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Single-cell transcriptomic analysis of craniogenesis in control and SOXC-mutant mice

ABSTRACT: SOXC genes (i.e., Sox4, Sox11 and Sox12) are important members of the SOX transcription factor family. They are involved in several developmental processes, including skeleton formation. However, their role in intramembranous ossification and, particularly, in skull development has not beed investigated yet. Here, we employed single-cell RNA-seq technology to better understand the roles of the SOXC genes in craniogenesis and how their inactivation could affect this process. We identified the expression of the SOXC genes in several cranial populations, including osteodermal and meningeal progenitors. Removal of the SOXC genes in the cranial mesenchyme with a Prx1Cre transgene showed changes in the proportions of progenitor clusters and deriving populations (dermal, hypodermal, periosteal, suture and bone cells). Mutant progenitors showed the downregulation of genes involved in cytoskeleton organization, cell adhesion and migration, cell proliferation and steorl biosynthesis. As a result, SOXC-mutant fetuses have underdeveloped bones, sutures, dermis and hypodermis, particularly in the apical regions.

ORGANISM(S): Mus musculus

PROVIDER: GSE174716 | GEO | 2022/06/08

REPOSITORIES: GEO

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Project description:During organogenesis, neural and mesenchymal progenitor cells give rise to many cell lineages, but their molecular requirements for self-renewal and lineage decisions are incompletely understood. Here we show that their survival critically relies on the redundantly acting SoxC transcription factors Sox4, Sox11 and Sox12. The more SoxC alleles are deleted in mouse embryos, the more severe and widespread organ hypoplasia is. SoxC triple-null embryos die at mid-gestation unturned and tiny, with normal patterning and lineage specification, but with massively dying neural and mesenchymal progenitor cells. Specific inactivation of SoxC genes in neural and mesenchymal cells leads to selective apoptosis of these cells, suggesting SoxC cell-autonomous roles. Tead2 functionally interacts with the SoxC genes in embryonic development, and is a direct target of the SoxC proteins. The SoxC genes therefore ensure neural and mesenchymal progenitor cell survival and act in part by activating this transcriptional mediator of the Hippo signaling pathway. During organogenesis, neural and mesenchymal progenitor cells give rise to many cell lineages, but their molecular requirements for self-renewal and lineage decisions are incompletely understood. Here we show that their survival critically relies on the redundantly acting SoxC transcription factors Sox4, Sox11 and Sox12. The more SoxC alleles are deleted in mouse embryos, the more severe and widespread organ hypoplasia is. SoxC triple-null embryos die at mid-gestation unturned and tiny, with normal patterning and lineage specification, but with massively dying neural and mesenchymal progenitor cells. Specific inactivation of SoxC genes in neural and mesenchymal cells leads to selective apoptosis of these cells, suggesting SoxC cell-autonomous roles. Tead2 functionally interacts with the SoxC genes in embryonic development, and is a direct target of the SoxC proteins. The SoxC genes therefore ensure neural and mesenchymal progenitor cell survival and act in part by activating this transcriptional mediator of the Hippo signaling pathway. Total RNA isolated from limb bud cells in culture treated with Cre recombinase expressing adenovirus to inactivate floxed SoxC genes was compared to total RNA isolated from cells treated with LacZ expressing adenovirus as well as untreated cells as controls.

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Single-cell transcriptomic analysis of craniogenesis in control and SOXC-mutant mice

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