Analysis of Sphingosine-1-phosphate signaling mutants reveals endodermal requirements for the growth but not dorsoventral patterning of jaw skeletal precursors

Balczerski, Bartosz; Matsutani, Megan; Castillo, Pablo E.; Osborne, Nicholas J.; Stainier, Didier Y. R.; Crump, J. Gage

doi:10.1016/j.ydbio.2011.12.010

Cited by 42 publications

(67 citation statements)

References 43 publications

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“…putative hypomorphic allele of smad5, we have shown that reduced Bmp signaling causes viscerocranial defects similar to those observed in some endoderm mutants (Swartz et al, 2011;Choe and Crump, 2014). Bmp signaling has been implicated in endoderm specification (Tiso et al, 2002), which is crucial for proper formation of the craniofacial skeleton (Balczerski et al, 2012;Couly et al, 2002;David et al, 2002). Data from a Bmp response element (BRE; derived from the X. laevis vent2 promoter) transgenic zebrafish line demonstrate that the endoderm receives Bmp signaling during pharyngeal arch development .…”

Section: Introductionsupporting

confidence: 56%

“…Mutants with disrupted endoderm morphogenesis exhibit defects to the viscerocranium (Balczerski et al, 2012;Choe et al, 2013;Choe and Crump, 2014) that are reminiscent of the phenotypes in Dorsomorphin-treated embryos. To determine if Bmp signaling mediates endoderm development, we treated sox17:dsRed transgenic embryos with Dorsomorphin and imaged the pharyngeal arches at 36 hpf.…”

Section: Proper Endoderm Morphology Requires Bmp Signalingmentioning

confidence: 98%

“…Studies in mouse (Couly et al, 2002), chicken (Graham et al, 2005) and zebrafish (Piotrowski and Nüsslein-Volhard, 2000;David et al, 2002) show a requirement for the endoderm in the patterning and morphogenesis of the craniofacial skeleton. This requirement can be both direct (Choe and Crump, 2014;Crump et al, 2004;Swartz et al, 2012) and indirect (Haworth et al, 2007;Balczerski et al, 2012), with loss of endoderm disrupting craniofacial development. Furthermore, disruption of endoderm morphogenesis causes defects in viscerocranial development (Choe et al, 2013;Choe and Crump, 2014;Piotrowski and Nüsslein-Volhard, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Bmp signaling mediates endoderm pouch morphogenesis by regulating Fgf signaling in zebrafish

et al. 2016

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The endodermal pouches are a series of reiterated structures that segment the pharyngeal arches and help pattern the vertebrate face. Multiple pathways regulate the complex process of endodermal development, including the Bone morphogenetic protein (Bmp) pathway. However, the role of Bmp signaling in pouch morphogenesis is poorly understood. Using genetic and chemical inhibitor approaches, we show that pouch morphogenesis requires Bmp signaling from 10-18 h post-fertilization, immediately following gastrulation. Blocking Bmp signaling during this window results in morphological defects to the pouches and craniofacial skeleton. Using genetic chimeras we show that Bmp signals directly to the endoderm for proper morphogenesis. Time-lapse imaging and analysis of reporter transgenics show that Bmp signaling is necessary for pouch outpocketing via the Fibroblast growth factor (Fgf) pathway. Double loss-of-function analyses demonstrate that Bmp and Fgf signaling interact synergistically in craniofacial development. Collectively, our analyses shed light on the tissue and signaling interactions that regulate development of the vertebrate face.

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Section: Introductionsupporting

confidence: 56%

Section: Proper Endoderm Morphology Requires Bmp Signalingmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Bmp signaling mediates endoderm pouch morphogenesis by regulating Fgf signaling in zebrafish

et al. 2016

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“…Interestingly, a recent study indicates that S1pr2 signaling in the endoderm is crucial for jaw development in zebrafish (Balczerski et al, 2012), further supporting the roles of this signaling pathway in endoderm development.…”

Section: Research Article Development 140 (4)mentioning

confidence: 72%

S1pr2/Gα13 signaling controls myocardial migration by regulating endoderm convergence

Lin

2013

Development

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SUMMARYA key process during vertebrate heart development is the migration of bilateral populations of myocardial precursors towards the midline to form the primitive heart tube. In zebrafish, signaling mediated by sphingosine-1-phosphate (S1P) and its cognate G proteincoupled receptor (S1pr2/Mil) is essential for myocardial migration, but the underlying mechanisms remain undefined. Here, we show that suppression of Ga 13 signaling disrupts myocardial migration, leading to the formation of two bilaterally located hearts (cardia bifida). Genetic studies indicate that Ga 13 acts downstream of S1pr2 to regulate myocardial migration through a RhoGEF-dependent pathway. Furthermore, disrupting any component of the S1pr2/Ga 13 /RhoGEF pathway impairs endoderm convergence during segmentation, and the endodermal defects correlate with the extent of cardia bifida. Moreover, endoderm transplantation reveals that the presence of wild-type anterior endodermal cells in Ga 13 -deficient embryos is sufficient to rescue the endoderm convergence defect and cardia bifida, and, conversely, that the presence of anterior endodermal cells defective for S1pr2 or Ga 13 in wild-type embryos causes such defects. Thus, S1pr2/Ga 13 signaling probably acts in the endoderm to regulate myocardial migration. In support of this notion, cardiac-specific expression of Ga 13 fails to rescue cardia bifida in the context of global Ga 13 inhibition. Our data demonstrate for the first time that the Ga 13 /RhoGEF-dependent pathway functions downstream of S1pr2 to regulate convergent movement of the endoderm, an event that is crucial for coordinating myocardial migration.

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“…We hypothesize that mandibular growth is regulated by a similar signaling feedback loop. Shh expression in the pharyngeal endoderm is essential for mandibular development, where it directs neural crest survival and outgrowth (Ahlgren and Bronner-Fraser, 1999;Balczerski et al, 2012;Brito et al, 2006;Brito et al, 2008;David et al, 2002;Jeong et al, 2004;Veitch et al, 1999). Exogenous Shh, when placed in the mandibular arch environment, activates Bmp4 and Fgf8 expression in the oral ectoderm, resulting in the development of supernumerary mandibles (Brito et al, 2008).…”

Section: Regulative Development Of the Mandiblementioning

confidence: 99%

Multiple developmental mechanisms regulate species-specific jaw size

et al. 2014

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Variation in jaw size during evolution has been crucial for the adaptive radiation of vertebrates, yet variation in jaw size during development is often associated with disease. To test the hypothesis that early developmental events regulating neural crest (NC) progenitors contribute to species-specific differences in size, we investigated mechanisms through which two avian species, duck and quail, achieve their remarkably different jaw size. At early stages, duck exhibit an anterior shift in brain regionalization yielding a shorter, broader, midbrain. We find no significant difference in the total number of pre-migratory NC; however, duck concentrate their premigratory NC in the midbrain, which contributes to an increase in size of the post-migratory NC population allocated to the mandibular arch. Subsequent differences in proliferation lead to a progressive increase in size of the duck mandibular arch relative to that of quail. To test the role of pre-migratory NC progenitor number in regulating jaw size, we reduced and augmented NC progenitors. In contrast to previous reports of regeneration by NC precursors, we find that neural fold extirpation results in a loss of NC precursors. Despite this reduction in their numbers, post-migratory NC progenitors compensate, producing a symmetric and normal-sized jaw. Our results suggest that evolutionary modification of multiple aspects of NC cell biology, including NC allocation within the jaw primordia and NC-mediated proliferation, have been important to the evolution of jaw size. Furthermore, our finding of NC post-migratory compensatory mechanisms potentially extends the developmental time frame for treatments of disease or injury associated with NC progenitor loss.

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Analysis of Sphingosine-1-phosphate signaling mutants reveals endodermal requirements for the growth but not dorsoventral patterning of jaw skeletal precursors

Cited by 42 publications

References 43 publications

Bmp signaling mediates endoderm pouch morphogenesis by regulating Fgf signaling in zebrafish

Bmp signaling mediates endoderm pouch morphogenesis by regulating Fgf signaling in zebrafish

S1pr2/Gα13 signaling controls myocardial migration by regulating endoderm convergence

Multiple developmental mechanisms regulate species-specific jaw size

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