Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA723890 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14304967_1.fastq.gz | Fastqsanger.gz | |||
| SRR14304967_2.fastq.gz | Fastqsanger.gz | |||
| SRR14304968_1.fastq.gz | Fastqsanger.gz | |||
| SRR14304968_2.fastq.gz | Fastqsanger.gz | |||
| SRR14304969_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed RNAseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptome.
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Project description:Binding sites of the Six1 transcription factor were identified in primary myoblasts and myotubes of mice using ChIP-sequencing
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Project description:Six1 is a critical transcription factor for specifying cell fates in multiple organs and shares common DNA-binding sites with Six2/4/5. However, its molecular function in defining the specificity of Six1-DNA interactions and in instructing cell fates is poorly understood. We performed Six1 ChIP-seq analyses in E10.5 mouse embryos and E13.5 cochleae to map genome-wide CRMs through which Six1 and its interacting TFs function in a combinatorial fashion to control the network of gene regulation necessary for proper development. Genome-wide characterization has identified a robust set of Six1 targets in embryos and auditory sensory epithelium, including genes participating in Wnt/Notch/Shh/Fgf signaling pathways and regulators critical for auditory hair cell formation. Our data provide insights into how Six1 acts in multiple regulatory networks operating in distinct cell types at different stages.
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Project description:Nephron endowment is determined by the self-renewal and induction of a nephron progenitor pool established at the onset of kidney development. In the mouse, the related transcriptional regulators Six1 and Six2 play non-overlapping roles in nephron progenitors. Transient Six1 activity prefigures, and is essential for, active nephrogenesis. In contrast, Six2 maintains later progenitor self-renewal from the onset of nephrogenesis. We compared Six2’s regulatory actions in mouse and human nephron progenitors by chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq). Surprisingly, SIX1 was identified as a SIX2 target unique to the human nephron progenitors. Further, RNA-seq and immunostaining revealed overlapping SIX1 and SIX2 progenitor activity in the 16 week human fetal kidney. Human SIX1 ChIP-seq revealed a similar set of targets to SIX2, and predicted both factors bind DNA through an identical recognition site. In contrast to the mouse where Six2 binds its own enhancers but doesn’t interact with DNA around Six1, both human SIX1 and SIX2 bind homologous SIX2 enhancers and putative enhancers positioned around SIX1. Transgenic analysis of a putative human SIX1 enhancer in the mouse revealed a transient, mouse-like, pre-nephrogenic, Six1 regulatory pattern. Together, these data demonstrate a divergence in SIX-factor regulation between mouse and human nephron progenitors. In the human, an auto/cross-regulatory loop drives continued SIX1 and SIX2 expression during active nephrogenesis. In contrast, the mouse establishes only an auto-regulatory Six2 loop. It is tempting to speculate that differential SIX-factor regulation may contribute to species differences in the duration of progenitor programs and nephron output.
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Project description:Craniofacial development requires intricate cooperation of multiple transcription factors and signaling pathways. Six1 is a critical transcription factor regulating craniofacial development. However, the exact function of Six1 during craniofacial development remains elusive. In this study, we investigated the function of Six1 in mandible development using a Six1 knockout mouse model (Six1-/-) and a cranial neural crest-specific, Six1 conditional knockout mouse model (Six1f/f; Wnt1-Cre). The Six1-/- mice exhibited multiple craniofacial deformities, including severe microsomia, high-arched palate, and uvula deformity. Importantly, the Six1f/f; Wnt1-Cre mice recapitulate the microsomia phenotype of Six1-/- mice, thus demonstrating that the expression of Six1 in ectomesenchyme is critical for mandible development. We further showed that the knockout of Six1 led to abnormal expression of osteogenic genes within the mandible. Moreover, the knockdown of Six1 in C3H10 T1/2 cells reduced their osteogenic capacity in vitro. Using RNA-seq, we showed that both the loss of Six1 in the E18.5 mandible and the Six1 knockdown in C3H10 T1/2 led to the dysregulation of genes involved in embryonal skeletal development. In particular, we showed that Six1 binds to the promoter of Bmp4, Fat4, Fgf18, and Fgfr2, and promotes their transcription. Collectively, our results suggest that Six1 plays a critical role in the regulation of mandibular skeleton formation during mouse embryogenesis.
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