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Transcriptome profiling of untreated and doxycycline-treated HeLa/TO-SmN

ABSTRACT: Purpose is to examine the effect of SmN expression to gene expression in HeLa

ORGANISM(S): Homo sapiens

PROVIDER: GSE54136 | GEO | 2015/01/16

SECONDARY ACCESSION(S): PRJNA235293

REPOSITORIES: GEO

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Transcriptome profiling of untreated and doxycycline-treated HeLa/TO-SmN

Project description:Purpose is to examine the effect of SmN expression to gene expression in HeLa Compare the differences between the transcriptome of untreated and doxycycline-treated HeLa/TO-SmN in which expression of SmN is under doxycycline control

2015-01-16 | E-GEOD-54136 | biostudies-arrayexpress

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Project description:Trimethylguanosine synthase 1 (TGS1) is a highly conserved enzyme that converts the 5' mono-methylguanosine cap of snRNAs to a trimethylguanosine cap. Here, we show that loss of TGS1 in C. elegans, D. melanogaster and D. rerio results in neurological phenotypes similar to those caused by Survival Motor Neuron (SMN) deficiency. Importantly, expression of human TGS1 ameliorates the SMN-dependent neurological phenotypes in both flies and worms, revealing that TGS1 can partly counteract the effects of SMN deficiency. TGS1 loss in HeLa cells leads to the accumulation of immature U2 and U4atac snRNAs with long 3' tails that are often uridylated. snRNAs with defective 3' terminations also accumulate in Drosophila Tgs1 mutants. Consistent with defective snRNA maturation, TGS1 and SMN mutant cells also exhibit partially overlapping transcriptome alterations that include aberrantly spliced and readthrough transcripts. Together, these results identify a neuroprotective function for TGS1 and reinforce the view that defective snRNA maturation affects neuronal viability and function.

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