Ectopic expression of mir-3 affects mef2 and tinman levels
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE28605 | GEO | 2015/04/01
SECONDARY ACCESSION(S): PRJNA143083
REPOSITORIES: GEO
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Project description:Loss of nautilus (MyoD) gene function results in a variable phenotype affecting muscle formation in embryos and larvae, larval movement, pupal eclosion, egg deposition, adult mobility and survival. 8-miR cluster deletion disrupts muscle formation in the embryo while affecting protein production from the nautilus, dMef2 , regulators of the muscle transcriptional network. We propose the complex phenotype in the nautilus null is due to the disruption of the regulatory interactions provided by the 8-miR cluster. The results demonstrate that nautilus is an integral regulator of the miRNA circuitry buffering the transcriptional network directing muscle development.
2015-04-01 | GSE28604 | GEO
Project description:Loss of nautilus (MyoD) gene function results in a variable phenotype affecting muscle formation in embryos and larvae, larval movement, pupal eclosion, egg deposition, adult mobility and survival. 8-miR cluster deletion disrupts muscle formation in the embryo while affecting protein production from the nautilus, dMef2 , regulators of the muscle transcriptional network. We propose the complex phenotype in the nautilus null is due to the disruption of the regulatory interactions provided by the 8-miR cluster. The results demonstrate that nautilus is an integral regulator of the miRNA circuitry buffering the transcriptional network directing muscle development. Two-condition experiment, wild type (w1118) vs. mutant (8-miR cluster null). Biological replicates: 3 wild type, 3 mutants, independently isolated. One of the biological replicate was dye swaped to avoid dye bias.
2015-04-01 | E-GEOD-28604 | biostudies-arrayexpress
Project description:Loss of nautilus (MyoD) gene function results in a variable phenotype affecting muscle formation in embryos and larvae, larval movement, pupal eclosion, egg deposition, adult mobility and survival. mir-3 over expression disrupts muscle formation in the embryo while affecting protein production from the dMef2 and tinman genes, global regulators of the muscle transcriptional network. We propose the complex phenotype in the nautilus null is due to the disruption of the regulatory interactions provided by the 8-miR cluster. The results demonstrate that nautilus is an integral regulator of the miRNA circuitry buffering the transcriptional network directing muscle development. Two-condition experiment, wild type (w1118) vs. mutant (mir-3 ectopic expressionl). Biological replicates: 3 wild type, 3 mutants, independently isolated. One of the biological replicate was dye swaped to avoid dye bias.
2015-04-01 | E-GEOD-28605 | biostudies-arrayexpress
Project description:To determine if the Drosophila MyoD homolog, nautilus, was activating any miRNA loci, similar to vertebrate MyoD, we compared the miRNA expression profiles between wild-type (w1118) and nautilus null embryos during the window of maximum nautilus expression (6-8hr AEL), using LNA arrays specifically designed to quantify miRNA levels in Drosophila (Exiqon). Expression levels for mir-309, mir-3, mir-286, mir-4, mir-5, and mir-6 from the 8-miR cluster, were significantly decreased in nautilus null embryos. It suggests that the intergenic 8-miR cluster, encoding eight miRNAs, is regulated by nautilus.
2015-04-01 | GSE28550 | GEO
Project description:To determine if the Drosophila MyoD homolog, nautilus, was activating any miRNA loci, similar to vertebrate MyoD, we compared the miRNA expression profiles between wild-type (w1118) and nautilus null embryos during the window of maximum nautilus expression (6-8hr AEL), using LNA arrays specifically designed to quantify miRNA levels in Drosophila (Exiqon). Expression levels for mir-309, mir-3, mir-286, mir-4, mir-5, and mir-6 from the 8-miR cluster, were significantly decreased in nautilus null embryos. It suggests that the intergenic 8-miR cluster, encoding eight miRNAs, is regulated by nautilus. Two-condition experiment, wild type (w1118) vs. mutant (nautilus null). Biological replicates: 3 wild type, 3 mutants, independently isolated.
2015-04-01 | E-GEOD-28550 | biostudies-arrayexpress
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2022-05-19 | PXD028554 | Pride
Project description:Muscle function relies on the precise architecture of dynamic contractile elements, which must be fine-tuned to maintain motility throughout life. Muscle is also highly plastic, and remodeled in response to stress, growth, neural and metabolic inputs. The evolutionarily conserved muscle microRNA, mir1, regulates distinct aspects of muscle biology during development, but whether it plays a role during ageing is unknown. Here we investigated the role of C. elegans mir-1 in muscle function in response to proteostatic stress during adulthood. mir-1 deletion results in improved mid-life muscle motility, pharyngeal pumping, and organismal longevity under conditions of polyglutamine repeat proteotoxic challenge. We identified multiple vacuolar ATPase subunits as subject to mir-1 control, and the regulatory subunit vha-13/ATP6VIA as a direct target downregulated via its 3’UTR to mediate mir-1 physiology. mir-1 further regulates nuclear localization of lysosomal biogenesis factor HLH-30/TFEB and lysosomal acidification. Our studies reveal that mir-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact muscle function and health during ageing.
2021-07-14 | PXD023544 | Pride
Project description:Proctor2017 - Identifying microRNA for muscle
regeneration during ageing (Mirs_in_muscle)
This model is described in the article:
Using computer simulation
models to investigate the most promising microRNAs to improve
muscle regeneration during ageing
Carole J. Proctor & Katarzyna
Goljanek-Whysall
Nature Scientific Reports
Abstract:
MicroRNAs (miRNAs) regulate gene expression through
interactions with target sites within mRNAs, leading to
enhanced degradation of the mRNA or inhibition of translation.
Skeletal muscle expresses many different miRNAs with important
roles in adulthood myogenesis (regeneration) and myofibre
hypertrophy and atrophy, processes associated with muscle
ageing. However, the large number of miRNAs and their targets
mean that a complex network of pathways exists, making it
difficult to predict the effect of selected miRNAs on
age-related muscle wasting. Computational modelling has the
potential to aid this process as it is possible to combine
models of individual miRNA:target interactions to form an
integrated network. As yet, no models of these interactions in
muscle exist. We created the first model of miRNA:target
interactions in myogenesis based on experimental evidence of
individual miRNAs which were next validated and used to make
testable predictions. Our model confirms that miRNAs regulate
key interactions during myogenesis and can act by promoting the
switch between quiescent/proliferating/differentiating
myoblasts and by maintaining the differentiation process. We
propose that a threshold level of miR-1 acts in the initial
switch to differentiation, with miR-181 keeping the switch on
and miR-378 maintaining the differentiation and miR-143
inhibiting myogenesis.
This model is hosted on
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MODEL1704110004.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
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2017-09-26 | MODEL1704110004 | BioModels