The Lsm1-7 complex transiently interacts with the decapping machinery and plays a minor role in unstable mRNA degradation
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PROVIDER: PRJNA1293427 | ENA |
REPOSITORIES: ENA
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Project description:Like-SM proteins (Lsm) assemble into heptameric complexes that are conserved in eukaryotes. The Lsm2-8 complex is involved in the function of spliceosomal RNAs, whereas the Lsm1-7/Pat1 complex associates with decapping complexes in the cytoplasm. It was proposed that the role of Lsm1-7 is to recruit the decapping machinery to unstable mRNA that are rapidly deadenylated. However, the role of deadenylation in RNA stability has been challenged by recent studies in yeast and other organisms. To better understand the potential role of Lsm1 in the degradation of unstable transcripts, we investigated the effects of rapid depletion of Lsm1 in an inducible degron system on transcripts degraded by decapping activation during nonsense-mediated mRNA decay (NMD). In contrast to previous studies that used deletion of LSM1, Lsm1 depletion, led to a slight increase in the abundance of NMD substrates, similar to what is observed following a minimal perturbation of decapping.
2025-07-31 | GSE303057 | GEO
Project description:We report the role of LSM1-7 complex in the Arabidopsis tolerance to abiotic stresses. LSM1-7 controls gene expression reprogramming at the post-transcriptional level by promoting the decapping of mRNA. This function is selectively achieve over selected stress-induced transcripts depending on stress nature.
2016-01-21 | GSE70491 | GEO
Project description:To assess the roles of the Dcp2 C-terminal domain and the decapping activators Pat1, Lsm1, and Dhh1 in mRNA decapping, we used RNA-Seq to analyze the expression profiles of yeast cells harboring a truncation of the Dcp2 C-terminal domain, mutations that render Dcp2 catalytically inactive, or deletions of the PAT1, LSM1, and DHH1 genes. Consistent with our recent model for decapping regulation, we found that: i) the Dcp2 C-terminal domain is an effector of both negative and positive regulation and that loss of these control functions causes significant deregulation of mRNA decapping; ii) rather than being global activators of decapping, Pat1, Lsm1, and Dhh1 directly target specific subsets of yeast mRNAs and loss of the functions of each of these factors has substantial indirect consequences for genome-wide mRNA expression; and iii) transcripts targeted by Pat1, Lsm1, and Dhh1 exhibit only partial overlap and, as expected, are targeted to decapping-dependent decay.
2017-12-09 | GSE107841 | GEO
Project description:To assess the role of the decapping activator Scd6 in mRNA decay, we used RNA-Seq to analyze the expression profile of yeast cells harboring a deletion of the SCD6 gene. Consistent with our recent model for decapping regulation, we found that Scd6 targets a small number of specific mRNAs in yeast cells. Interestingly, degradation of Scd6-targeted transcripts also requires the functions of the decapping activators Pat1, Lsm1, and Dhh1, suggesting that Scd6 functions together with Pat1, Lsm1, and Dhh1 in promoting mRNA decapping.
2018-05-15 | GSE114428 | GEO
Project description:We analyzed mRNA expression profiles in Drosophila melanogaster S2 cells that had been depleted of proteins known as mRNA decapping co-activators. mRNA decapping is catalyzed by DCP2, and DCP2 activity is stimulated by decapping co-activators. This group of proteins includes DCP1, Hedls (also known as Ge-1), LSm16 (also known as EDC3), rck/p54 (also known as DHH1 or Me31B), Pat1, and the heptameric LSm1-7 complex. We used the RNA interference technology to deplete cultured S2 cells of DCP1 (CG11183), Ge-1 (CG6181), Pat1 (CG5208), LSm16 (CG6311), and LSm1 (CG4279). We used Affymetrix oligonucleotide microarrays to analyze two independent samples for each depletion. We included the following controls: mock RNAi treatment and GFP dsRNA treatment (two profiles each). We also profiled AGO1 (CG6671) depleted cells (3 independent samples). AGO1 is a key protein required for miRNA-mediated gene silencing. We had shown previously that silencing by miRNAs involves decapping of target mRNAs.
2007-09-03 | E-MEXP-1012 | biostudies-arrayexpress
Project description:Characterization of the lsm1a lsm1b transcriptional profile. LSM1 protein is involved in RNA decay through decapping facilitation. The performed array help us to understand the transcription level alterations produced by the absence of LSM1.
2013-01-16 | GSE39630 | GEO
Project description:Characterization of the lsm1a lsm1b transcriptional profile. LSM1 protein is involved in RNA decay through decapping facilitation. The performed array help us to understand the transcription level alterations produced by the absence of LSM1. One-condition experiment, Col-0 vs. lsm1a lsm1b plants. Biological replicates: 3 control replicates.
2013-01-16 | E-GEOD-39630 | biostudies-arrayexpress
Project description:The Dcp2 and Nudt16 Nudix hydrolases, are mRNA decapping enzymes that preferentially modulate stability of a subset of mRNAs. Here we report Nudt3 is a third Nudix protein that possess mRNA decapping activity in cells and is a modulator of cell migration in MCF-7 breast cancer cells. Genome-wide analysis of Nudt3 compromised cells identified increases in mRNAs involved in cell motility including integrin β6, lipocalin-2 and fibronectin. The increase in mRNA levels was dependent on Nudt3 decapping activity where integrin β6 and lipocalin-2 were modulated directly through mRNA stability, while fibronectin was indirectly controlled. Moreover, increased cell migration observed in Nudt3 depleted cells was mediated through the extracellular integrin β6 and fibronectin protein nexus. We conclude, Nudt3 is an mRNA decapping enzyme that orchestrates expression of a subset of mRNAs to modulate cell migration and further substantiates the existence of multiple decapping enzymes functioning in distinct cellular pathways in mammals. Stably transformed MCF-7 cell lines constitutively expressing either a short hairpin RNA (shRNA) directed against Nudt3 (Nudt3KD) or a non-targeted control shRNA (ConKD) were used, with three replicate cultures used per group (n=3).
2016-07-21 | E-GEOD-75146 | biostudies-arrayexpress
Project description:Candidatus Nitrosotenuis cloacae strain:LSM1 Genome sequencing and assembly
| PRJNA903657 | ENA
Project description:The rupture of unstable atherosclerotic plaques, leading to debilitating or fatal thrombotic events, is a major health burden worldwide. Limited understanding as to the molecular drivers of plaque instability and rupture hinders efforts in diagnosis and treatment prior to thrombotic events. Utilising an advanced pre-clinical mouse model (Tandem stenosis (TS) model), which presents human-like unstable atherosclerotic disease, we apply high-end omic methods to characterize the molecular signatures associated with plaque instability in atherosclerotic arteries. Through quantitative proteomic profiling, we depict unique proteome signatures of unstable plaques compared to stable plaques and healthy arteries. Coupled with single-cell RNA-sequencing of leukocytes, we describe the heterodimer complex S100a8/S100a9 as unique to unstable plaque, with neutrophils implicated as the transcriptional drivers of S100a8/a9 expression. We confirm S100a9 expression in human carotid atherosclerotic plaques and we further utilise the TS pre-clinical model to pharmacologically inhibit S100a8/S100a9, resulting in plaque stabilisation. Thus, we establish the TS model as a sophisticated translational tool for the profiling of unstable atherosclerotic plaques and demonstrate that unstable and stable atherosclerosis are highly different disease entities.
2023-05-10 | PXD030857 | Pride