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Endogenous transcripts direct microRNA degradation in Drosophila, and this targeted degradation is required for proper embryonic development

ABSTRACT: Endogenous transcripts direct microRNA degradation in Drosophila, and this targeted degradation is required for proper embryonic development

PROVIDER: PRJNA807525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18048500.fastq.gz	Fastqsanger.gz
	SRR18048501.fastq.gz	Fastqsanger.gz
	SRR18048502.fastq.gz	Fastqsanger.gz
	SRR18048503.fastq.gz	Fastqsanger.gz
	SRR18048504.fastq.gz	Fastqsanger.gz

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Endogenous transcripts direct microRNA degradation in Drosophila, and this targeted degradation is required for proper embryonic development

Project description:MicroRNAs (miRNAs) typically direct degradation of their mRNA targets. However, five miRNA targets in vertebrate animals are reported to have unusual miRNA-binding sites that direct degradation of cognate miRNAs. Here, we identify six sites, five in mRNAs and one in a non-coding RNA named Marge, that serve this purpose in Drosophila cells or embryos, which shows that target-directed miRNA degradation (TDMD) shapes endogenous miRNA levels in some invertebrate animals. The six sites direct miRNA degradation without collateral target degradation, helping to explain the potency of this miRNA-degradation pathway. Mutations that disrupt this pathway in Drosophila are lethal, with many flies dying as embryos. Derepression of miR-3 and its paralog miR-309 is responsible for some of this lethality, whereas the loss of Marge-directed degradation of miR-310 miRNAs causes defects in embryonic cuticle development. Thus, TDMD is strongly implicated in the viability of an animal and is required for its proper development.

2022-09-14 | GSE196837 | GEO

Endogenous transcripts direct microRNA degradation in Drosophila, and this targeted degradation is required for proper embryonic development.

Project description:MicroRNAs (miRNAs) typically direct degradation of their mRNA targets. However, some targets have unusual miRNA-binding sites that direct degradation of cognate miRNAs. Although this target-directed miRNA degradation (TDMD) is thought to shape the levels of numerous miRNAs, relatively few sites that endogenously direct degradation have been identified. Here, we identify six sites, five in mRNAs and one in a noncoding RNA named Marge, which serve this purpose in Drosophila cells or embryos. These six sites direct miRNA degradation without collateral target degradation, helping explain the effectiveness of this miRNA-degradation pathway. Mutations that disrupt this pathway are lethal, with many flies dying as embryos. Concomitant derepression of miR-3 and its paralog miR-309 appears responsible for some of this lethality, whereas the loss of Marge-directed degradation of miR-310 miRNAs causes defects in embryonic cuticle development. Thus, TDMD is implicated in the viability of an animal and is required for its proper development.

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Novel endogenous antisense transcripts in mouse

Project description:This SuperSeries is composed of the following subset Series: GSE14372: Novel endogenous antisense transcripts (data for the mouse normal tissues) GSE14557: Novel endogenous antisense transcripts (data for the mouse mammary tumors) Refer to individual Series Unpublished data has been masked in the supplementary feature extraction files.

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Project description:We developed Trim-Away as a a technique to degrade endogenous proteins acutely in mammalian cells without prior modification of the genome or mRNA. Trim-Away is able to remove unmodified native proteins within minutes of application by making use of the TRIM21 ubiquitin ligase that regognises antibody-protein complexes and harnesses the cellular degradation machinery. We performed transcriptome profiling (RNAseq) on NIH3T3 and NIH3T3-mCherry-mTRIM21 cells following electroporation with non-targeting antibody (IgG), bovine serum albumin (BSA), or buffer (PBS). We found that a total of only 8 protein-encoding transcripts were consistently downregulated more than 2-fold in the NIH3T3-mCherry-mTRIM21 cells (Kdm5d, Ddx3y, Eif2s3y, Uty, Asb4, Fat4, Papss2 and Lama2), although we cannot rule out the possibility that this is an indirect consequence of lentivirus construct integration rather than a direct consequence of TRIM21 overexpression. Notably, transcripts encoding previously described ligands of TRIM21, IRF-3, IRF-5, Skp2, DAXX, DDX41, and SQSTM1 were not significantly increased or decreased upon overexpression of TRIM21. Our experiments suggest that the cells overexpressing TRIM21 behave similar to wild-types.

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