Molecular patterning of the embryonic cranial mesenchyme revealed by genome-wide transcriptional profiling

Dasgupta, Krishnakali; Chung, Jong Uk; Asam, Kesava; Jeong, Juhee

doi:10.1016/j.ydbio.2019.07.015

Cited by 21 publications

(16 citation statements)

References 81 publications

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“…Staining was also observed in the limb buds (Figure 6F, G), the choroid plexus (Figure 6G, middle and left panel), and in the mesenchyme surrounding the dorsal root ganglia. Our results confirm and extend the previously published study reporting the expression of Sned1 using in‐situ hybridization in the limb buds, tail, sclerotome, vertebrae and ribs, lung, kidney, adrenal gland, cerebellum, choroid plexus and head mesenchyme, 25,48 and with gene expression data reporting Sned1 expression in the mandible and frontonasal region of E10.5 to E12.5 embryos 49,50 …”

Section: Resultssupporting

confidence: 92%

“…G, Sagittal sections of Lac-Z-stained E13.5 LacZ Sned1 WT/LacZ-Neo embryo (from left to right: lateral to the midline). CP, choroid plexus; DRG, dorsal root ganglia; FL, forelimb; HL, hindlimb; Hu, humerus; Lu B, lung bud; MC, site of apposition in the midline of Meckel's cartilages; NP, nasal process; NS, cartilage primordium of nasal septum; RP, Rathke's pouch; Sc, blade of scapula; So, somites; T, tongue; V, cartilage primordium of the vertebrae; VO, vomeronasal organ choroid plexus and head mesenchyme, 25,48 and with gene expression data reporting Sned1 expression in the mandible and frontonasal region of E10.5 to E12.5 embryos. 49,50 2.8 | Deletion of Sned1 in the neural crest cells does not affect mouse survival…”

Section: Sned1 Is Expressed In Skeletal and Craniofacial Precursorsmentioning

confidence: 99%

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Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Barqué

Jan

Fuente

et al. 2020

Developmental Dynamics

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Background The extracellular matrix (ECM) is a fundamental component of multicellular organisms that orchestrates developmental processes and controls cell and tissue organization. We previously identified the novel ECM protein SNED1 as a promoter of breast cancer metastasis and showed that its level of expression negatively correlated with breast cancer patient survival. Here, we sought to identify the roles of SNED1 during murine development. Results We generated two novel Sned1 knockout mouse strains and showed that Sned1 is essential since homozygous ablation of the gene led to early neonatal lethality. Phenotypic analysis of the surviving knockout mice revealed a role for SNED1 in the development of craniofacial and skeletal structures since Sned1 knockout resulted in growth defects, nasal cavity occlusion, and craniofacial malformations. Sned1 is widely expressed in embryos, notably by cell populations undergoing epithelial‐to‐mesenchymal transition, such as the neural crest cells. We further show that mice with a neural‐crest‐cell‐specific deletion of Sned1 survive, but display facial anomalies partly phenocopying the global knockout mice. Conclusions Our results demonstrate requisite roles for SNED1 during development and neonatal survival. Importantly, the deletion of 2q37.3 in humans, a region that includes the SNED1 locus, has been associated with facial dysmorphism and short stature.

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Section: Resultssupporting

confidence: 92%

Section: Sned1 Is Expressed In Skeletal and Craniofacial Precursorsmentioning

confidence: 99%

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Barqué

Jan

Fuente

et al. 2020

Developmental Dynamics

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show abstract

“…Our results confirm and extend the previously published study reporting the expression of Sned1 using in-situ hybridization, 22,45 and with gene expression data reporting Sned1 expression in the mandible and frontonasal region of E10.5 to E12.5 embryos. 46,47…”

Section: Sned1 Is Expressed In Skeletal and Craniofacial Precursorssupporting

confidence: 92%

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Barqué

Jan

Fuente

et al. 2018

Preprint

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AbstractBackgroundThe extracellular matrix (ECM) is a fundamental component of multicellular organisms that orchestrates developmental processes and controls cell and tissue organization. We previously identified the novel ECM protein SNED1 as a promoter of breast cancer metastasis and showed that its level of expression negatively correlated with survival of breast cancer patients. Here we sought to identify the roles of SNED1 during murine development and in physiology.ResultsWe generated two novel Sned1 knockout mouse strains and showed that Sned1 is essential since homozygous ablation of the gene led to ~67% early neonatal lethality. Phenotypic analysis of the surviving knockout mice obtained revealed a role for SNED1 in the development of craniofacial and skeletal structures since Sned1 knockout resulted in growth defects, nasal cavity occlusion, and craniofacial malformations. Sned1 is widely expressed in embryos, notably in neural-crest derivatives. We further show here that mice with a neural-crest-cell-specific deletion of Sned1 survive, but display facial anomalies partly phenocopying the global knockout mice.ConclusionsOur results demonstrate requisite roles for SNED1 during development and neonatal survival. Importantly, the deletion of 2q37.3 in humans, a region that includes the SNED1 locus, has been associated with facial dysmorphism and short stature.

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“…The close proximity of each cell type results in cross-talk of cell signaling and communication between cell populations. Furthermore, there are mechanical cues and regional differences in the composition and signaling of the extracellular matrix in the cranial mesenchyme as the cranial bones expand apically [58]. These regional differences can impact how cell fate decisions are made and are difficult to recapitulate in vitro , leading to an incomplete understanding of cell signaling mechanisms across tissue types.…”

Section: Discussionmentioning

confidence: 99%

Wnt-dependent activation of ERK mediates repression of chondrocyte fate during calvarial development

Ibarra

Machen

Atit

2021

Preprint

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Wnt signaling regulates cell fate decisions in diverse contexts during development, and loss of Wnt signaling in the cranial mesenchyme results in a robust and binary cell fate switch from cranial bone to ectopic cartilage. The Extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) and Wnt signaling pathways are activated during calvarial osteoblast cell fate selection. Here, we test the hypothesis that ERK signaling is a mediator of Wnt-dependent cell fate decisions in the cranial mesenchyme. First, we show that loss ofErk1/2 in the cranial mesenchyme results in a diminished domain of osteoblast marker expression and increased expression of cartilage fate markers and ectopic cartilage formation in the frontal bone primordia. Second, we show that mesenchyme Wnt/β-catenin signaling andWntlessare required for ERK activation in calvarial osteoblasts. Third, we demonstrate that Wnt and ERK signaling pathways function together to repress Sox9 expression in mouse cranial mesenchyme. Our results demonstrate a link between the Wnt and ERK signaling pathways in regulating lineage selection in a subset of calvarial cells and provide new insights into Wnt-dependent cell fate decisions.

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Molecular patterning of the embryonic cranial mesenchyme revealed by genome-wide transcriptional profiling

Cited by 21 publications

References 81 publications

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Wnt-dependent activation of ERK mediates repression of chondrocyte fate during calvarial development

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