SoxC transcription factors shape the epigenetic landscape to establish competence for sensory differentiation in the mammalian organ of Corti
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ABSTRACT:
PROVIDER: PRJNA889032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21854259_1.fastq.gz | Fastqsanger.gz | |||
| SRR21854259_2.fastq.gz | Fastqsanger.gz | |||
| SRR21854260_1.fastq.gz | Fastqsanger.gz | |||
| SRR21854260_2.fastq.gz | Fastqsanger.gz | |||
| SRR21854261.fastq.gz | Fastqsanger.gz |
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Project description:Understanding the molecular basis of competence acquisition by the lineage-specific progenitor cells can provide mechanistic insights into tissue development and regeneration. The sensory epithelium of the inner ear represents a convenient model to study this process, as only two cell types – the mechanosensory hair cells and their associated supporting cells – are specified from a single pool of progenitors in this lineage. Here we show that competence to respond to Atoh1, a transcriptional master regulator both necessary and sufficient for induction of mechanosensory hair cells, is established in the organ of Corti progenitor cells between E12.0 and 13.5. The transition to the competent state is rapid and is associated with extensive remodeling of the epigenetic landscape controlled by the SoxC group of transcription factors. Conditional loss of Sox4 and Sox11 – the two homologous family members transiently expressed in the inner ear at the time of competence establishment – blocks the ability of sensory progenitors to differentiate into hair cells. Mechanistically, we show that Sox4 binds to and establishes accessibility of early sensory lineage-specific regulatory elements, including ones associated with Atoh1 itself and its direct downstream targets. Consistent with these observations, overexpression of Sox4 or Sox11 prior to developmental establishment of competence precociously induces hair cell differentiation in the cochlear progenitors. Further, reintroducing Sox4 or Sox11 expression restores the ability of postnatal supporting cells to differentiate as hair cells in vitro and in vivo. Our findings demonstrate the pivotal role of SoxC family members as agents of epigenetic and transcriptional changes necessary for establishing competence for sensory receptor differentiation in the inner ear.
2023-08-01 | GSE215171 | GEO
Project description:The auditory organ of Corti is comprised of only two major cell types-the mechanosensory hair cells and their associated supporting cells-both specified from a single pool of prosensory progenitors in the cochlear duct. Here, we show that competence to respond to Atoh1, a transcriptional master regulator necessary and sufficient for induction of mechanosensory hair cells, is established in the prosensory progenitors between E12.0 and 13.5. The transition to the competent state is rapid and is associated with extensive remodeling of the epigenetic landscape controlled by the SoxC group of transcription factors. Conditional loss of Sox4 and Sox11-the two homologous family members transiently expressed in the inner ear at the time of competence establishment-blocks the ability of prosensory progenitors to differentiate as hair cells. Mechanistically, we show that Sox4 binds to and establishes accessibility of early sensory lineage-specific regulatory elements, including ones associated with Atoh1 and its direct downstream targets. Consistent with these observations, overexpression of Sox4 or Sox11 prior to developmental establishment of competence precociously induces hair cell differentiation in the cochlear progenitors. Further, reintroducing Sox4 or Sox11 expression restores the ability of postnatal supporting cells to differentiate as hair cells in vitro and in vivo. Our findings demonstrate the pivotal role of SoxC family members as agents of epigenetic and transcriptional changes necessary for establishing competence for sensory receptor differentiation in the inner ear.
| S-EPMC10450657 | biostudies-literature
Project description:Transcription factor SoxC is required for all neural development in purple sea urchin S. purpuratus embryos. To begin to develop a gene regulatory network for neural development, we used RNA-Seq to compare transcript populations in SoxC knockdown and control embryos. SoxC function was knocked down by morpholino oligo injection. RNA from about 1000 embryos were collected for both control and knockdown samples.
2015-12-16 | E-GEOD-76067 | biostudies-arrayexpress
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.
2010-04-15 | GSE20740 | GEO
Project description:Transcription factor SoxC is required for all neural development in purple sea urchin S. purpuratus embryos. To begin to develop a gene regulatory network for neural development, we used RNA-Seq to compare transcript populations in SoxC knockdown and control embryos.
2015-12-16 | GSE76067 | GEO
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.
2010-04-28 | E-GEOD-20740 | biostudies-arrayexpress
Project description:SOXC genes (i.e., SOX4, SOX11 and SOX12) encode for transcription factors controlling survival, proliferation, commitment and differentiation of several cell types from development onwards. Although human diseases indicate crucial roles for SOXC in bone development and maintenance, SOXC activities in osteoblastic cells remain elusive. Here, we used a mouse model to inactivate SOXC genes in the osteoblast lineage cells using an OsxCre transgene (Sox4fl/fl Sox11fl/fl Sox12fl/fl OsxCre mice referred to as SOXCOsxCre mice) and we used single-cell RNA-sequencing assays to characterize gene expression changes in bone and bone marrow cells in adulthood.
2024-03-04 | GSE241637 | GEO
Project description: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.
2022-06-08 | GSE174716 | GEO
Project description:Mesocestoides corti transcriptome
| PRJEB97085 | ENA