miR-92b regulates Mef2 levels through a negative-feedback circuit during <i>Drosophila</i> muscle development

Chen, Zhimin; Liang, Shanshan; Ying, Zhao; Han, Zhe

doi:10.1242/dev.082719

Cited by 51 publications

(41 citation statements)

References 49 publications

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“…Immunostaining of Drosophila embryos was performed as described (Chen et al, 2012). The following primary antibodies were used: α-Mef2 (a gift from B. Paterson), α-Even-skipped (Developmental Studies Hybridoma Bank, the University of Iowa).…”

Section: Methodsmentioning

confidence: 99%

Wnt4 is required for ostia development in the Drosophila heart

Chen

Zhu

et al. 2016

Developmental Biology

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The Drosophila ostia are valve-like structures in the heart with functional similarity to vertebrate cardiac valves. The Wnt/ -catenin signaling pathway is critical for valve development in zebrafish and mouse, but the key ligand(s) for valve induction remains unclear. We observed high levels of Wnt4 gene expression in Drosophila ostia progenitor cells, immediately prior to morphological differentiation of these cells associated with ostia formation. This differentiation was blocked in Wnt4 mutants and in flies expressing canonical Wnt signaling pathway inhibitors but not inhibitors of the planar cell polarity pathway. High levels of Wnt4 dependent activation of a canonical Wnt signaling reporter was observed specifically in ostia progenitor cells. In vertebrate valve formation Wnt signaling is active in cells undergoing early endothelial-mesenchymal transition (EMT) and the Wnt9 homologue of Drosophila Wnt4 is expressed in valve progenitors. In demonstrating an essential role for Wnt4 in ostia development we have identified similarities between molecular and cellular events associated with early EMT during vertebrate valve development and the differentiation and partial delamination of ostia progenitor cells in the process of ostia formation.

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Section: Methodsmentioning

confidence: 99%

Wnt4 is required for ostia development in the Drosophila heart

Chen

Zhu

et al. 2016

Developmental Biology

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“…One question is whether it is significant that these particular miRNAs are co-expressed together in the blastoderm embryo. Of the early expressed miRNAs, loss-of-function mutations have been made in miR-309 as mentioned above, miR-1 (Sokol and Ambros, 2005), miR-9a (Li et al, 2006), miR-11 (Truscott et al, 2011), miR-iab-4/4as (Bender, 2008), miR-10 ( Lemons et al, 2012) and miR-92a (Chen et al, 2012b). Curiously, none of these mutants displayed early morphological phenotypes despite the fact that miRNA targets for some were identified and verified.…”

Section: Co-activation Of Mirnas By Zelda Is Crucial For Normal Develmentioning

confidence: 99%

Co-activation of microRNAs by Zelda is essential for early Drosophila development

Nien

Liang

et al. 2014

Development

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Transcription factors and microRNAs (miRNAs) are two important classes of trans-regulators in differential gene expression. Transcription factors occupy cis-regulatory motifs in DNA to activate or repress gene transcription, whereas miRNAs specifically pair with seed sites in target mRNAs to trigger mRNA decay or inhibit translation. Dynamic spatiotemporal expression patterns of transcription factors and miRNAs during development point to their stage-and tissuespecific functions. Recent studies have focused on miRNA functions during development; however, much remains to explore regarding how the expression of miRNAs is initiated and how dynamic miRNA expression patterns are achieved by transcriptional regulatory networks at different developmental stages. Here, we focused on the identification, regulation and function of miRNAs during the earliest stage of Drosophila development, when the maternal-tozygotic transition (MZT) takes place. Eleven miRNA clusters comprise the first set of miRNAs activated in the blastoderm embryo. The transcriptional activator Zelda is required for their proper activation and regulation, and Zelda binding observed in genome-wide binding profiles is predictive of enhancer activity. In addition, other blastoderm transcription factors, comprising both activators and repressors, the activities of which are potentiated and coordinated by Zelda, contribute to the accurate temporal and spatial expression of these miRNAs, which are known to function in diverse developmental processes. Although previous genetic studies showed no early phenotypes upon loss of individual miRNAs, our analysis of the miR-1; miR-9a double mutant revealed defects in gastrulation, demonstrating the importance of co-activation of miRNAs by Zelda during the MZT.

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“…The concept was proved by showing that deletion of miR-92b caused abnormally high MEF2 expression, leading to muscle defects and lethality. In addition, overexpression of miR-92b reduced MEF2 levels and caused muscle defects similar to those seen in MEF2 RNAi [47]. In another study, miR-26a was induced in an injury/regeneration animal model.…”

Section: Muscle-specific Microrna and Myogenesismentioning

confidence: 99%

MicroRNA in myogenesis and muscle atrophy

Wang

2013

Current Opinion in Clinical Nutrition and Metabolic Care

132

103

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Purpose of review To understand the impact of microRNA on myogenesis and muscle wasting in order to provide valuable information for clinical investigation. Recent findings Muscle wasting increases the risk of morbidity/mortality in primary muscle diseases, secondary muscle disorders and elderly population. Muscle mass is controlled by several different signalling pathways. Insulin-like growth factor/PI3K/Akt is a positive signalling pathway, as it increases muscle mass by increasing protein synthesis and decreasing protein degradation. This pathway is directly and/or indirectly downregulated by miR-1, miR-133, miR-206 or miR-125b, and upregulated by miR-23a or miR-486. Myostatin and the transforming growth factor-β signalling pathway are negative regulators that cause muscle wasting. An increase of miR-27 reduces myostatin and increases muscle cell proliferation. Muscle regeneration capacity also plays a significant role in the regulation of muscle mass. This review comprehensively describes the effect of microRNA on myoblasts proliferation and differentiation, and summarizes the varied influences of microRNA on different muscle atrophy. Summary Growing evidence indicates that microRNAs significantly impact muscle growth, regeneration and metabolism. MicroRNAs have a great potential to become diagnostic and/or prognostic markers, therapeutic agents and therapeutic targets.

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miR-92b regulates Mef2 levels through a negative-feedback circuit during Drosophila muscle development

Cited by 51 publications

References 49 publications

Wnt4 is required for ostia development in the Drosophila heart

Wnt4 is required for ostia development in the Drosophila heart

Co-activation of microRNAs by Zelda is essential for early Drosophila development

MicroRNA in myogenesis and muscle atrophy

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