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Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41

ABSTRACT: Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41

PROVIDER: PRJNA318055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3356480.fastq.gz	Fastqsanger.gz
	SRR3356490.fastq.gz	Fastqsanger.gz
	SRR3356500.fastq.gz	Fastqsanger.gz
	SRR3356510.fastq.gz	Fastqsanger.gz
	SRR3356520.fastq.gz	Fastqsanger.gz

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Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41 [RNA-seq]

Project description:We perform RNA sequencing and ribosome profiling time course experiments to examine the effect of fully dysregulating all let-7 targets (in let-7(n2853) animals), partially dysregulating only LIN41 (in lin-41(xe11) animals) or fully dysregulating all let-7 targets while partially dysregulating LIN41 in lin-41(xe11); let-7(n2853) double mutant animals. We conclude that effects on gene expression in let-7 mutant animals are largely and quantitatively explained by dysregulation of LIN41 as its primary target. Furthermore, we identify direct LIN41 target genes regulated on the level of translation or mRNA abundance.

2017-07-17 | GSE80157 | GEO

Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41 [Ribosome footprinting]

2017-07-17 | GSE80133 | GEO

Simultaneous activation of Tor and suppression of ribosome biogenesis by TRIM-NHL proteins promotes terminal differentiation

Project description:Tissue development and homeostasis depend on the balance between growth and terminal differentiation, but the mechanisms coordinating these processes remain elusive. Accumulating evidence indicates that ribosome biogenesis (RiBi) and protein synthesis, two cellular processes sustaining growth, are tightly regulated and yet can be uncoupled during stem cell differentiation. Using the Drosophila adult female germline stem cell (GSC) and larval neuroblast (NB) systems, we show that Mei-P26 and Brat, two Drosophila TRIM-NHL paralogs, are responsible for uncoupling RiBi and protein synthesis during differentiation. In differentiating cells, Mei-P26 and Brat activate the Target of rapamycin (Tor) kinase to promote translation, while concomitantly repressing RiBi. Depletion of Mei-P26 or Brat results in defective terminal differentiation, which can be rescued by ectopic activation of Tor together with suppression of RiBi. Our results indicate that uncoupling RiBi and translation activities by TRIM-NHL activity creates the conditions required for terminal differentiation.

2023-03-03 | GSE218205 | GEO

RNA co-immunoprecipitation coupled to RNA sequencing (RIP-seq) to identify somatic target mRNAs of the TRIM-NHL protein LIN41

Project description:RNA co-immunoprecipitation coupled to RNA sequencing (RIP-seq) to identify somatic target mRNAs of the TRIM-NHL protein LIN41

| PRJNA493005 | ENA

RNA co-immunoprecipitation coupled to RNA sequencing (RIP-seq) to identify somatic target mRNAs of the TRIM-NHL protein LIN41

Project description:We perform RIP-seq experiments with two C. elegans worm lines: i) lin-41(n2914); him-5(e1490) with transgenic expression of a rescuing flag::gfp::lin-41 transgene (Aeschimann et al., Mol Cell, 2017) and ii) him-5(e1490) with transgenic expression of flag::gfp::sart-3 (Rüegger et al., NAR, 2015) as a control. The him-5(e1490) genetic background results in an increased frequency of males in the population. We used an anti-FLAG antibody for the IP and semi-synchronous populations of animals in the L3 and L4 larval stages as samples. The purpose of the experiment was to identify LIN41 mRNA targets in the soma. From the three independent replicates, we determined a set of LIN41-bound mRNAs using edgeR and FDR < 0.05 as a cutoff. This set contained only seven mRNAs, the previously known targets lin-29, mab-10, mab-3 and dmd-3 (Aeschimann et al., Mol Cell, 2017), as well as lin-41 and the unannotated genes F18C5.10 and C31H5.5. We conclude that LIN41 likely only binds to a few somatic mRNA targets. Intersecting this experiment with differential gene expression experiments upon dys-regulation of LIN41 (Aeschimann et al., Mol Cell, 2017) and phenotypic analysis of mutant strains, we further conclude that during larval development, LIN41 likely regulates only a four direct targets, namely lin-29, mab-10, mab-3 and dmd-3. Additionally, the lin-41 mRNA could be directly targeted by LIN41 as well, but the detection of lin-41 mRNA in the IPs may result from the immunoprecipitation of nascent FLAG::GFP::LIN41 protein, still bound to the translating ribosome on its own mRNA.

2018-11-15 | GSE120405 | GEO

Caenorhabditis elegans

Project description:Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41 [Ribosome footprinting]

| PRJNA318047 | ENA

Caenorhabditis elegans

Project description:Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41 [RNA-seq]

| PRJNA318054 | ENA

Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-07-17 | GSE80159 | GEO

Simultaneous activation of Tor and suppression of ribosome biogenesis by TRIM-NHL proteins promotes terminal differentiation

Project description:Simultaneous activation of Tor and suppression of ribosome biogenesis by TRIM-NHL proteins promotes terminal differentiation

| PRJNA902740 | ENA

Casein kinase II suppresses autophagy by activating Filamin-NHL containing TRIM proteins

Project description:Autophagy is a tightly regulated process integral to cellular homeostasis and innate immunity. As such, dysregulation of autophagy is associated with cancer, neurodegenerative disorders, and infectious diseases. While many factors have been characterized that promote autophagy, key players preventing excessive autophagy are less well understood. Here, we identify Casein kinase II (CK2) as a negative regulator of autophagy. Pharmacological inhibition of CK2 activity or siRNA-mediated depletion of CK2 increased basal autophagic flux in cell lines and primary human lung cells. Vice versa, ectopic expression of CK2 reduced autophagic flux. Mechanistically, CK2 interacts with tripartite motif (TRIM) family members TRIM2, TRIM3 and TRIM71 at their shared C-terminal NHL domain. This interaction was required for autophagy inhibition by CK2. TRIM3 was highly phosphorylated by CK2 at serine 661, and a phosphorylation-defective mutant of TRIM3 was unable to reduce autophagy induction. Targeting of the CK2-TRIM axis promoted autophagy during influenza A virus (IAV) and measles virus (MeV) infection. In line with this, inhibition of CK2 enhanced autophagy-dependent restriction of IAV, MeV and human immunodeficiency virus 1 (HIV-1). Thus, our results identify the CK2-TRIM2/3/71 axis as a key regulatory pathway that limits autophagy. Targeting this axis may allow therapeutic induction of autophagy against viral infections and diseases associated with dysregulated autophagy.

2023-05-16 | MSV000091956 | MassIVE

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