell fate decision occurs at the morula stage and gives rise to two distinct types of cells that constitute the trophectoderm (TE) and inner cell mass (ICM). The cell fate determinant, Cdx2, is induced in TE cells and plays an essential role in their differentiation and maintenance. Notch and Hippo signaling cascades are assumed to converge onto regulatory elements of Cdx2, however, the underlying molecular mechanisms are largely unknown. Here, we show involvement of Strawberry Notch1 (Sbno1), a novel chromatin factor of the helicase superfamily 2, during preimplantation development. Sbno1 knockout embryos die at the preimplantation stage without forming a blastocoel, and Cdx2 is not turned on even though both Yap and Tead4 reside normally in nuclei. Accordingly, Sbno1 acts on the trophectoderm-enhancer (TEE) of Cdx2, ensuring its robust and synergistic activation by the Yap/Tead4 and NICD/Rbpj complexes. Interestingly, this synergism is enhanced when cells are mechanically stretched, which might reflect that TE cells are continuously stretched by the expanding ICM and blastocoel cavity. In addition, the histone chaperone, FACT (FAcilitates Chromatin Transcription) physically interacts with Sbno1. Our data provide new evidence on TE specification, highlighting unexpected but essential functions of the highly conserved chromatin factor, Sbno1.

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“…Hindbrain efferent neurons. Whole mount in situ hybridization of the mouse embryos showed specific expression of Reelin in rhombomere 4 from E11.5, which is much earlier than the neuronal migration takes place, suggesting that Reelin function is involved not only in neuronal migration, but also in some biochemical changes of neural stem cells (Baba et al . 2006).…”

mentioning

confidence: 99%

Developmental anatomy of reeler mutant mouse

Katsuyama

Terashima

2009

Dev Growth Differ

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The reeler mouse is one of the most famous spontaneously occurring mutants in the research field of neuroscience, and this mutant has been used as a model animal to understand mammalian brain development. The classical observations emphasized that laminar structures of the reeler brain are highly disrupted. Molecular cloning of Reelin, the gene responsible for reeler mutant provided insights into biochemistry of Reelin signal, and some models had been proposed to explain the function of Reelin signal in brain development. However, recent reports of reeler found that non-laminated structures in the central nervous system are also affected by the mutation, making function of Reelin signal more controversial. In this review, we summarized reported morphological and histological abnormalities throughout the central nervous system of the reeler comparing to those of the normal mouse. Based on this overview of the reeler abnormalities, we discuss possible function of Reelin signal in the neuronal migration and other morphological events in mouse development.

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A mouse homologue of Strawberry Notch is transcriptionally regulated by Reelin signal

Cited by 9 publications

References 34 publications

Interaction between Reelin and Notch Signaling Regulates Neuronal Migration in the Cerebral Cortex

Interaction between Reelin and Notch Signaling Regulates Neuronal Migration in the Cerebral Cortex

Notch and Hippo signaling converge on Strawberry Notch 1 (Sbno1) to synergistically activate Cdx2 during specification of the trophectoderm

Developmental anatomy of reeler mutant mouse

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