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Novel insights into Emx2 and Dmrta2 cooperation during cortex development and evidence for Dmrta2 function in choroid plexus

ABSTRACT: To understand the genes deregulated in WT us Emx2 Knockout dorsal telencephalon at E12.5. We then performed gene expression profiling analysis using data obtained from RNA-seq of 5 different WT and Emx2KO dorsal telencephalon samples at E12.5

ORGANISM(S): Mus musculus

PROVIDER: GSE277662 | GEO | 2025/07/09

REPOSITORIES: GEO

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Novel insights into Emx2 and Dmrta2 cooperation during cortex development and evidence for Dmrta2 function in choroid plexus

Project description:Early dorsal telencephalon development is coordinated by an interplay of transcription factors that exhibit a graded expression pattern in neural progenitors. How they function together to orchestrate cortical development remains largely unknown. The Emx2 and Dmrta2 genes encode TFs that are expressed in a similar caudomedialhigh/ rostrolaterallow gradient in the ventricular zone of the developing dorsal telencephalon with, in the medial pallium, Dmrta2 but not Emx2 expressed in the developing choroid plexus. Their constitutive loss has been shown to impart similar cortical abnormalities, and their combined deletion exacerbates the phenotypes, suggesting possible cooperation during cortex development. In this study, we utilized molecular and genetic approaches to dissect how Emx2 functions with Dmrta2 during cortical development. Our results show that while they regulate a similar set of genes, their common direct targets are limited but include key regulators of cortical development. Identification of the interaction partners of Emx2 suggests that it coordinates with the LIM-domain binding protein Ldb1 to execute the activation and repression of some of its downstream targets. Finally, while Emx2 is known to suppress choroid plexus development, we also provide evidence that Dmrta2 is in contrast required for choroid plexus since in its absence in medial telencephalic progenitors, mice develop hydrocephalous postnatally, a phenotype that appears to be due to a compromised cytoarchitecture. Together, these data indicate that Emx2 and Dmrta2 have similar but also distinct functions in telencephalon development and provide the first insights into Emx2 mechanism of action.

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Project description:Early dorsal telencephalon development is coordinated by an interplay of transcription factors that exhibit a graded expression pattern in neural progenitors. How they function together to orchestrate cortical development remains largely unknown. The Emx2 and Dmrta2 genes encode TFs that are expressed in a similar caudomedialhigh/ rostrolaterallow gradient in the ventricular zone of the developing dorsal telencephalon with, in the medial pallium, Dmrta2 but not Emx2 expressed in the developing choroid plexus. Their constitutive loss has been shown to impart similar cortical abnormalities, and their combined deletion exacerbates the phenotypes, suggesting possible cooperation during cortex development. In this study, we utilized molecular and genetic approaches to dissect how Emx2 functions with Dmrta2 during mouse cortical development. Our results show that while they regulate a similar set of genes, their common direct targets are limited but include key regulators of cortical development. The identification of the interaction partners of Emx2 suggests that it coordinates with the LIM-domain binding protein Ldb1 to execute the activation and repression of some of its downstream targets. Finally, while Emx2 is known to suppress choroid plexus development, we also provide evidence that Dmrta2 is, in contrast, required for choroid plexus since in its absence in medial telencephalic progenitors, mice develop hydrocephalus postnatally, a phenotype that appears to be due to a compromised cytoarchitecture. Together, these data indicate that Emx2 and Dmrta2 have similar but also distinct functions in telencephalon development and provide the first insights into Emx2 mechanism of action.

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