Fgf receptors Fgfr1a and Fgfr2 control the function of pharyngeal endoderm in late cranial cartilage development

Larbuisson, Arnaud; Dalcq, Julia; Martial, Joseph; Müller, Marc

doi:10.1016/j.diff.2013.07.006

Cited by 33 publications

(39 citation statements)

References 54 publications

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“…Bmp signaling may regulate the Fgf response directly and recent work has shown that fgfr1a and fgfr2 in the endoderm are important in craniofacial development (Larbuisson et al, 2013). However, neither receptor is expressed until at least 24 hpf, after our time window of Bmp dependence.…”

Section: Bmp Signaling Interacts With Fgf Signaling For Proper Endodementioning

confidence: 97%

“…The autonomous requirement of the endoderm for Bmp signaling suggests that it regulates the reception of Fgf signaling. There are five Fgf receptors in zebrafish and fgfr1a and fgfr2 are not expressed before 24 hpf (Larbuisson et al, 2013). The expression of fgfr1b, fgfr3 and fgfr4 has not been examined.…”

Section: Fgf-dependent Pouch Segmentation Requires Bmp Signalingmentioning

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: Bmp Signaling Interacts With Fgf Signaling For Proper Endodementioning

confidence: 97%

Section: Fgf-dependent Pouch Segmentation Requires Bmp Signalingmentioning

confidence: 99%

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

et al. 2016

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“…S3C). As both molecules have important roles in other contexts, especially in neural crest development (Larbuisson et al, 2013;Walshe and Mason, 2003), and SU5402 can affect other receptor tyrosine kinase pathways (Mohammadi et al, 1997;Sun et al, 1999), it cannot be concluded whether these pathways act directly or indirectly on scxa expression. Nevertheless, our results are consistent with previously established roles for these pathways in other systems.…”

Section: Role Of Muscle In Tendon and Ligament Developmentmentioning

confidence: 99%

The development of zebrafish tendon and ligament progenitors

2014

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Despite the importance of tendons and ligaments for transmitting movement and providing stability to the musculoskeletal system, their development is considerably less well understood than that of the tissues they serve to connect. Zebrafish have been widely used to address questions in muscle and skeletal development, yet few studies describe their tendon and ligament tissues. We have analyzed in zebrafish the expression of several genes known to be enriched in mammalian tendons and ligaments, including scleraxis (scx), collagen 1a2 (col1a2) and tenomodulin (tnmd), or in the tendon-like myosepta of the zebrafish (xirp2a). Co-expression studies with muscle and cartilage markers demonstrate the presence of scxa, col1a2 and tnmd at sites between the developing muscle and cartilage, and xirp2a at the myotendinous junctions. We determined that the zebrafish craniofacial tendon and ligament progenitors are neural crest derived, as in mammals. Cranial and fin tendon progenitors can be induced in the absence of differentiated muscle or cartilage, although neighboring muscle and cartilage are required for tendon cell maintenance and organization, respectively. By contrast, myoseptal scxa expression requires muscle for its initiation. Together, these data suggest a conserved role for muscle in tendon development. Based on the similarities in gene expression, morphology, collagen ultrastructural arrangement and developmental regulation with that of mammalian tendons, we conclude that the zebrafish tendon populations are homologous to their force-transmitting counterparts in higher vertebrates. Within this context, the zebrafish model can be used to provide new avenues for studying tendon biology in a vertebrate genetic system.

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“…The chondrocytes from patients have reduced responsiveness to extracellular FGF18 and deficient plasma-membrane localization of FGFR2 (Merrill et al 2012). In zebrafish, fgfr2 is required for mesenchyme condensation and later chondrogenic differentiation (Larbuisson et al 2013). Targeted disruption of Fgfr2IIIC leads to narrowing of the proliferative and hypertrophic chondrocyte zones with decreased IHH and PTHRP expression and retarded ossification with a decrease in the transcription of secreted phosphoprotein 1 and RUNX2 (Eswarakumar et al 2002).…”

Section: Introduction On Growth Plate Developmentmentioning

confidence: 99%

RECENT RESEARCH ON THE GROWTH PLATE: Advances in fibroblast growth factor signaling in growth plate development and disorders

Xie

Zhou

Chen

et al. 2014

Journal of Molecular Endocrinology

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Skeletons are formed through two distinct developmental actions, intramembranous ossification and endochondral ossification. During embryonic development, most bone is formed by endochondral ossification. The growth plate is the developmental center for endochondral ossification. Multiple signaling pathways participate in the regulation of endochondral ossification. Fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling has been found to play a vital role in the development and maintenance of growth plates. Missense mutations in FGFs and FGFRs can cause multiple genetic skeletal diseases with disordered endochondral ossification. Clarifying the molecular mechanisms of FGFs/FGFRs signaling in skeletal development and genetic skeletal diseases will have implications for the development of therapies for FGF-signaling-related skeletal dysplasias and growth plate injuries. In this review, we summarize the recent advances in elucidating the role of FGFs/FGFRs signaling in growth plate development, genetic skeletal disorders, and the promising therapies for those genetic skeletal diseases resulting from FGFs/FGFRs dysfunction. Finally, we also examine the potential important research in this field in the future.

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Fgf receptors Fgfr1a and Fgfr2 control the function of pharyngeal endoderm in late cranial cartilage development

Cited by 33 publications

References 54 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

The development of zebrafish tendon and ligament progenitors

RECENT RESEARCH ON THE GROWTH PLATE: Advances in fibroblast growth factor signaling in growth plate development and disorders

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