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Transcription factor Pbx4 regulates limb development and hematopoiesis in mice

ABSTRACT: Transcription factor Pbx4 regulates limb development and hematopoiesis in mice

PROVIDER: PRJNA930734 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23318981_1.fastq.gz	Fastqsanger.gz
	SRR23318981_2.fastq.gz	Fastqsanger.gz
	SRR23318982_1.fastq.gz	Fastqsanger.gz
	SRR23318982_2.fastq.gz	Fastqsanger.gz
	SRR23318983_1.fastq.gz	Fastqsanger.gz

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Transcription factor Pbx4 regulates limb development and hematopoiesis in mice

Project description:To characterize Pbx4-binding sites on the genome, we conducted ChIP-seq analyses by using testicular lysates from Pbx4-FLAG KI mice. We found Pbx4 preferentially binds to promoters of a large number of genes including other HD-containing protein and ribosomal protein genes, of which mutations are related to anemia. PBX4 binding sites are enriched in motifs similar to those of other HD-containing proteins indicating PBX4, like other PBX members, may act as a cofactor of other proteins. Together, these results show that PBX4 participates limb development and hematopoiesis although its expression in spermatogenic cells but not in other cell types in adult mice is detected.

2024-01-22 | GSE224369 | GEO

Transcription factor Pbx4 regulates limb development and hematopoiesis in mice

Project description:Transcription factor Pbx4 regulates limb development and hematopoiesis in mice

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Transcription factor Pbx4 regulates limb development and hematopoiesis in mice [RNA-seq]

Project description:Transcription factor Pbx4 regulates limb development and hematopoiesis in mice [RNA-seq]

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Transcription factor Pbx4 regulates limb development and hematopoiesis in mice [RNA-seq]

Project description:We carried out RNA-seq analysis to identify genes that are potentially regulated by PBX4 in hindlimb bud cells of the E11.5 mice by comparing gene expression in KO vs WT mice.

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Transcription factor Pbx4 regulates limb development and hematopoiesis in mice

Project description:This SuperSeries is composed of the SubSeries listed below.

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Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

Project description:Development of the vertebrate heart requires the appropriate integration of temporally-distinct differentiating progenitor populations. While factors that promote accrual of later-differentiating second heart field (SHF)-derived cells to the outflow tract (OFT) have been intensively investigated, few signals are understood that specifically restrict the size of the vertebrate OFT. Here, we show that improper specification and proliferation of SHF progenitors in zebrafish lazarus (lzr) mutants, which lack the transcription factor Pbx4, produces enlarged hearts with a specific increase in ventricular cardiomyocytes and smooth muscle cells within the OFT. Specifically, optogenetic lineage-tracing demonstrates Pbx4 initially promotes the proper partitioning of the SHF into anterior progenitors, which contribute to the OFT, and adjacent endothelial cell progenitors, which contribute to posterior pharyngeal arch arteries. Subsequently, Pbx4 also limits the size of the SHF through repressing SHF progenitor proliferation. Single-cell RNA sequencing of nkx2.5+ cells revealed that the enlarged SHF progenitor population within Pbx4-deficient embryos assimilates characteristics of normally distinct proliferative and more anterior, differentiated cardiomyocyte populations. Therefore, the generation of proper OFT size and great arteries in vertebrates requires Pbx-dependent stratification of unique progenitor differentiation states to facilitate homeotic-like transformations and limit progenitor production within the SHF.

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HoxC5 and Pbx4 repress hTERT to limit telomerase activity

Project description:Telomere elongation by telomerase is critical for the proliferation of human stem cells and >85-90% of cancer cells. The repression of telomerase activity during cellular differentiation promotes replicative aging and function as a physiological barrier for tumorigenesis in long-lived mammals, including humans. However, the underlying mechanisms remain unclear. We found that HoxC5 repressed hTERT, via a previously uncharacterized upstream enhancer element. HoxC5 interacts with co-repressors Pbx4 and Meis3, and recruits Class I histone deacetylases, to mediate repression of hTERT. The upstream enhancer element are conserved in long-lived primates, and HOXC5 are activated upon differentiation, consistent with diminished telomerase activity. Thus, HoxC5/Pbx4/Meis3 together constitute a developmental-controlled regulatory loop that coordinates transcriptional repression of hTERT.

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Project description:NF-YA and Pbx4 ChIP-seq on pooled whole zebrafish embryos at 3.5 hours post fertilisation (hpf)

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Project description:The pluripotency factor NANOG controls primitive hematopoiesis and directly regulates Tal1.

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