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RNAseq anaysis of ventral striatum cholinergic cells of p11 cKO mice

ABSTRACT: RNAseq anaysis of ventral striatum cholinergic cells of p11 cKO mice

PROVIDER: PRJNA416696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6241830.fastq.gz	Fastqsanger.gz
	SRR6241831.fastq.gz	Fastqsanger.gz
	SRR6241832.fastq.gz	Fastqsanger.gz
	SRR6241826.fastq.gz	Fastqsanger.gz
	SRR6241827.fastq.gz	Fastqsanger.gz

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RNAseq anaysis of ventral striatum cholinergic cells of p11 cKO mice

Project description:Purpose: To identify gene expression changes in cholinergic neurons of the ventral striatum of p11 cKO mice Method: Translating Ribosome Affinity Purification (TRAP) to isolate RNA from ChAT+ cells and, cDNA synthesisi and next generation RNAseq using Illumina Hiseq sequencer. Results: Biostatistical analysis identified 113 genes that were altered by p11. 59 genes were up-regulated and 54 down-regulated.

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Expression data from PyMT P11-KO or P11-WT mammary tumours

Project description:S100A10 (p11) is a plasminogen receptor that regulatess cellular plasmin generation by cancer cells. In the current study we used the MMTV-PyMT mouse breast cancer model to investigate the role of p11 in oncogenesis. Genetic deletion of p11 resulted in significantly decreased tumor onset, growth rate and spontaneous pulmonary metastatic burden in the PyMT/p11-KO mice. This phenotype was accompanied by substantial reduction in Ki67 positivity, macrophage infiltration and decreased vascular density in the primary tumors, and appearance of invasive carcinoma and pulmonary metastasis. Surprisingly, immunohistochemical analysis of wild-type MMTV-PyMT mice failed to detect p11 expression in the tumors or metastatic tumor cells and loss of p11 did not decrease plasmin generation in the PyMT tumors and cells. Furthermore, tumor cells expressing p11 displayed dramatically reduced lung metastasis when injected into p11-depleted mice, further strengthening the stromal role of p11. Transcriptome analysis of the p11-depleted tumors showed marked reduction in genes involved in breast cancer development, progression, and inflammation such as AREG, MUC1 and S100A8. The PyMT/p11-KO tumors displayed remarkable increase in inflammatory cytokines such as IL-6, IL-10 and IFN-γ. Gene expression profiling and immunohistochemistry primary breast cancer samples showed that p11 mRNA and protein was significantly higher in tumors compared to normal mammary tissue. The mRNA expression was significantly associated with poor patient prognosis and significantly elevated in high grade, triple negative tumors and tumors with high proliferative index. We used microarray to detail the global programme of gene expression underlying reduced growth/establishment of P11-KO PyMT tumours.

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Human p11-mediated re-direction of phagosomes to the recycling endosome-expulsion pathway induced by fungal pathogen

Project description:Aspergillus fumigatus invades pulmonary epithelial cells by induced phagocytosis, and survives for some time in phagosomes. Although dihydroxynaphthalene melanin on fungal conidia has been intensively investigated for its role in inhibiting phagosome maturation, a proportion of melanin-lacking mutant conidia still escaped killing by phagosomes, implying that additional mechanisms must be in place. Here, we identified the fungal surface-exposed heat shock protein HscA as an effector protein that binds the human p11 protein. A. fumigatus induces and increases the amount of p11 and anchors p11 and Annexin A2 to phagosomes and phagocytic cups, the latter facilitates phagocytosis of conidia by epithelial cells. We identified a SNP in the in the non-coding region of the human p11 gene resulting in heightened susceptibility for invasive aspergillosis in hematopoietic stem-cell transplant recipients. This finding can help for stratification of donors for hematopoietic stem cell transplantation. On phagosomes, HscA triggers an increase of p11 on the phagosomal membrane, which prevents directing the phagosome to the degradative pathway by re-directing the p11-positive phagosome to the recycling endosomal pathway. Therefore, a surface-located heat shock protein enables fungal conidia to escape phagolysosome killing.

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