Mouse <i>Ripply2</i> is downstream of Wnt3a and is dynamically expressed during somitogenesis

Biris, Kristin K.; Dunty, William C.; Yamaguchi, Terry P.

doi:10.1002/dvdy.21342

Cited by 28 publications

(25 citation statements)

References 31 publications

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“…The protocol was as described in Biris et al (Biris et al, 2007) with the following changes: embryos were washed for 1 hour six times in maelic acid buffer (MAB; 0.1 M maelic acid pH 7.5, 0.15 M NaCl, 0.1% Tween-20 and 0.002 M levamisole) followed by a 16 hour overnight wash at room temperature. Color reactions were allowed to develop overnight and images were taken prior to storage in 80% glycerol.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

sonic hedgehog is required in pulmonary endoderm for atrial septation

et al. 2009

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The genesis of the septal structures of the mammalian heart is central to understanding the ontogeny of congenital heart disease and the evolution of cardiac organogenesis. We found that Hedgehog (Hh) signaling marked a subset of cardiac progenitors specific to the atrial septum and the pulmonary trunk in the mouse. Using genetic inducible fate mapping with Gli1CreERT2, we marked Hh-receiving progenitors in anterior and posterior second heart field splanchnic mesoderm between E8 and E10. In the inflow tract, Hh-receiving progenitors migrated from the posterior second heart field through the dorsal mesocardium to form the atrial septum,including both the primary atrial septum and dorsal mesenchymal protrusion(DMP). In the outflow tract, Hh-receiving progenitors migrated from the anterior second heart field to populate the pulmonary trunk. Abrogation of Hh signaling during atrial septal progenitor specification resulted in atrial and atrioventricular septal defects and hypoplasia of the developing DMP. Hedgehog signaling appeared necessary and sufficient for atrial septal progenitor fate:Hh-receiving cells rendered unresponsive to the Hh ligand migrated into the atrium in normal numbers but populated the atrial free wall rather than the atrial septum. Conversely, constitutive activation of Hh signaling caused inappropriate enlargement of the atrial septum. The close proximity of posterior second heart field cardiac progenitors to pulmonary endoderm suggested a pulmonary source for the Hh ligand. We found that Shh is required in the pulmonary endoderm for atrial septation. Therefore, Hh signaling from distinct pulmonary and pharyngeal endoderm is required for inflow and outflow septation, respectively. These data suggest a model in which respiratory endoderm patterns the morphogenesis of cardiac structural components required for efficient cardiopulmonary circulation.

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Section: In Situ Hybridizationmentioning

confidence: 99%

sonic hedgehog is required in pulmonary endoderm for atrial septation

et al. 2009

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“…Single and double whole-mount in situ hybridization (WISH) was performed as previously described (Biris et al, 2007). Embryos were photographed on a Leica stereoscope or a Zeiss Axiophot compound microscope.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Wnt3a/β-catenin signaling controls posterior body development by coordinating mesoderm formation and segmentation

et al. 2008

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Somitogenesis is thought to be controlled by a segmentation clock, which consists of molecular oscillators in the Wnt3a, Fgf8 and Notch pathways. Using conditional alleles of Ctnnb1 (␤-catenin), we show that the canonical Wnt3a/␤-catenin pathway is necessary for molecular oscillations in all three signaling pathways but does not function as an integral component of the oscillator. Small, irregular somites persist in abnormally posterior locations in the absence of ␤-catenin and cycling clock gene expression. Conversely, Notch pathway genes continue to oscillate in the presence of stabilized ␤-catenin but boundary formation is delayed and anteriorized. Together, these results suggest that the Wnt3a/␤-catenin pathway is permissive but not instructive for oscillating clock genes and that it controls the anterior-posterior positioning of boundary formation in the presomitic mesoderm (PSM). The Wnt3a/␤-catenin pathway does so by regulating the activation of the segment boundary determination genes Mesp2 and Ripply2 in the PSM through the activation of the Notch ligand Dll1 and the mesodermal transcription factors T and Tbx6. Spatial restriction of Ripply2 to the anterior PSM is ensured by the Wnt3a/␤-catenin-mediated repression of Ripply2 in posterior PSM. Thus, Wnt3a regulates somitogenesis by activating a network of interacting target genes that promote mesodermal fates, activate the segmentation clock, and position boundary determination genes in the anterior PSM.

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“…In situ hybridization and βGal staining Whole-mount in situ hybridization was performed using a modification (Biris et al, 2007) of previously described methods (Harland, 1991) with antisense RNA probes using digoxigenin-or fluorescein-labeled UTP (Roche) for synthesis of Sox2, T and Uncx4.1 RNA probes (Invitrogen). For color development, NBT/BCIP (dark purple, Roche), BCIP alone (light blue) or magenta phosphate (magenta, Goldbio) were used as substrates.…”

Section: Histology and Immunohistochemistrymentioning

confidence: 99%

Lineage tracing of neuromesodermal progenitors reveals novel Wnt-dependent roles in trunk progenitor cell maintenance and differentiation

et al. 2015

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In the development of the vertebrate body plan, Wnt3a is thought to promote the formation of paraxial mesodermal progenitors (PMPs) of the trunk region while suppressing neural specification. Recent lineage-tracing experiments have demonstrated that these trunk neural progenitors and PMPs derive from a common multipotent progenitor called the neuromesodermal progenitor (NMP). NMPs are known to reside in the anterior primitive streak (PS) region; however, the extent to which NMPs populate the PS and contribute to the vertebrate body plan, and the precise role that Wnt3a plays in regulating NMP self-renewal and differentiation are unclear. To address this, we used cell-specific markers (Sox2 and T) and tamoxifen-induced Cre recombinase-based lineage tracing to locate putative NMPs in vivo. We provide functional evidence for NMP location primarily in the epithelial PS, and to a lesser degree in the ingressed PS. Lineage-tracing studies in Wnt3a/β-catenin signaling pathway mutants provide genetic evidence that trunk progenitors normally fated to enter the mesodermal germ layer can be redirected towards the neural lineage. These data, combined with previous PS lineage-tracing studies, support a model that epithelial anterior PS cells are Sox2 + T + multipotent NMPs and form the bulk of neural progenitors and PMPs of the posterior trunk region. Finally, we find that Wnt3a/β-catenin signaling directs trunk progenitors towards PMP fates; however, our data also suggest that Wnt3a positively supports a progenitor state for both mesodermal and neural progenitors.

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Mouse Ripply2 is downstream of Wnt3a and is dynamically expressed during somitogenesis

Cited by 28 publications

References 31 publications

sonic hedgehog is required in pulmonary endoderm for atrial septation

sonic hedgehog is required in pulmonary endoderm for atrial septation

Wnt3a/β-catenin signaling controls posterior body development by coordinating mesoderm formation and segmentation

Lineage tracing of neuromesodermal progenitors reveals novel Wnt-dependent roles in trunk progenitor cell maintenance and differentiation

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