mir-234 controls neuropeptide release at the Caenorhabditis elegans neuromuscular junction

Snieckute, Goda; Baltaci, Oguzhan; Liu, Haowen; Li, Lei; Hu, Zhitao; Pocock, Roger

doi:10.1016/j.mcn.2019.06.001

Cited by 8 publications

(10 citation statements)

References 39 publications

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“…Likewise, miR-234, which was expressed and AGO-loaded exclusively in the nervous system (Supplementary Fig. 10b), was recently demonstrated to regulate genes involved in neuropeptide release 41 .…”

Section: Reads Per Millionmentioning

confidence: 94%

Cell-type-specific profiling of loaded miRNAs from Caenorhabditis elegans reveals spatial and temporal flexibility in Argonaute loading

2021

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Multicellularity has coincided with the evolution of microRNAs (miRNAs), small regulatory RNAs that are integrated into cellular differentiation and homeostatic gene-regulatory networks. However, the regulatory mechanisms underpinning miRNA activity have remained largely obscured because of the precise, and thus difficult to access, cellular contexts under which they operate. To resolve these, we have generated a genome-wide map of active miRNAs in Caenorhabditis elegans by revealing cell-type-specific patterns of miRNAs loaded into Argonaute (AGO) silencing complexes. Epitope-labelled AGO proteins were selectively expressed and immunoprecipitated from three distinct tissue types and associated miRNAs sequenced. In addition to providing information on biological function, we define adaptable miRNA:AGO interactions with single-cell-type and AGO-specific resolution. We demonstrate spatial and temporal dynamicism, flexibility of miRNA loading, and suggest miRNA regulatory mechanisms via AGO selectivity in different tissues and during ageing. Additionally, we resolve widespread changes in AGO-regulated gene expression by analysing translatomes specifically in neurons.

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Section: Reads Per Millionmentioning

confidence: 94%

Cell-type-specific profiling of loaded miRNAs from Caenorhabditis elegans reveals spatial and temporal flexibility in Argonaute loading

2021

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“…miRNAs are a class of endogenous nucleotide non-protein-encoding RNAs with 21–23 bases, and regulate eukaryotic gene expression at the post-transcriptional level 21 , 22 . miRNAs inhibit gene expression primarily by binding to certain sites of the 3′ untranslated regions (3′ UTRs) of target mRNAs, which results in degradation of mRNA and inhibition of protein translation 23 – 25 . In C. elegans , miRNAs also play important roles in response to the toxicity of certain carbon nanomaterials.…”

Section: Introductionmentioning

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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“…In particular, in a mouse model of spinal muscular atrophy, miR-146a overexpression results in loss of motoneurons, while its abrogation prevents motoneurons loss [ 146 ]. Further analyses revealed that mir-234 may be responsible for NMJ dysfunctions through its ability to control the expression of target genes that are important for the maturation and transport of neuropeptides in Caenorhabditis elegans [ 147 ]. Although more research is needed, these studies highlight a possible role for miRNAs in regulating neurodegeneration in sarcopenia ( Table 1 ).…”

Section: Epigenetic Regulation Of Nmj Dysfunctionmentioning

confidence: 99%

Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications

Dobrowolny

Barbiera

Sica

et al. 2021

Cells

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With advancing aging, a decline in physical abilities occurs, leading to reduced mobility and loss of independence. Although many factors contribute to the physio-pathological effects of aging, an important event seems to be related to the compromised integrity of the neuromuscular system, which connects the brain and skeletal muscles via motoneurons and the neuromuscular junctions (NMJs). NMJs undergo severe functional, morphological, and molecular alterations during aging and ultimately degenerate. The effect of this decline is an inexorable decrease in skeletal muscle mass and strength, a condition generally known as sarcopenia. Moreover, several studies have highlighted how the age-related alteration of reactive oxygen species (ROS) homeostasis can contribute to changes in the neuromuscular junction morphology and stability, leading to the reduction in fiber number and innervation. Increasing evidence supports the involvement of epigenetic modifications in age-dependent alterations of the NMJ. In particular, DNA methylation, histone modifications, and miRNA-dependent gene expression represent the major epigenetic mechanisms that play a crucial role in NMJ remodeling. It is established that environmental and lifestyle factors, such as physical exercise and nutrition that are susceptible to change during aging, can modulate epigenetic phenomena and attenuate the age-related NMJs changes. This review aims to highlight the recent epigenetic findings related to the NMJ dysregulation during aging and the role of physical activity and nutrition as possible interventions to attenuate or delay the age-related decline in the neuromuscular system.

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mir-234 controls neuropeptide release at the Caenorhabditis elegans neuromuscular junction

Cited by 8 publications

References 39 publications

Cell-type-specific profiling of loaded miRNAs from Caenorhabditis elegans reveals spatial and temporal flexibility in Argonaute loading

Cell-type-specific profiling of loaded miRNAs from Caenorhabditis elegans reveals spatial and temporal flexibility in Argonaute loading

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

Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications

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