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The SWI/SNF protein ATRX co-regulates pseudoautosomal genes that have translocated to autosomes in the mouse genome

ABSTRACT: Pseudoautosomal regions (PAR1 and PAR2) in eutherians retain homologous regions between the X and Y chromosomes that play a critical role in the obligatory X-Y crossover during male meiosis. Genes that reside in the PAR1 are exceptional in that they are rich in repetitive sequences and undergo a very high rate of recombination. Remarkably, murine PAR1 homologs have translocated to various autosomes, reflecting the complex recombination history during the evolution of the mammalian X chromosome. We now report that the SNF2-type chromatin remodeling protein ATRX controls the expression of eutherians ancestral PAR1 genes that have translocated to autosomes in the mouse. In addition, we have identified two potentially novel mouse PAR1 orthologs. We propose that the ancestral PAR1 genes share a common epigenetic environment that allows ATRX to control their expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE12454 | GEO | 2009/08/01

SECONDARY ACCESSION(S): PRJNA113013

REPOSITORIES: GEO

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The SWI/SNF protein ATRX co-regulates pseudoautosomal genes that have translocated to autosomes in the mouse genome

Project description:Pseudoautosomal regions (PAR1 and PAR2) in eutherians retain homologous regions between the X and Y chromosomes that play a critical role in the obligatory X-Y crossover during male meiosis. Genes that reside in the PAR1 are exceptional in that they are rich in repetitive sequences and undergo a very high rate of recombination. Remarkably, murine PAR1 homologs have translocated to various autosomes, reflecting the complex recombination history during the evolution of the mammalian X chromosome. We now report that the SNF2-type chromatin remodeling protein ATRX controls the expression of eutherians ancestral PAR1 genes that have translocated to autosomes in the mouse. In addition, we have identified two potentially novel mouse PAR1 orthologs. We propose that the ancestral PAR1 genes share a common epigenetic environment that allows ATRX to control their expression. At E13.5, n = 3 biological replicates of littermate-matched wt/ko pairs. RNA from 2 forebrains were pooled to generate enough RNA for each sample. At P0.5, n = 4 biological replicates of littermate-matched wt/ko pairs (for pair #2 there is one wt and 2 Atrx-null samples (2A & 2B) and we count this as 2 pairs).

2009-08-01 | E-GEOD-12454 | biostudies-arrayexpress

Gene expression data from human prostate cancer cell line PC3 and PAR1 and PAR-2-knockout PC3 cells generated using CRISPR/Cas9 targeting

Project description:We found that PC3 cells secrete proteases that cleavae and activate PAR1 and PAR2. In order to understand gene regulation by this autocrine signaling loop, PAR1 and PAR2 knockout cell gene expression was compared to WT PC3 cell gene expression. Proteinase activated receptors (PARs) are G protein-coupled receptors (GPCRs) activated by limited N-terminal proteolysis. A variety of proteolytic enzymes derived from the coagulation cascade and inflammatory milieu activate PARs, however specific activators in different physiological and pathophysiological contexts remain poorly defined. PARs are highly expressed in many cancer cells and regulate various aspects of tumor growth and metastasis. Endogenous proteinases that regulate PARs in the setting of various tumors however remains unresolved. Prostate cancer (PCa) remains a major cause of mortality in men despite advances in early detection and clinical intervention. PAR expression has been reported in PCa, however, their role here remains poorly defined. In androgen independent PC3 cells, we find functional expression of PAR1 and PAR2 but not PAR4. Using genetically encoded PAR cleavage biosensors, we find that PCa cells secrete proteolytic enzymes that cleave PARs and trigger autocrine signaling. Deletion of PAR1 and PAR2 using CRISPR/Cas9 combined with microarray analysis revealed genes that are differentially regulated by this autocrine signalling mechanism. Interestingly, several genes that are known PCa prognostic factors or biomarker were differentially expressed in PAR1-KO and PAR2-KO PC3 cells. We also examined PAR1 and PAR2 regulation of PCa cell proliferation and migration using PAR1 and PAR2-KO PC3 cells, as well as PAR1 and PAR2 specific agonists and antagonists. We find that PAR1 and PAR2 have opposite effects on PC3 cell proliferation and migration. In summary, we have identified an autocrine signaling mechanism through PARs as a regulator of PCa cell function.

2022-08-24 | GSE211813 | GEO

KLK6 expression in skin induces PAR1-mediated psoriasiform dermatitis and inflammatory joint disease

Project description:Kallikrein-related peptidase 6 (KLK6) is a secreted serine protease hypothesized to promote inflammation via cleavage of protease-activated receptors (PAR)1 and PAR2. KLK6 levels are elevated in multiple inflammatory and autoimmune conditions, but no definitive role in pathogenesis has been established. Here, we show that skin-targeted overexpression of KLK6 causes generalized, severe psoriasiform dermatitis with spontaneous development of debilitating psoriatic arthritis-like joint disease. The psoriatic skin and joint phenotypes are reversed by normalization of skin KLK6 levels and attenuated following genetic elimination of PAR1 but not PAR2. Conservation of this regulatory pathway was confirmed in human psoriasis using vorapaxar, an FDA-approved PAR1 antagonist, on explanted lesional skin from psoriasis patients. Beyond defining a critical role for KLK6-PAR1 signaling in promoting psoriasis, our results demonstrate that KLK6-PAR1-mediated inflammation in the skin alone is sufficient to drive inflammatory joint disease. Further, we identify PAR1 as a promising cytokine-independent target in therapy of psoriasis and psoriatic arthritis.

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Mus musculus

Project description:The SWI/SNF protein ATRX co-regulates pseudoautosomal genes that have translocated to autosomes in the mouse genome

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Project description:The gut microbiome of translocated populations of the Seychelles warbler

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CRISPR enhancer scan to detect critical elements for the regulation of EVI1 in a translocated enhancer

Project description:To uncover, in an unbiased fashion, which elements of the 18 kb translocated region control EVI1 transcription, we devised a CRISPR/Cas9-based enhancer scanning approach. We considered all possible sgRNA target sites containing a canonical Cas9 PAM site (NGG) on both strands of the minimal 18 kb translocated region. Deep-sequencing libraries were generated by PCR amplification of sgRNA guide strands using primers that tag the product with standard Illumina adapters and a 4 bp sample barcode in a 2 step-PCR protocol.

2021-07-26 | E-MTAB-9948 | biostudies-arrayexpress

The maleless gene mitigates global aneuploid effect and evolutionary shift from X to autosomes

Project description:During sexual dimorphism, the loss of one entire X chromosome in Drosophila males is achieved largely via a broad genome-wide aneuploid effect. Exploring how MSL proteins and two large non coding RNAs (roX1 and roX2) modulate trans-acting aneuploid effect for equality to females, we employ a system biology approach (microarray) to investigate the global aneuploid effect of maleless(mle) mutation by disrupting MSL binding. A large number of the genes (144) that encode a broad spectrum of cellular transport proteins and transcription factors are located in the autosomes of Drosophila melanogaster. We find these autosomal targets are sensitive to the aneuploid effect and are poorly conserved in primitive Drosophila species and Anopheles gambiae autosomes. It is expected that during evolutionary process, they shifted gradually from their X chromosomal position in primitive Drosophila to autosomes in melanogaster, suggesting that MSL favors inverse counteraction of these autosomal targets along with X-linked genes. These findings suggest a remarkable and previously unsuspected level of complexity among aneuploid-sensitive genes, that creates a functional shift of the aneuploid effect from X to autosomes during evolution, which is resolved by the binding of MSL complex on the X chromosome..

2016-03-31 | GSE78227 | GEO

RNA sequencing of 13 T-cell acute lymphoblastic leukemia patients (5 TCRAD-MYC translocated T-ALL_8TAL1-LMO2 T-ALL)

Project description:RNA sequencing analysis revealed a different expression profile between two different T-ALL subgroups, namely MYC-TCRAD translocated T-ALL vs TAL1-LMO2 T-ALL.

2018-07-01 | GSE106699 | GEO

The SWI/SNF protein ATRX co-regulates pseudoautosomal genes that have translocated to autosomes in the mouse genome.

Project description:BACKGROUND: Pseudoautosomal regions (PAR1 and PAR2) in eutherians retain homologous regions between the X and Y chromosomes that play a critical role in the obligatory X-Y crossover during male meiosis. Genes that reside in the PAR1 are exceptional in that they are rich in repetitive sequences and undergo a very high rate of recombination. Remarkably, murine PAR1 homologs have translocated to various autosomes, reflecting the complex recombination history during the evolution of the mammalian X chromosome. RESULTS: We now report that the SNF2-type chromatin remodeling protein ATRX controls the expression of eutherian ancestral PAR1 genes that have translocated to autosomes in the mouse. In addition, we have identified two potentially novel mouse PAR1 orthologs. CONCLUSION: We propose that the ancestral PAR1 genes share a common epigenetic environment that allows ATRX to control their expression.

| S-EPMC2577121 | biostudies-literature

Array CGH data of A. oryzae strains bearing translocated chromosomal duplication and triplication

Project description:In this study, we achieved translocated chromosomal duplication and triplication of a 1.4-Mb targeted chromosomal region by directly introducing I-SceI meganuclease into A. oryzae protoplast cells. Strains with duplication and triplication of chromosome 2 showed substantial increases in the activity of protease and amylase. Gene dosage effects were enhanced by combining the structural gene and its regulatory gene, indicating that segmental duplications of chromosomes play important phenotypic roles in koji mold strains.

2018-10-23 | GSE120604 | GEO

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