A micro
            <scp>RNA</scp>
            switch controls dietary restriction‐induced longevity through Wnt signaling

Xu, Yunpeng; He, Zhidong; Song, Mengjiao; Zhou, Yifei; Shen, Yi-Dong

doi:10.15252/embr.201846888

Cited by 22 publications

(26 citation statements)

References 66 publications

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“…When pry-1 was knocked down in mom-2(or42) and cwn-2(ok895) backgrounds, life span extension was significantly reduced in mom-2 mutants (13.6% reduction in mean life span, p < 0.05, Figure 3 A; Table S2 ) but remained unchanged in the cwn-2 animals ( Figure 3 B; Table S2 ). We also analyzed the requirements of bar-1 / β-catenin , a component of the canonical WNT signaling that plays a role in aging ( Xu et al., 2019 ; Zhang et al., 2018 ), in the mom-2 - pry-1 pathway. Since pry-1 -mediated WNT signaling negatively regulates bar-1 , removing bar-1 function is expected to suppress the phenotype of pry-1 mutants.…”

Section: Resultsmentioning

confidence: 99%

Axin-Mediated Regulation of Lifespan and Muscle Health in C. elegans Requires AMPK-FOXO Signaling

et al. 2020

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Aging is a significant risk factor for several diseases. Studies have uncovered multiple signaling pathways that modulate aging, including insulin/insulin-like growth factor-1 signaling (IIS). In Caenorhabditis elegans, the key regulator of IIS is DAF-16/FOXO. One of the kinases that affects DAF-16 function is the AMPK catalytic subunit homolog AAK-2. In this study, we report that PRY-1/Axin plays an essential role in AAK-2 and DAF-16-mediated regulation of life span. The pry-1 mutant transcriptome contains many genes associated with aging and muscle function. Consistent with this, pry-1 is strongly expressed in muscles, and muscle-specific overexpression of pry-1 extends life span, delays muscle aging, and improves mitochondrial morphology in AAK-2-DAF-16-dependent manner. Furthermore, PRY-1 is necessary for AAK-2 phosphorylation. Taken together, our data demonstrate that PRY-1 functions in muscles to promote the life span of animals. This study establishes Axin as a major regulator of muscle health and aging.

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Section: Resultsmentioning

confidence: 99%

Axin-Mediated Regulation of Lifespan and Muscle Health in C. elegans Requires AMPK-FOXO Signaling

et al. 2020

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“…No defects in dauer arrest or development have been reported for these miRNAs, however cel - mir - 235 is required for maintaining L1 arrest, when eggs hatch in the absence of food 12 , while dietary restriction of C . elegans adult worms induces expression of mir - 235 31 , mir - 228 and mir - 71 32 .…”

Section: Resultsmentioning

confidence: 99%

Profiling microRNAs through development of the parasitic nematode Haemonchus identifies nematode-specific miRNAs that suppress larval development

Marks

Winter

et al. 2019

Sci Rep

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Parasitic nematodes transition between dramatically different free-living and parasitic stages, with correctly timed development and migration crucial to successful completion of their lifecycle. However little is known of the mechanisms controlling these transitions. microRNAs (miRNAs) negatively regulate gene expression post-transcriptionally and regulate development of diverse organisms. Here we used microarrays to determine the expression profile of miRNAs through development and in gut tissue of the pathogenic nematode Haemonchus contortus. Two miRNAs, mir-228 and mir-235, were enriched in infective L3 larvae, an arrested stage analogous to Caenorhabditis elegans dauer larvae. We hypothesized that these miRNAs may suppress development and maintain arrest. Consistent with this, inhibitors of these miRNAs promoted H. contortus development from L3 to L4 stage, while genetic deletion of C. elegans homologous miRNAs reduced dauer arrest. Epistasis studies with C. elegans daf-2 mutants showed that mir-228 and mir-235 synergise with FOXO transcription factor DAF-16 in the insulin signaling pathway. Target prediction suggests that these miRNAs suppress metabolic and transcription factor activity required for development. Our results provide novel insight into the expression and functions of specific miRNAs in regulating nematode development and identify miRNAs and their target genes as potential therapeutic targets to limit parasite survival within the host.

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“…In C. elegans, miRNAs have been shown to participate in the regulation of metabolic processes, cell development and lifespan determination 31,32 . Increasing evidence suggests that some miRNAs play critical roles in response to the toxicity of nanomaterials 20,30 .…”

Section: Discussionmentioning

confidence: 99%

“…mir-235, a sole orthologue of mammalian miR-92 in oncogenic miR-17-92 cluster, acts in the hypodermis and glial cells to arrest postembryonic developmental events in neuroblasts and mesoblasts 31 . mir-235 is induced by dietary restriction at the end of larval development, which subsequently suppresses Wnt signaling by inhibiting cwn-1/WNT4 and thereby promotes longevity 32 . Our previous study found that mir-235(n4504) mutants display a sensitive property to GO toxicity 30 .…”

mentioning

confidence: 99%

The C. elegans miR-235 regulates the toxicity of graphene oxide via targeting the nuclear hormone receptor DAF-12 in the intestine

Guo

Cheng

Zhao

et al. 2020

Sci Rep

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The increased application of graphene oxide (GO), a new carbon-based engineered nanomaterial, has generated a potential toxicity in humans and the environment. Previous studies have identified some dysregulated microRNAs (miRNAs), such as up-regulated mir-235, in organisms exposed to GO. However, the detailed mechanisms of the dysregulation of miRNA underlying GO toxicity are still largely elusive. In this study, we employed Caenorhabditis elegans as an in vivo model to investigate the biological function and molecular basis of mir-235 in the regulation of GO toxicity. After low concentration GO exposure, mir-235 (n4504) mutant nematodes were sensitive to GO toxicity, implying that mir-235 mediates a protection mechanism against GO toxicity. Tissue-specific assays suggested that mir-235 expressed in intestine is required for suppressing the GO toxicity in C. elegans. daf-12, a gene encoding a member of the steroid hormone receptor superfamily, acts as a target gene of mir-235 in the nematode intestine in response to GO treatment, and RNAi knockdown of daf-12 suppressed the sensitivity of mir-235(n4503) to GO toxicity. Further genetic analysis showed that DAF-12 acted in the upstream of DAF-16 in insulin/IGF-1 signaling pathway and PMK-1 in p38 MAPK signaling pathway in parallel to regulate GO toxicity. Altogether, our results revealed that mir-235 may activate a protective mechanism against GO toxicity by suppressing the DAF-12-DAF-16 and DAF-12-PMK-1 signaling cascade in nematodes, which provides an important molecular basis for the in vivo toxicity of GO at the miRNA level.

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A micro RNA switch controls dietary restriction‐induced longevity through Wnt signaling

Cited by 22 publications

References 66 publications

Axin-Mediated Regulation of Lifespan and Muscle Health in C. elegans Requires AMPK-FOXO Signaling

Axin-Mediated Regulation of Lifespan and Muscle Health in C. elegans Requires AMPK-FOXO Signaling

Profiling microRNAs through development of the parasitic nematode Haemonchus identifies nematode-specific miRNAs that suppress larval development

The C. elegans miR-235 regulates the toxicity of graphene oxide via targeting the nuclear hormone receptor DAF-12 in the intestine

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