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Zeb2 regulates the balance between retinal interneurons and Muller glia by inhibition of BMP-Smad signaling

ABSTRACT: Zeb2 regulates the balance between retinal interneurons and Muller glia by inhibition of BMP-Smad signaling

PROVIDER: PRJNA658914 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12507016.fastq.gz	Fastqsanger.gz
	SRR12507017.fastq.gz	Fastqsanger.gz
	SRR12507018.fastq.gz	Fastqsanger.gz
	SRR12507019.fastq.gz	Fastqsanger.gz
	SRR12507020.fastq.gz	Fastqsanger.gz

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Similar Datasets

Zeb2 regulates the balance between retinal interneurons and Muller glia by inhibition of BMP-Smad signaling

Project description:In order to identify the roles of the transcription factor Zeb2, Zeb2 was inactivated in the peripheral retina of Zeb2 mouse embryos using the αCre transgene which is acrive in the peripheral retina as early as E10.5. RNA was extracted from the whole retinae of control and Zeb2 mutant mice pups at P2.

2023-07-25 | GSE156730 | GEO

Zeb2 regulates the balance between retinal interneurons and Muller glia by inhibition of BMP-Smad signaling.

Project description:The interplay between signaling molecules and transcription factors during retinal development is key to controlling the correct number of retinal cell types. Zeb2 (Sip1) is a zinc-finger multidomain transcription factor that plays multiple roles in central and peripheral nervous system development. Haploinsufficiency of ZEB2 causes Mowat-Wilson syndrome, a congenital disease characterized by intellectual disability, epilepsy and Hirschsprung disease. In the developing retina, Zeb2 is required for generation of horizontal cells and the correct number of interneurons; however, its potential function in controlling gliogenic versus neurogenic decisions remains unresolved. Here we present cellular and molecular evidence of the inhibition of Müller glia cell fate by Zeb2 in late stages of retinogenesis. Unbiased transcriptomic profiling of control and Zeb2-deficient early-postnatal retina revealed that Zeb2 functions in inhibiting Id1/2/4 and Hes1 gene expression. These neural progenitor factors normally inhibit neural differentiation and promote Müller glia cell fate. Chromatin immunoprecipitation (ChIP) supported direct regulation of Id1 by Zeb2 in the postnatal retina. Reporter assays and ChIP analyses in differentiating neural progenitors provided further evidence that Zeb2 inhibits Id1 through inhibition of Smad-mediated activation of Id1 transcription. Together, the results suggest that Zeb2 promotes the timely differentiation of retinal interneurons at least in part by repressing BMP-Smad/Notch target genes that inhibit neurogenesis. These findings show that Zeb2 integrates extrinsic cues to regulate the balance between neuronal and glial cell types in the developing murine retina.

| S-EPMC8638546 | biostudies-literature

RNA-seq to investigate the adult mouse Muller glia transcriptome

Project description:These data serve as a reference transcriptomic profile for adult mouse retinal Muller glia. Retinas were dissociated into single cell suspensions and sorted into two fractions: a Muller glia-enriched fraction on the basis of Muller glia-specific tdTomato expression and a second fraction containing the remaining retinal cells that were tdTomato-negative. Both fractions were sequenced.

2020-08-02 | E-MTAB-7058 | biostudies-arrayexpress

Differential expression in Muller glia of injured zebrafish in a mycb-/- context

Project description:This experiment studies retinal regeneration using a zebrafish model with a focus on Muller glia reprogramming.

2024-05-10 | GSE249116 | GEO

Differential expression in Muller glia of injured zebrafish in a mych-/- context

Project description:This experiment studies retinal regeneration using a zebrafish model with a focus on Muller glia reprogramming.

2024-05-10 | GSE249115 | GEO

DAPT-dependent regulation of zebrafish Muller glial cell gene expression

Project description:In this work we identify genes differentially expressed in Muller glia from uninjured retina in zebrafish treated with and without DAPT for 1 day.

2021-07-31 | GSE160047 | GEO

Injury and apobec2-dependent regulation of zebrafish Muller glial cell gene expression

Project description:In this work we identify genes differentially expressed in Muller glia form uninjured and injured retina with and without apobec2a knockdown

2020-05-19 | GSE145330 | GEO

DN-MAML-dependent regulation of zebrafish Muller glial cell gene expression

Project description:In this work we identify genes differentially expressed in Muller glia from uninjured retina in zebrafish treated with and without DN-MAML for 1 day.

2021-07-31 | GSE160051 | GEO

Reprogramming effect of Neurog2-9SA on adult mouse Muller glial cells [mutliomics]

Project description:This study examines the reprogramming effect of Neurog2-9SA on adult mouse Muller glial cells. Generated neurons were characterized using immunohistochemistry, single-cell omics and electrophysiology. We found that AAV-mediated expression of Neurog20-9SA induces reprogramming of Muller glia into bipolar, amacrine-like neurons, and small subset of cells expressing phototreceptor marker

2025-10-02 | GSE309445 | GEO

Zeb2 is Essential for Bergmann Glial Development and Cerebellar Organization

Project description:Cerebellar circuitry is critical for balance and motor control among a wide array of functions and largely consists of granule and Purkinje neurons. Bergmann glia in the cerebellum form distinct morphological structures that facilitate granule neuron migration during development and that maintain the cerebellar organization and functional integrity. At present, molecular control of the formation and morphogenesis of Bergmann glia remains obscure. In this study, we found that Zeb2 (a.k.a. Sip1 or Zfhx1b), a Mowat-Wilson syndrome-associated transcriptional regulator, is highly restricted to Bergmann glia and is essential for their development and maturation. The mice with Zeb2 ablation in the cerebellar neural progenitor exhibit dysgenesis of cerebellar cortical lamination and locomotion defects. Deletion of Zeb2 markedly reduced Bergmann glial proliferation, differentiation and the establishment of the normal radial scaffold, disrupting migration of granule cell progenitors from external to internal granular layers. Transcriptome profiling indicated that Zeb2 regulates multiple pathways including FGF and Notch signaling as well as axonal guidance cues including Netrin G2 and Gdf10 to control Bergmann glial development. Our data reveal that Zeb2 acts as a transcriptional integrator of diverse signaling pathways to regulate the formation and morphogenesis of Bergmann glia ensuring maintenance of cerebellar integrity, suggesting that Zeb2 dysfunction in Bergmann glia might contribute to motor deficits in Mowat-Wilson syndrome.

2018-06-25 | GSE84098 | GEO

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