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Genome-wide analysis of gene expression in control and Lats1/2 deficient neonatal mice

ABSTRACT: Genome-wide analysis of gene expression in control and Lats1/2 deficient neonatal mice

PROVIDER: PRJNA292381 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2153330_1.fastq.gz	Fastqsanger.gz
	SRR2153330_2.fastq.gz	Fastqsanger.gz
	SRR2153323_1.fastq.gz	Fastqsanger.gz
	SRR2153323_2.fastq.gz	Fastqsanger.gz
	SRR2153324_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of livers of control and Lats1/2 deficient neonatal mice [Microarray expression]

Project description:Lats1-/-;Lats2fl/fl;Alb-Cre pups and control pups were sacrificed at 1 day after birth Total mRNA obtained from livers in control and Lats1/2 deficient neonatal mice

2016-06-29 | E-GEOD-71872 | biostudies-arrayexpress

Genome-wide analysis of gene expression using in vitro cultured control and Lats1/2 deficient hepatoblasts [RNA-Seq]

Project description:RNA-sequencing results with in vitro cultured control and Lats1/2 deficient hepatoblasts, in vitro differentiated control and Lats1/2 deficient hepatocytes and biliary epithelial cells To investigate changes in gene expression by loss of Lats1 and Lats2 during hepatocyte or biliary epithelial cell differentiation, we performed multiplex RNA-sequecing with in vitro cultured hepatoblasts, in vitro differentiated hepatocytes and biliary epithelial cells

2016-06-29 | E-GEOD-71873 | biostudies-arrayexpress

Genome-wide analysis of gene expression using in vitro cultured control and Lats1/2 deficient hepatoblasts [RNA-Seq]

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Genome-wide analysis of livers of control and Lats1/2 deficient neonatal mice [Microarray expression]

Project description:Lats1-/-;Lats2fl/fl;Alb-Cre pups and control pups were sacrificed at 1 day after birth

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Genome-wide expression analysis in Control and Atg5-deficient eosinophils.

Project description:Genome-wide expression analysis in Control and Atg5-deficient eosinophils.

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Reprogramming of Schwann Cells by LATS1/2-TAZ/YAP Signaling Drives Malignant Peripheral Nerve Sheath Tumorigenesis

Project description:Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive Schwann cell (SC)-lineage derived sarcomas with poor prognosis. The molecular events underlying SC lineage cells-to-MPNST transformation remain elusive. Here, we show that human MPNSTs exhibit elevated HIPPO-TAZ/YAP expression, and that TAZ/YAP hyperactivity in SCs caused by Lats1/2 loss potently induces high-grade nerve-associated tumors with full penetrance. Lats1/2 deficiency reprograms SCs to a cancerous, progenitor-like phenotype and promotes hyper-proliferation. Conversely, disruption of TAZ/YAP activity alleviates tumor burden in Lats1/2-deficient mice and inhibits human MPNST cell proliferation. Moreover, genome-wide target profiling reveals that TAZ/YAP-TEAD1 directly activates a set of oncogenic programs in SCs including PDGFR/RAF signaling. Co-targeting TAZ/YAP and PDGFR/RAF signaling efficaciously reduces tumorigenicity in Lats1/2-deficient tumors. Thus, our findings establish a previously unrecognized convergence between LATS1/2-TAZ/YAP pathway and MPNST pathogenesis, suggesting that combined inhibition of TAZ/YAP-PDGFR/RAF signaling may be beneficial in MPNSTs.

2018-02-13 | GSE99040 | GEO

Hippo deficient cardiac fibroblasts differentiate into osteochondroprogenitors (ST)

Project description:We investigated how Hippo-deficient cardiac fibroblasts (CFs) alter their cell state and interact with immune cells during cardiac fibrosis. To study the role of the Hippo pathway in CFs, we conditionally knocked out Lats1/2 specifically in the CFs of mouse hearts (Lats1/2CKO). To test the role of Hippo-deficient CF-induced macrophages, we treated the control and Lats1/2CKO mice with or without CSF1R inhibitor to block macrophage expansion and performed ST.

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Lats1/2 control TGF-beta directed EMT in the dorsal cranial neuroepithelium through YAP regulation

Project description:Hippo signaling, an evolutionarily conserved pathway involved in organ size control, has been implicated to play key roles in developmental processes of various tissues, but its role in craniofacial development has not been largely explored. To examine the function of the Hippo signaling kinase cascade, we inactivated Hippo components Lats1 and Lats2 in the cranial neuroepithelium of mouse embryos using a Wnt1CreSOR driver. Double conditional knock out (DCKO) of Lats1/2 resulted in neural tube and craniofacial defects. Lats1/2 DCKO mutant embryos presented a minute head with delayed and defective neural tube closure. Furthermore, neuroepithelial cell polarity and cell integrity were disrupted within the cranial neural tube in Lats1/2 DCKO mutants. Embryonic neural tube RNA-seq revealed increased TGF-beta signaling in absence of Lats1/2. Moreover, markers of epithelial-to-mesenchymal transition (EMT) were upregulated in the cranial neural tube. Notably, modulation of Hippo signaling downstream effectors Yap and Taz prevented neuroepithelial defects, aberrant EMT, and TGF-beta dysregulation caused by Lats1/2 deficiency, indicating that Lats1/2 function via canonical Hippo-Yap pathway. Together, our findings revealed important roles for Hippo signaling kinases in pre-migratory neural crest EMT and migration.

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Expression profiling in primary embryonic fibroblasts deficient for the N-terminal truncation of Lats1

Project description:Lats1 and Lats2 are the mediators of the Hippo pathway that regulates tissue growth and proliferation. Lats1 and Lats2 kinases share 85% sequence identity in the kinase domain. However, their non-kinase regions at the N-terminus are distinct except for Lats conserved domain 1 (LCD1) and LCD2, suggesting that their N-terminal regions are important for Lats1/2-specific functions. In this study, we generated Lats1 knockout mice disrupting the N-terminal region containing LCD1 (Lats1M-NM-^TN/M-NM-^TN). We show that some Lats1M-NM-^TN/M-NM-^TN mice were born safely and grew normally. However, mouse embryonic fibroblasts (MEFs) from Lats1M-NM-^TN/M-NM-^TN mice displayed drastic defects in mitosis, showing enhanced centrosome overduplication, chromosomal misalignment, multipolar spindle formation, chromosome bridging, and cytokinesis failure. Moreover, they displayed accelerated cell cycle and cell growth bypassing a cell-cell contact inhibition like tumor cells, and exhibited anchorage independent growth. Indeed, Lats1M-NM-^TN/M-NM-^TN MEFs produced tumors in nude mice after subcutaneous injection, although the tumor growth rate was much slower than ordinary cancer cells. Furthermore, Yap, the key transcriptional co-activator in the Hippo pathway, was overexpressed and retained stable in Lats1M-NM-^TN/M-NM-^TN MEFs under high cell density, and expression of Lats2 mRNA were down-regulated. Total RNAs were extracted from MEFs under high or low cell density using miRNeasy extraction kit (Qiagen). A Dye-swapped experiment was performed by hybridizing complimentary RNA (cRNA) labeled with either Cyanine (Cy) -3 or Cy-5 (Perkin-Elmer) onto Whole Mouse Genome Oligo Microarray (G4122F; Agilent Technologies). Co-hybridizations were performed and data from Cy3 or Cy5 channels were analyzed as normalized signal intensities rather than as log ratios corresponding to each array.

2012-12-17 | E-GEOD-37871 | biostudies-arrayexpress

Raw RNA-seq data of small intestine tissue from control and Lats1/2 knock out mice

Project description:Raw RNA-seq data of small intestine tissue from control and Lats1/2 knock out mice

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