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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

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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 of different combination of transcription factors

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

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

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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

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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/+)

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Pabpn1-driven cytoskeletal rearrangement induces muscle wasting

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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

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

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