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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

Quantitative proteomics of the SMAD transcription factor family reveals IPO5 as a BMP Receptor-SMAD specific importin

Project description:Gene-specific transcription factors (GSTFs) control of gene transcription by DNA binding and specific protein complex recruitment, which regulates promoter accessibility for transcription initiation by RNA polymerase II. GSTFs that are frequently mutated in colon and rectal carcinomas are Suppressor of Mothers Against Decapentaplegic 2 (SMAD2) and SMAD4, which play an important role in the TGF-β signaling pathways controlling cell fate and proliferation (ref.). The SMAD protein family is a diverse and it can be divided into three subclasses: receptor activated SMADs, inhibitory SMADs and the common SMAD4 co-activator. To study protein interactors of the SMAD protein family we generated a quantitative proteomics pipeline that allows for inducible expression of GFP-tagged SMAD proteins followed by affinity purification and MS analysis. The nuclear importin IPO5 was identified as a novel interacting protein of SMAD1. Overexpression of IPO5 shows forced BMP R-SMAD nuclear localization confirming a functional relationship between BMP but not TGF-β R-SMADs and IPO5. Finally we provide evidence that the length of the lysine stretch in the NLS is involved in importin selection.

2016-10-10 | PXD004529 | Pride

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

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

ASCL1 induces neurogenesis in human Muller glia

Project description:ASCL1 induces neurogenesis in human Muller glia

| PRJNA1031951 | ENA

ASCL1 induces neurogenesis in human Muller glia

Project description:In mammals, loss of retinal cells due to disease or trauma is an irreversible process which can lead to blindness. Interestingly, regeneration of retinal neurons is a well-established process in some non-mammalian vertebrates and is driven by the Muller glia (MG), which are able to re-enter the cell cycle and reprogram into neurogenic progenitors upon retinal injury or disease. Progress has been made to restore this mechanism in mammals to promote retinal regeneration: MG can be stimulated to generate new neurons in vivo in the adult mouse retina after the over-expression of the pro-neural transcription factor Ascl1. In this study, we applied the same strategy to reprogram human MG derived from fetal retina and retinal organoids into neurons. Combining scRNA-seq, scATAC-seq, Immunofluorescence, and electrophysiology we demonstrate that human MG can be reprogrammed into neurogenic cells in vitro.

2023-10-30 | GSE246169 | GEO

Zeb2 regulates myogenic differentiation in pluripotent stem cells

Project description:Zinc finger E-box-binding homeobox 2 (ZEB2, also known as SMAD interacting protein 1 or Zfhx1b) protein is a transcription factor involved in the transforming growth factor β (TGFβ) and bone morphogenetic proteins (BMPs) signaling pathways. ZEB2 is a two-handed zinc-finger closely related to ZEB1 (ZFHX1a/δEF1) and it is present in many tissues including cardiac and skeletal muscles. Skeletal muscle development and adult myogenesis are regulated by helix-loop-helix proteins, including MyoD, Myf5, myogenin and MRF-4. It has been shown that ZEB1 (ZFHX1a/δEF1) competes with the myogenic regulatory factors for their consensus sequences on some target genes during muscle differentiation, however the role of ZEB2 in myogenesis is still unknown. In the present study, we evaluated the myogenic potential of Zeb2-null and R26_Zeb2 mouse embryonic stem cells by single-cell RNA-sequencing and tested muscle engraftment capability of the respective myogenic progenitors. Our results support the implication of Zeb2 in promoting myogenesis in pluripotent stem cells and myogenic progenitors by modulating specific genes encoding components of the TGFβ/BMP signaling system.

2020-03-31 | GSE147744 | GEO

ZEB2 protects the heart from ischemic damage

Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.

2021-03-23 | PXD022212 | Pride

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