Dll1 is a downstream target of Tbx6 in the paraxial mesoderm

White, Phillip H.; Chapman, Deborah L.

doi:10.1002/gene.20140

Cited by 52 publications

(67 citation statements)

References 28 publications

(50 reference statements)

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“…In embryos of Tbx6 hypomorphic mutant mice, Dll1 expression in the tailbud and posterior PSM is greatly reduced (40). Promoter analyses of Dll1 have demonstrated that Tbx6, in synergy with Wnt signaling, activates Dll1 expression by binding to T-binding consensus sequences (20,41). Taken together, our present results demonstrate that Tbx6 and Notch signaling constitute a regulatory network that controls somite formation via the regulation of Mesp2 expression.…”

Section: Biologysupporting

confidence: 64%

“…Tbx6 protein exists also in S-1 (20). Mesp2 is not expressed in the PSM of Tbx6-null mouse embryos (7), suggesting that it is a downstream target of Tbx6.…”

Section: Tbx6 Binds To Cis-regulatory Elements Of the Mesp2 Gene Andmentioning

confidence: 99%

“…3), indicating that Tbx6 functions as a transcriptional activator of Mesp2. In somitestage embryos, Tbx6 is expressed throughout the PSM and also in the tailbud region (20,23), whereas Mesp2 expression is restricted to the anterior PSM just before somite formation, and the expression overlaps only in the anterior limit of the Tbx6 expression domain (Fig. 6E).…”

Section: The Notch Intracellular Domain (Nicd) Activates a Mesp2 Repomentioning

confidence: 99%

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Tbx6-mediated Notch signaling controls somite-specific Mesp2 expression

Yasuhiko

Haraguchi²,

Kitajima³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

124

142

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Mesp2 is a transcription factor that plays fundamental roles in somitogenesis, and its expression is strictly restricted to the anterior presomitic mesoderm just before segment border formation. The transcriptional on-off cycle is linked to the segmentation clock. In our current study, we show that a T-box transcription factor, Tbx6, is essential for Mesp2 expression. Tbx6 directly binds to the Mesp2 gene upstream region and mediates Notch signaling, and subsequent Mesp2 transcription, in the anterior presomitic mesoderm. Our data therefore reveal that a mechanism, via Tbx6-dependent Notch signaling, acts on the transcriptional regulation of Mesp2. This finding uncovers an additional component of the interacting network of various signaling pathways that are involved in somitogenesis.enhancer ͉ transgenic mouse ͉ RBPJ ͉ luciferase assay

show abstract

Section: Biologysupporting

confidence: 64%

“…Tbx6 protein exists also in S-1 (20). Mesp2 is not expressed in the PSM of Tbx6-null mouse embryos (7), suggesting that it is a downstream target of Tbx6.…”

Section: Tbx6 Binds To Cis-regulatory Elements Of the Mesp2 Gene Andmentioning

confidence: 99%

Section: The Notch Intracellular Domain (Nicd) Activates a Mesp2 Repomentioning

confidence: 99%

See 1 more Smart Citation

Tbx6-mediated Notch signaling controls somite-specific Mesp2 expression

Yasuhiko

Haraguchi²,

Kitajima³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

124

142

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show abstract

“…However, the question of whether P2PSME is indispensable for Mesp2 expression during somitogenesis remained to be addressed. Because of differences in the expression patterns of Mesp2 and Tbx6 -Tbx6 is expressed throughout the PSM and tailbud (Chapman et al, 1996;White and Chapman, 2005) whereas Mesp2 expression is observed only in the anterior PSM (Saga et al, 1997) -another open question was whether Tbx6 actually binds to P2PSME.…”

Section: Introductionmentioning

confidence: 99%

Functional importance of evolutionally conserved Tbx6 binding sites in the presomitic mesoderm-specific enhancer ofMesp2

et al. 2008

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The T-box transcription factor Tbx6 controls the expression of Mesp2, which encodes a basic helix-loop-helix transcription factor that has crucial roles in somitogenesis. In cultured cells, Tbx6 binding to the Mesp2 enhancer region is essential for the activation of Mesp2 by Notch signaling. However, it is not known whether this binding is required in vivo. Here we report that an Mesp2 enhancer knockout mouse bearing mutations in two crucial Tbx6 binding sites does not express Mesp2 in the presomitic mesoderm. This absence leads to impaired skeletal segmentation identical to that reported for Mesp2-null mice, indicating that these Tbx6 binding sites are indispensable for Mesp2 expression. T-box binding to the consensus sequences in the Mesp2 upstream region was confirmed by chromatin immunoprecipitation assays. Further enhancer analyses indicated that the number and spatial organization of the T-box binding sites are critical for initiating Mesp2 transcription via Notch signaling. We also generated a knock-in mouse in which the endogenous Mesp2 enhancer was replaced by the core enhancer of medaka mespb, an ortholog of mouse Mesp2. The homozygous enhancer knock-in mouse was viable and showed normal skeletal segmentation, indicating that the medaka mespbenhancer functionally replaced the mouse Mesp2 enhancer. These results demonstrate that there is significant evolutionary conservation of Mesp regulatory mechanisms between fish and mice.

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“…We found three sites resembling a Tbox half site (Kispert and Herrmann, 1993;Conlon et al, 2001;White and Chapman, 2005) positioned at 113 (T1), 141 (T2), and 201 (T3) nucleotides upstream from the pMesogenin2 transcriptional start site (Fig. 4A, B).…”

Section: Pmesogenin2 5 Regulatory Region Contains Potential T-box Binmentioning

confidence: 67%

pMesogenin1 and 2 function directly downstream of Xtbx6 in Xenopus somitogenesis and myogenesis

Tazumi

Yabe

Yokoyama

et al. 2008

Developmental Dynamics

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T-box transcription factor tbx6 and basic-helix-loop-helix transcription factor pMesogenin1 are reported to be involved in paraxial mesodermal differentiation. To clarify the relationship between these genes in Xenopus laevis, we isolated pMesogenin2, which showed high homology with pMesogenin1. Both pMesogenin1 and 2 appeared to be transcriptional activators and were induced by a hormone-inducible version of Xtbx6 without secondary protein synthesis in animal cap assays. The pMesogenin2 promoter contained three potential T-box binding sites with which Xtbx6 protein was shown to interact, and a reporter gene construct containing these sites was activated by Xtbx6. Xtbx6 knockdown reduced pMesogenin1 and 2 expressions, but not vice versa. Xtbx6 and pMesogenin1 and 2 knockdowns caused similar phenotypic abnormalities including somite malformation and ventral body wall muscle hypoplasia, suggesting that Xtbx6 is a direct regulator of pMesogenin1 and 2, which are both involved in somitogenesis and myogenesis including that of body wall muscle in Xenopus laevis. Developmental Dynamics 237: 3749 -3761, 2008.

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Dll1 is a downstream target of Tbx6 in the paraxial mesoderm

Cited by 52 publications

References 28 publications

Tbx6-mediated Notch signaling controls somite-specific Mesp2 expression

Tbx6-mediated Notch signaling controls somite-specific Mesp2 expression

Functional importance of evolutionally conserved Tbx6 binding sites in the presomitic mesoderm-specific enhancer ofMesp2

pMesogenin1 and 2 function directly downstream of Xtbx6 in Xenopus somitogenesis and myogenesis

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