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PAX5 promotes heterocharomatin formation

ABSTRACT: PAX5 promotes heterocharomatin formation

PROVIDER: PRJNA693009 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13477610_1.fastq.gz	Fastqsanger.gz
	SRR13477610_2.fastq.gz	Fastqsanger.gz
	SRR13477612_1.fastq.gz	Fastqsanger.gz
	SRR13477612_2.fastq.gz	Fastqsanger.gz
	SRR13477614_1.fastq.gz	Fastqsanger.gz

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PAX5 promotes heterocharomatin formation

Project description:Heterochromatin has a high density of DNA and low rates of gene transcription.H3k9me3 is a conserved histone modification, and is best known for its role in constitutive heterochromatin formation.H1155, which is a neuroendocrine large cell lung cancer cell line, has a dense nucleus and a high level of occupancy of H3K9me3. PAX5 is a neurogenesis and B lymphocyte development transcription factor, and endogenous expressed in neuroendocrine carcinoma, including H1155 cell line. To assess whether PAX5 promotes heterochromatin formation in H1155, we knock out PAX5 in H1155 cell (KO-PAX5) by CRISPR/Cas9 and use H3K9me3 to performed ChIP-seq.

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PAX5 promotes progression of SCLC

Project description:RNAseq of SCLC cell line H1155 with PAX5.knocked out. The goals of this study are to identify the function of PAX5 in SCLC.

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The PAX5-JAK2 translocation acts as a dual-hit mutation that promotes aggressive B-cell leukemia via nuclear STAT5 activation

Project description:While PAX5 is an important tumor suppressor in B-ALL, it is also involved in oncogenic translocations coding for PAX5 fusion proteins. PAX5-JAK2 encodes a protein consisting of the PAX5 DNA-binding region fused to the constitutively active JAK2 kinase domain. Here, we studied the oncogenic function of PAX5-JAK2 in a mouse model expressing it from the endogenous Pax5 locus. The Pax5Jak2/+ mice rapidly developed an aggressive B-ALL in the absence of another cooperating mutation. The DNA-binding function and kinase activity of Pax5-Jak2, as well as IL-7 signaling, all contributed to leukemia development. Interestingly, all Pax5Jak2/+ tumors lost the wild-type Pax5 allele, allowing efficient DNA binding of Pax5-Jak2. While we could not find evidence for a nuclear role of Pax5-Jak2 as an epigenetic regulator, active phosphorylated Stat5 was present at a high level in Pax5Jak2/+ B-ALL tumors, consistent with increased expression of Stat5 target genes. Together, these data identified Pax5-Jak2 as an important nuclear driver of leukemia formation by maintaining phosphorylated Stat5 levels in the nucleus.

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PAX5 transduction of Pax5-/- pro-B cells

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Gene expression analysis of Pax5-/- proB cells transduced with control or EBF retrovirus.

Project description:We have determined that sustained expression of EBF suppresses alternate lineage genes independently of Pax5. Keywords: Transcription factor EBF restricts alternate lineage options and promotes B cell fate commitment independently of Pax5.

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Project description:Pax5 controls B-cell commitment, development and immunity by repressing B-lineage-inappropriate genes and activating B-cell-specific genes. In addition to the N-terminal DNA-binding paired domain, Pax5 contains a conserved octapeptide, partial homeodomain and C-terminal sequences with transactivating and inhibitory potential. To understand how the C-terminal domains of Pax5 contribute to the repression and activation function of Pax5, we performed Pax5 pulldown combined with mass spectrometry to identify coactivator or corepressor complexes that bind to the C-terminal regions of Pax5.

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