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Genome-wide identification of mRNAs involved in BCL2L2-PABNP1 regulation

ABSTRACT: RNA-Seq technology was used to explore mechanisms of BP on adipogenesis in cells transfected with adenoviruses expressing BP at a condition of MOI 300 and 48 h which was predetermined with fluorescence microscope and qPCR analysis . A total of 3,074 DEmRs were obtained by RNA-Seq analysis, among which 1,476 were upregulated and 1,598 were downregulated in cells overexpressing BCL2L2–PABPN1 compared with control groups .

ORGANISM(S): Sus scrofa

PROVIDER: GSE192412 | GEO | 2022/03/01

REPOSITORIES: GEO

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Genome wide RNA-sequencing of human pluripotent stem-cell derived endothelial cells 48h after transduction with adenoviruses expressing either empty vector or single transcription factor

Project description:To induce barrier of stem-cell derived endothelial cells in vitro cells have been transduced with adenoviruses overexpressing transcription factors with potential role in endothelial cell barrier stabilization. Adenoviruses overexpressing either ETS1 or FOXC1 or FOXF2 or KLF11 or SOX18 or SOX7 or TAL1 or LEF1 or LMO2 have been been used at 80 MOI. As control adenovirus overexpressing empty vectors has been used (80 MOI).

2020-03-05 | GSE142130 | GEO

Genome wide RNA-sequencing of human pluripotent stem-cell derived endothelial cells 48h after transduction with adenoviruses expressing either empty vector of different combination of transcription factors

Project description:To induce barrier of stem-cell derived endothelial cells in vitro cells have been transduced with a mixture of adenovirus overexpressing transcription factors with potential role in endothelial cell barrier stabilization. Adenoviruses overexpressing ETS1, SOX18 and SOX7 have been part of both transcription factor mixtures. As fourth transcription factor in the mixture included TAL1 while the other mixture included LEF1. Each transcription factor was used at 20 MOI. As control adenovirus overexpressing empty vectors has been used (80 MOI).

2020-03-05 | GSE142131 | GEO

Genome-wide identification of mRNAs involved in BCL2L2-PABNP1 regulation

Project description:Genome-wide identification of mRNAs involved in BCL2L2-PABNP1 regulation

| PRJNA791373 | ENA

OPMD_mouse_celline (I & II)

Project description:stable transfected cell lines IM2 = untransfected WTA = wildtype pabpn1 transfected high WTD = wildtype pabpn1 transfected low D7E = mutant pabpn1 transfected high D7F = mutant pabpn1 transfected low 5 cell lines triplicate cultures dye-swap

2006-04-20 | E-GEOD-2734 | biostudies-arrayexpress

OPMD_mouse_celline (I & II)

2006-04-20 | GSE2734 | GEO

Thorax transcriptome from control and PABPN1-17ala-expressing flies

Project description:Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset syndrome characterized by progressive degeneration of particular muscles. OPMD is caused by short GCG repeat expansions within the gene encoding the nuclear poly(A)-binding protein 1 (PABPN1) that extend an N-terminal polyalanine tract in the protein. Mutant PABPN1 aggregates as nuclear inclusions in OMPD patient muscles. We have created a Drosophila model of OPMD that recapitulates the features of the human disorder: progressive muscle degeneration, with muscle defects proportional to the number of alanines in the tract, and formation of PABPN1 nuclear inclusions. Wild-type human PABPN1 contains a stretch of 10 alanines following the initial methionine, which is expanded to 12–17 alanines in OPMD patients. In Drosophila, the PABPN1 homolog is the poly(A)-binding protein 2 (PABP2), which has the same function as PABPN1 in nuclear polyadenylation but lacks a polyalanine tract at the N-terminus. We used the UAS/Gal4 system to express mammalian PABPN1 in Drosophila. An alanine-expanded PABPN1 cDNA (encoding the 17 alanine tract) was cloned downstream of UAS sequences (UAS-PABPN1). Transgenic lines containing this construct were crossed to a Mhc-Gal4 driver, leading to muscle-specific expression. To gain insight into the molecular and physiological defects in OPMD we performed a transcriptomic analysis in OPMD fly muscles. Using microarrays, thorax gene expression was compared between control flies (Mhc-Gal4/+) and flies expressing PABPN1-17ala in thoracic muscles (UAS-PABPN1-17ala/+; Mhc-Gal4/+), at three time points (days 2, 6 and 11). Transcriptome of thorax RNA samples from control (Mhc-Gal4/+) flies and flies expressing PABPN1-17ala (UAS-PABPN1-17ala/+; Mhc-Gal4/+)

2014-12-12 | GSE64094 | GEO

Pabpn1-driven cytoskeletal rearrangement induces muscle wasting

Project description:Poly(A) binding protein nuclear 1 (PABPN1) is a multifunctional regulator of mRNA processing. PABPN1 inhibits alternative polyadenylation (APA), and in conditions with reduced PABPN1 levels APA utilization causes genome-wide mRNA dysregulation. PABPN1 levels decline from midlife onwards in Oculopharyngeal Muscular Dystrophy (OPMD) and in aged muscles. Reduced PABPN1 levels cause muscle atrophy by altering mRNA levels of the ubiquitin proteasome system. The effect of PABPN1-mediated APA utilization on the proteome has not been investigated yet. We report the PABPN1-mediated proteome in Tibialis anterior (TA) mouse muscles, signifying functional impact for the mitochondria, cytoskeleton and translation cellular machineries. Central nucleation and split myofibers marked PABPN1-derived muscle histology. We show that up-regulation of the cytoskeletal proteins: Murc, Pfn1 and Csrp3, is highly associated with PABPN1-mediated muscle pathology and with reduced PABPN1 levels. Elevation of PABPN1 levels by sirtinol treatment reversed muscle pathology and restored levels of those cytoskeletal proteins. We suggest that restoration of PABPN1 levels in aged muscles could be a novel therapeutic strategy to mitigate muscle waste.

2020-07-06 | PXD004865 | Pride

Next generation sequencing identifies polyadenylated species of hTR

Project description:The paired-end next-generation sequencing of all hTR versions of less than 200 nucleotides in length was used to analyze the 3’ end distribution of hTR associated to Flag-tagged versions of PABPN1, hTERT and Dyskerin. In total, we obtained 2,716,342, 3,152,013, and 3,077,395 hTR-specific reads for the PABPN1, hTERT, and Dyskerin purifications, respectively. We found that the majority of polyadenylated telomerase RNA recovered in the PABPN1, hTERT, and Dyskerin purifications had poly(A) tails starting immediately after the annotated hTR 3’ end. However, a greater proportion of poly(A) tails were found on genome-encoded 3’-extentions in the PABPN1-bound fraction compared to the population of hTR that was copurified with hTERT and DKC1: 15.5% for PABPN1, 6.9% for hTERT, and 6.5% for Dyskerin. Notably, the population of polyadenylated telomerase RNA recovered with PABPN1 was significantly different in terms of poly(A) tail length compared to polyadenylated hTR retrieved in the hTERT- and Dyskerin-bound fractions (P-value=5.551e-16, Kolmogorov-Smirnov test), showing a tendency toward longer poly(A) tails in the PABPN1-bound fraction. The enrichment of telomerase RNA with long poly(A) tails in the PABPN1-bound fraction is consistent with a role of PABPN1 in a maturation pathway that depends on hTR 3’ end polyadenylation. Moreover, our results indicate that a fraction of hTERT and Dyskerin are associated with polyadenylated versions of hTR.

2015-10-21 | GSE74186 | GEO

Deacetylation inhibition reverses PABPN1-dependent muscle wasting

Project description:Reduced PABPN1 levels cause aging-associated muscle wasting. PABPN1 is a multi-functional regulator of mRNA processing. To elucidate the molecular mechanisms causing PABPN1-mediated muscle wasting, we compared the transcriptome to the proteome in mouse muscles expressing shRNA to PABPN1 (shPab). We found greater variations in the proteome as compared to mRNA expression profiles. Protein accumulation in the shPab proteome was concomitant with reduced proteasomal activity. Notably, protein acetylation appeared to be enriched in shPab versus control proteomes (63%). An acetylome study in shPab muscles revealed prominent peptide deacetylation associated with elevated sirtuin-1 (SIRT1) deacetylase. We show that SIRT1 mRNA levels are controlled by PABPN1 via an alternative polyadenylation site utilization. SIRT1 inhibition reversed PABPN1 activity and muscle cell function. Moreover, deacetylation inhibition increased PABPN1 levels and reversed muscle wasting. We suggest that perturbation of a multifactorial regulatory loop involving PABPN1 and SIRT1 plays an imperative role in aging-associated muscle wasting.

2022-02-28 | PXD011534 | Pride

Genome-wide analysis of the effect of knockdown of the nuclear poly(A) binding proteins, PABPN1 and ZC3H14 on steady-state mRNA levels

Project description:The polyadenosine RNA binding proteins (Pabs) represent one class of RNA binding proteins that play critical roles in gene expression. This class includes the well-studied nuclear and cytoplasmic Pabs, PABPN1 and PABPC1, respectively, as well as the newly characterized nuclear Pab, zinc finger CCCH-type containing #14, or ZC3H14. ZC3H14 was recently linked to a form of intellectual disability, suggesting a critical role for ZC3H14 in neurons; however, the post-transcriptional function of ZC3H14 is unknown. In this study, we performed a microarray analysis of cells depleted of ZC3H14 or PABPN1 in MCF-7 breast cancer cells. These results revealed that PABPN1 significantly affected ~17% of expressed transcripts as compared to ZC3H14, which affected ~1% of expressed transcripts, suggesting that ZC3H14 has specific mRNA targets. The differentially expressed mRNAs identified in this analysis not only provide information about the classes and types of transcripts that are regulated by these proteins, but also represent a set of transcripts that could be directly bound by ZC3H14 and/or PABPN1. Total RNA isolated from MCF-7 cells treated for 48 hours with siRNA targeting PABPN1, ZC3H14 (all splice variants), or a control scramble siRNA.

2014-10-06 | E-GEOD-62067 | biostudies-arrayexpress

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