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ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

ABSTRACT: To investigate the downstream genes of Isl1 and Pou4f1 in CVGs, we examined the gene expression level of each single knockout and double knockout compared with control.

ORGANISM(S): Mus musculus

PROVIDER: GSE233755 | GEO | 2024/05/31

REPOSITORIES: GEO

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ISL1 and POU4F1 Directly Interact to Regulate the Differentiation and Survival of Inner Ear Sensory Neurons

Project description:Isl1 and Pou4f1 regulate a unique set of CVG gene cooperatively or individually. GO term analysis shows these genes are crucial for CVGs development. To estimate Isl1 and Pou4f1 directly or indirectly regulate these downstream genes and how they act to affect these genes, we performed the CUT&Tag of ISL1 and POU4F1 with the histone modifications, H3K4me3, H3K27ac and H3K27me3 in CVGs. The identity of the peaks were characterized and big chromatin profiles were obtained.

2024-05-31 | GSE233840 | GEO

ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

Project description:The inner ear sensory neurons play a pivotal role in auditory processing and balance control. Though significant progresses have been made, the underlying mechanisms controlling the differentiation and survival of the inner ear sensory neurons remain largely unknown. During development, ISL1 and POU4F transcription factors are co-expressed and are required for terminal differentiation, pathfinding, axon outgrowth and the survival of neurons in the central and peripheral nervous systems. However, little is understood about their functional relationship and regulatory mechanism in neural development. Here, we have knocked out Isl1 or Pou4f1 or both in mice of both sexes. In the absence of Isl1, the differentiation of cochleovestibular ganglion (CVG) neurons is disturbed and with that Isl1-deficient CVG neurons display defects in migration and axon pathfinding. Compound deletion of Isl1 and Pou4f1 causes a delay in CVG differentiation and results in a more severe CVG defect with a loss of nearly all of spiral ganglion neurons (SGNs). Moreover, ISL1 and POU4F1 interact directly in developing CVG neurons and act cooperatively as well as independently in regulating the expression of unique sets of CVG-specific genes crucial for CVG development and survival by binding to the cis-regulatory elements including the promoters of Fgf10, Pou4f2, and Epha5 and enhancers of Eya1 and Ntng2 These findings demonstrate that Isl1 and Pou4f1 are indispensable for CVG development and maintenance by acting epistatically to regulate genes essential for CVG development.

2024-05-31 | GSE233706 | GEO

ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

Project description:ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

| PRJNA977627 | ENA

ISL1 and POU4F1 Directly Interact to Regulate the Differentiation and Survival of Inner Ear Sensory Neurons

Project description:ISL1 and POU4F1 Directly Interact to Regulate the Differentiation and Survival of Inner Ear Sensory Neurons

| PRJNA978073 | ENA

ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

Project description:ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

| PRJNA977700 | ENA

ISL1

Project description:ISL1

| PRJNA312204 | ENA

Sox2 and Fgf interact with Atoh1 to promote sensory competence throughout the zebrafish inner ear.

Project description:Atoh1 is required for differentiation of sensory hair cells in the vertebrate inner ear. Moreover, misexpression of Atoh1 is sufficient to establish ectopic sensory epithelia, making Atoh1 a good candidate for gene therapy to restore hearing. However, competence to form sensory epithelia appears to be limited to discrete regions of the inner ear. To better understand the developmental factors influencing sensory-competence, we examined the effects of misexpressing atoh1a in zebrafish embryos under various developmental conditions. Activation of a heat shock-inducible transgene, hs:atoh1a, resulted in ectopic expression of early markers of sensory development within 2h, and mature hair cells marked by brn3c:GFP began to accumulate 9h after heat shock. The ability of atoh1a to induce ectopic sensory epithelia was maximal when activated during placodal or early otic vesicle stages but declined rapidly thereafter. At no stage was atoh1a sufficient to induce sensory development in dorsal or lateral non-sensory regions of the otic vesicle. However, co-misexpression of atoh1a with fgf3, fgf8 or sox2, genes normally acting in the same gene network with atoh1a, stimulated sensory development in all regions of the otic vesicle. Thus, expression of fgf3, fgf8 or sox2 strongly enhances competence to respond to Atoh1.

| S-EPMC3171634 | biostudies-literature

POU4F1 is associated with t(8;21) AML and contributes directly to its unique transcriptional signature

Project description:POU4F1 is associated with t(8;21) acute myeloid leukemia (AML) and contributes directly to its unique transcriptional signature To identify targets of POU4F1, we performed gene expression profiling, comparing Pou4f1+/+ or Pou4f1-/- fetal liver cells to cells overexpressing POU4F1 and identified 140 differentially expressed genes.

2010-04-09 | E-GEOD-19997 | biostudies-arrayexpress

CUT&Tag analysis uncovered Pou4f1-bound DNA elements in E16.5 retinas

Project description:To understand how Pou4f1 functions in RGC lineage specification and subtype formation, we performed “Cleavage Under Targets & Tagmentation” (CUT&Tag) analysis using a rabbit anti-Pou4f1 antibody and embryonic 16.5 (E16.5) retinal cells to generate barcoded PCR libraries that are enriched for Pou4f1-mediated binding. In parallel, rabbit IgG was used as a negative control for peak calling analysis, and rabbit anti-H3K9ac antibody was used to mark active enhancers and promoters.

2023-04-30 | GSE221209 | GEO

Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer

Project description:Basal-like breast cancer (BLBC) is the most aggressive molecular subtype of breast cancer with worse prognosis and fewer treatment options. The underlying mechanisms upon BLBC transcriptional dysregulation and its upstream transcription factors (TFs) remain unclear. Here, among the hyperactive candidate TFs of BLBC identified by bioinformatic analysis, POU4F1 is uniquely upregulated in BLBC and is associated with poor prognosis. POU4F1 is necessary for the tumor growth and malignant phenotypes of BLBC through regulating G1/S transition by direct binding at the promoter of CDK2 and CCND1. More importantly, POU4F1 maintains BLBC identity by repressing ERα expression through CDK2-mediated EZH2 phosphorylation and subsequent H3K27me3 modification in ESR1 promoter. Knocking out POU4F1 in BLBC cells reactivates functional ERa expression, rendering BLBC sensitive to tamoxifen treatment. In-depth epigenetic analysis reveals that the subtype-specific re-configuration and activation of the bivalent chromatin in the POU4F1 promoter contributes to its unique expression in BLBC, which is maintained by DNA demethylase TET1. Together, these results reveal a subtype-specific epigenetically activated TF with critical role in promoting and maintaining BLBC, suggesting that POU4F1 is a potential therapeutic target for BLBC.

2024-03-14 | GSE261462 | GEO

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