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Nonsense mediated decay and a novel protein Period-2 regulate casein kinase I in an opposing manner to control circadian period in Neurospora crassa

ABSTRACT: Nonsense mediated decay and a novel protein Period-2 regulate casein kinase I in an opposing manner to control circadian period in Neurospora crassa

PROVIDER: PRJNA656289 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12424531_1.fastq.gz	Fastqsanger.gz
	SRR12424531_2.fastq.gz	Fastqsanger.gz
	SRR12424532_1.fastq.gz	Fastqsanger.gz
	SRR12424532_2.fastq.gz	Fastqsanger.gz
	SRR12424533_1.fastq.gz	Fastqsanger.gz

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Nonsense mediated decay and a novel protein Period-2 regulate casein kinase I in an opposing manner to control circadian period in Neurospora crassa

Project description:The period-2 (prd-2) mutant of Neurospora crassa is characterized by recessive inheritance of a 26-hour long period phenotype of the circadian clock. PRD-2 encodes a putative RNA-binding protein. To identify PRD-2 target genes and its role in the clock, we performed transcript profiling in delta prd-2 compared to control samples using RNA-Sequencing. Hundreds of genes are affected by loss of prd-2, including decreased levels of Casein Kinase I (ck-1a, NCU00685). The circadian period length in Neurospora is exquisitely sensitive to ck-1a levels, and we attribute the long period length defect in the prd-2 mutant to low levels of ck-1a transcript, decreased ck-1a transcript stability, and lower levels of CKI protein. Thus, Casein Kinase I gene expression is subject to complex regulation in the circadian clock.

2020-12-09 | GSE155999 | GEO

Nonsense-mediated decay in Plasmodium falciparum

Project description:We have HA-tagged two nonsense-mediated decay proteins, UPF1 and UPF2, in the malaria parasite Plasmodium falciparum. We then performed co-immunoprecipitation experiments to determine the protein-protein interactions of these nonsense-mediated decay components.

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Regulated endocleavage balances the degradation of nonsense-mediated decay substrates

Project description:Nonsense-mediated mRNA decay (NMD) controls gene expression by eliminating mRNAs with premature or aberrant translation termination. Degradation of NMD substrates is initiated by the central NMD factor UPF1, which recruits the endonuclease SMG6 and the deadenylation-promoting SMG5/7 complex. Here we map transcriptome-wide sites of SMG6-mediated endocleavage via 3′ fragment capture and degradome sequencing.

2017-06-01 | E-MTAB-3625 | biostudies-arrayexpress

Analysis of nonsense-mediated mRNA decay in daf-2 mutants

Project description:To exmine the role of nonsense-mediated mRNA decay process in the longevity regulation of daf-2 mutants, we sequenced transcriptomes from day 1 adult Caenorhabditis elegans: Bristol N2 (wild-type), and smg-2(qd101), daf-2(e1370) and smg-2(qd101); daf-2(e1370) mutants.

2017-03-17 | GSE94077 | GEO

Ultraconserved elements are associated with control of splicing regulators by alt splicing and nonsense mediated decay

Project description:We blocked nonsense-mediated mRNA decay (NMD) pathway and used a custom alternative transcript sensitive Affymetrix microarray to seek alternatively spliced RNAs whose levels increased compared to controls. Keywords: Nonsense Mediated Decay (NMD)

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Inhibition of nonsense-mediated RNA decay by the tumor microenvironment promotes tumorigenesis

2011-07-08 | GSE30499 | GEO

The application of nonsense-mediated mRNA decay inhibition to the identification of breast cancer susceptibility genes

Project description:Identification of novel, highly penetrant, breast cancer susceptibility genes will require the application of additional strategies beyond that of traditional linkage and candidate gene approaches. Approximately one-third of inherited genetic diseases, including breast cancer susceptibility, are caused by frameshift or nonsense mutations that truncate the protein product [1]. Transcripts harbouring premature termination codons are selectively and rapidly degraded by the nonsense-mediated mRNA decay (NMD) pathway. Blocking the NMD pathway in any given cell will stabilise these mutant transcripts, which can then be detected using gene expression microarrays. This technique, known as gene identification by nonsense-mediated mRNA decay inhibition (GINI), has proved successful in identifying sporadic nonsense mutations involved in many different cancer types. However, the approach has not yet been applied to identify germline mutations involved in breast cancer. We therefore attempted to use GINI on lymphoblastoid cell lines (LCLs) from multiple-case, non-BRCA1/2 breast cancer families in order to identify additional high-risk breast cancer susceptibility genes. We applied GINI to a total of 24 LCLs,established from breast-cancer affected and unaffected women from three multiple-case non-BRCA1/2 breast cancer families. We then used Illumina gene expression microarrays to identify transcripts stabilised by the NMD inhibition. Total RNA obtained from the lymphoblastoid cell lines derived from 24 individuals.

2012-04-11 | E-GEOD-37210 | biostudies-arrayexpress

Human Nonsense-Mediated RNA Decay Initiates Widely by Endonucleolysis and Targets snoRNA Host Genes

Project description:Eukaryotic RNAs with premature termination codons (PTCs) are eliminated by nonsense-mediated decay (NMD). While human nonsense RNA degradation can be initiated either by an endonucleolytic cleavage event near the PTC or through decapping, the individual contribution of these activities on endogenous substrates has remained unresolved. Here we unambiguously establish that SMG6-catalyzed endonucleolysis is the primary initiating step in human nonsense RNA decay. We also show that both protein-coding and ‘non-coding’ genes hosting snoRNAs in their introns produce considerable amounts of NMD-sensitive splice variants, suggesting that these RNAs are merely by-products of a primary snoRNA production process. Finally, genes encoding multiple snoRNAs generally yield elevated numbers of alternative transcript isoforms, enabling the differential expression of individual snoRNAs. These findings demonstrate a hitherto unappreciated potential for decoupling of the individual expression levels of functional exon- and intron-encoded species from such composite genes. HEK293 Flp-In T-Rex cells were subjected to siRNA-mediated depletion of XRN1 and co-depletion of XRN1 with either SMG6 or UPF1. All the treated samples together with the controls were subjected to both RNA-seq and 5'-end-seq. RNA-seq was used for detecting NMD isoforms and their expression levels. 5'-end-seq was used for finding NMD decay intermediates (decapped and endocleaved molecules). CAGE was used to distinguish decapped from endocleaved RNA fragments.

2014-11-18 | E-GEOD-57433 | biostudies-arrayexpress

Human Nonsense-Mediated RNA Decay Initiates Widely by Endonucleolysis and Targets snoRNA Host Genes

Project description:Eukaryotic RNAs with premature termination codons (PTCs) are eliminated by nonsense-mediated decay (NMD). While human nonsense RNA degradation can be initiated either by an endonucleolytic cleavage event near the PTC or through decapping, the individual contribution of these activities on endogenous substrates has remained unresolved. Here we unambiguously establish that SMG6-catalyzed endonucleolysis is the primary initiating step in human nonsense RNA decay. We also show that both protein-coding and ‘non-coding’ genes hosting snoRNAs in their introns produce considerable amounts of NMD-sensitive splice variants, suggesting that these RNAs are merely by-products of a primary snoRNA production process. Finally, genes encoding multiple snoRNAs generally yield elevated numbers of alternative transcript isoforms, enabling the differential expression of individual snoRNAs. These findings demonstrate a hitherto unappreciated potential for decoupling of the individual expression levels of functional exon- and intron-encoded species from such composite genes. ------------------------------------------------------------------------------------- This article was corrected in http://genesdev.cshlp.org/content/30/9/1128.short Completely mapped 5'p-end sequencing data from the corrigendum have been updated in corresponding samples.

2014-11-18 | GSE57433 | GEO

Inhibition of nonsense-mediated RNA decay by the tumor microenvironment promotes tumorigenesis

Project description:Nonsense-mediated RNA decay (NMD) is regulated by a variety of cellular stresses. We expose U2OS cells to several stresses and assess RNA expression in the absence of transcription (i.e. stability). These studies identify transcripts that are stabilized by the physiological inhibition of NMD. U2OS cells rendered hypoxia for three hours, treated with tunicamycin for three hours, treated with emetine for three hours, or depleted of Upf1/Rent1 were treated with DRB, and RNA was collected at 0, 1.5, 3 and 4.5 hrs.

2011-07-08 | E-GEOD-30499 | biostudies-arrayexpress

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