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Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE60421 | GEO | 2015/06/05

SECONDARY ACCESSION(S): PRJNA258214

REPOSITORIES: GEO

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Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans.

Project description:In animals, microRNAs frequently form families with related sequences. The functional relevance of miRNA families and the relative contribution of family members to target repression have remained, however, largely unexplored. Here, we used the Caenorhabditis elegans miR-58 miRNA family, composed primarily of the four highly abundant members miR-58.1, miR-80, miR-81, and miR-82, as a model to investigate the redundancy of miRNA family members and their impact on target expression in an in vivo setting. We found that miR-58 family members repress largely overlapping sets of targets in a predominantly additive fashion. Progressive deletions of miR-58 family members lead to cumulative up-regulation of target protein and RNA levels. Phenotypic defects could only be observed in the family quadruple mutant, which also showed the strongest change in target protein levels. Interestingly, although the seed sequences of miR-80 and miR-58.1 differ in a single nucleotide, predicted canonical miR-80 targets were efficiently up-regulated in the mir-58.1 single mutant, indicating functional redundancy of distinct members of this miRNA family. At the aggregate level, target binding leads mainly to mRNA degradation, although we also observed some degree of translational inhibition, particularly in the single miR-58 family mutants. These results provide a framework for understanding how miRNA family members interact to regulate target mRNAs.

| S-EPMC4617964 | biostudies-literature

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans

Project description:Comparative proteomic study between C. elegans wild type, mir-58.1 single, mir-80; mir-58.1 double and mir-80; mir-58.1; mir-81-82 quadruple mutants.

2015-08-06 | PXD001998 | Pride

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-06-05 | E-GEOD-60421 | biostudies-arrayexpress

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [miRNA-Seq]

2015-06-05 | E-GEOD-60419 | biostudies-arrayexpress

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [RNA-Seq]

2015-06-05 | E-GEOD-60420 | biostudies-arrayexpress

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [RNA-Seq]

2015-06-05 | GSE60420 | GEO

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans [miRNA-Seq]

2015-06-05 | GSE60419 | GEO

miR-58 family and TGF-β pathways regulate each other in Caenorhabditis elegans.

Project description:Despite the fact that microRNAs (miRNAs) modulate the expression of around 60% of protein-coding genes, it is often hard to elucidate their precise role and target genes. Studying miRNA families as opposed to single miRNAs alone increases our chances of observing not only mutant phenotypes but also changes in the expression of target genes. Here we ask whether the TGF-β signalling pathways, which control many animal processes, might be modulated by miRNAs in Caenorhabditis elegans. Using a mutant for four members of the mir-58 family, we show that both TGF-β Sma/Mab (controlling body size) and TGF-β Dauer (regulating dauer, a stress-resistant larval stage) are upregulated. Thus, mir-58 family directly inhibits the expression of dbl-1 (ligand), daf-1, daf-4 and sma-6 (receptors) of TGF-β pathways. Epistasis experiments reveal that whereas the small body phenotype of the mir-58 family mutant must invoke unknown targets independent from TGF-β Sma/Mab, its dauer defectiveness can be rescued by DAF-1 depletion. Additionally, we found a negative feedback loop between TGF-β Sma/Mab and mir-58 and the related mir-80. Our results suggest that the interaction between mir-58 family and TGF-β genes is key on decisions about animal growth and stress resistance in C. elegans and perhaps other organisms.

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MicroRNA destabilization enables dynamic regulation of the miR-16 family in response to cell-cycle changes.

Project description:The miR-16 family, which targets genes important for the G1-S transition, is a known modulator of the cell cycle, and members of this family are often deleted or downregulated in many types of cancers. Here, we report the reciprocal relationship-that of the cell cycle controlling the miR-16 family. Levels of this family increase rapidly as cells are arrested in G0. Conversely, as cells are released from G0 arrest, levels of the miR-16 family rapidly decrease. Such rapid changes are made possible by the unusual instabilities of several family members. The repression mediated by the miR-16 family is sensitive to these cell-cycle changes, which suggests that the rapid upregulation of the miR-16 family reinforces cell-cycle arrest in G0. Upon cell-cycle re-entry, the rapid decay of several members allows levels of the family to decrease, alleviating repression of target genes and allowing proper resumption of the cell cycle.

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Tissue expression pattern of PMK-2 p38 MAPK is established by the miR-58 family in C. elegans.

Project description:Analyses of gene expression profiles in evolutionarily diverse organisms have revealed a role for microRNAs in tuning tissue-specific gene expression. Here, we show that the relatively abundant and constitutively expressed miR-58 family of microRNAs sharply defines the tissue-specific expression of the broadly transcribed gene encoding PMK-2 p38 MAPK in Caenorhabditis elegans. Whereas PMK-2 functions redundantly with PMK-1 in the nervous system to regulate neuronal development and behavioral responses to pathogenic bacteria, the miR-58, miR-80, miR-81, and miR-82 microRNAs function redundantly to destabilize pmk-2 mRNA in non-neuronal cells with switch-like potency. Our data suggest a role for the miR-58 family in the establishment of neuronal-specific gene expression in C. elegans, and support a more general role for microRNAs in the establishment of tissue-specific gene expression.

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