Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

P0.5 WT or Ftsj1 KO mouse brain or liver total mRNA or ribosome-contained mRNA

ABSTRACT: P0.5 WT or Ftsj1 KO mouse brain or liver ribosome-contained mRNAs or total mRNAs, and were sequenced using MiSeq and HiSeq.

ORGANISM(S): Mus musculus

PROVIDER: GSE153797 | GEO | 2021/03/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

P0.5 WT or Ftsj1 KO mouse brain or liver total mRNA or ribosome-contained mRNA

Project description:P0.5 WT or Ftsj1 KO mouse brain or liver total mRNA or ribosome-contained mRNA

| PRJNA644116 | ENA

8-week WT or Ftsj1 KO mouse brain total mRNAs and ribosome-contained mRNAs

Project description:8-week WT or Ftsj1 KO mouse brain total mRNAs and ribosome-contained mRNAs

| PRJNA643980 | ENA

8-week WT or Ftsj1 KO mouse brain total mRNAs and ribosome-contained mRNAs

Project description:8-week mouse brain ribosome-contained mRNAs and total mRNAs were collected and sequenced.

2021-03-31 | GSE153756 | GEO

Next Generation Sequencing identifies differential genes regulated by FTSJ1 overexpression

Project description:We report the application of RNA-sequencing for high-throughput profiling of transcriptomes in PC9 cells transfected with stably expressed FTSJ1.

2020-05-19 | GSE146604 | GEO

The ribose methylation enzyme FTSJ1 has a conserved role in neuron morphology and learning performance

Project description:FTSJ1 is a conserved human 2’-O-methyltransferase (Nm-MTase) that modifies several transfer RNAs (tRNAs) at position 32 and the wobble position 34 in the AntiCodon Loop (ACL). Its loss of function has been linked to Non-Syndromic X-Linked Intellectual Disability (NSXLID), and more recently to cancers. However, the molecular mechanisms underlying these pathologies are currently unclear. Here we report a novel FTSJ1 pathogenic variant from a NSXLID patient. Using blood cells derived from this patient and other affected individuals carrying FTSJ1 mutations, we performed an unbiased and comprehensive RiboMethSeq analysis to map the ribose methylation (Nm) on all tRNAs and identify novel targets. In addition, we performed a transcriptome analysis in these cells and found that several genes previously associated with intellectual disability and cancers were deregulated. We also found changes in the miRNA population that suggest potential cross-regulation of some miRNAs with these key mRNA targets. Finally, we show that differentiation of FTSJ1-depleted human neuronal progenitor cells (NPC) into neurons displays long and thin spine neurites compared to control cells. These defects are also observed in Drosophila and are associated with long term memory deficit in this organism. Altogether, our study adds insight into FTSJ1 pathologies in human by the identification of novel FTSJ1 targets and the defect in neuron morphology.

2023-01-06 | GSE179384 | GEO

8-week WT or Ftsj1 KO mouse brain tRNA and tRF MiSeq

Project description:8-week WT or Ftsj1 KO mouse brain tRNA and tRF MiSeq

| PRJNA643981 | ENA

WT or Ftsj1 KO mouse brain

Project description:WT or Ftsj1 KO mouse brain

| PRJNA643976 | ENA

8-week WT or Ftsj1 KO mouse brain tRNA and tRF MiSeq

Project description:8-week brain total tRNA, total tRNA fragments (tRFs), and ribosome-contained tRNAs were sequenced using MiSeq.

2021-03-31 | GSE153757 | GEO

Distinct ribosome states trigger diverse mRNA quality control pathways

Project description:Key protein adapters couple translation to mRNA decay on specific classes of problematic mRNAs in eukaryotes. Slow decoding on nonoptimal codons leads to codon-optimality-mediated decay (COMD) and prolonged arrest at stall sites leads to no-go decay (NGD). The identities of the decay factors underlying these processes and the mechanisms by which they respond to translational distress remain open areas of investigation. We use carefully-designed reporter mRNAs to perform genetic screens and functional assays in S. cerevisiae. We characterize the roles of Hel2 and Syh1 in coordinating translational repression and mRNA decay on NGD reporter mRNAs, finding that Syh1 acts as the primary link to mRNA decay in NGD. Importantly we, observe that these NGD factors are not involved in the degradation of mRNAs enriched in nonoptimal codons. Further, we establish that key factors previously implicated in COMD, Not5 and Dhh1 , contribute modestly to the degradation of an NGD-targeted mRNA. Finally, we use ribosome profiling to reveal distinct ribosomal states associated with each reporter mRNA that readily rationalize the contributions of NGD and COMD factors to degradation of these reporters. Taken together, these results provide new mechanistic insight into the role of Syh1 in NGD and define the molecular triggers that determine how distinct pathways target mRNAs for degradation in yeast.

2022-08-08 | PXD030076 | Pride

Next Generation Sequencing identifies differential genes regulated by FTSJ1 overexpression

Project description:Next Generation Sequencing identifies differential genes regulated by FTSJ1 overexpression

| PRJNA611060 | ENA