Drosophila Erect wing (Ewg) controls mitochondrial fusion during muscle growth and maintenance by regulation of the <i>Opa1-like</i> gene

Rai, Mamta; Katti, Prasanna; Nongthomba, Upendra

doi:10.1242/jcs.135525

Cited by 35 publications

(42 citation statements)

References 73 publications

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“…6a ). Dp-depleted muscles failed to properly remodel mitochondria, which remained thin and elongated, resembling mitochondria at earlier time points of muscle development 33 . E2F/Dp was shown to regulate mitochondrial function by directly controlling the expression of mitochondria-associated genes in the eye 34 .…”

Section: Resultsmentioning

confidence: 90%

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E2F function in muscle growth is necessary and sufficient for viability in Drosophila

Zappia

Frolov

2016

Nat Commun

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The E2F transcription factor is a key cell cycle regulator. However, the inactivation of the entire E2F family in Drosophila is permissive throughout most of animal development until pupation when lethality occurs. Here we show that E2F function in the adult skeletal muscle is essential for animal viability since providing E2F function in muscles rescues the lethality of the whole-body E2F-deficient animals. Muscle-specific loss of E2F results in a significant reduction in muscle mass and thinner myofibrils. We demonstrate that E2F is dispensable for proliferation of muscle progenitor cells, but is required during late myogenesis to directly control the expression of a set of muscle-specific genes. Interestingly, E2f1 provides a major contribution to the regulation of myogenic function, while E2f2 appears to be less important. These findings identify a key function of E2F in skeletal muscle required for animal viability, and illustrate how the cell cycle regulator is repurposed in post-mitotic cells.

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Section: Resultsmentioning

confidence: 90%

“…During DLM growth, mitochondria undergo extensive fusion, increase in size 33 and become large and tubular as revealed by mitog FP marker ( Fig. 6a ).…”

Section: Resultsmentioning

confidence: 99%

E2F function in muscle growth is necessary and sufficient for viability in Drosophila

Zappia

Frolov

2016

Nat Commun

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“…OPA1, the inner mitochondrial fusion protein, has been identified to be crucial for muscle development (Rai et al . ; Sin et al . ) and, in the present study, OPA1 was changed from fusion‐ to fission‐preferred format across postnatal muscle growth (Fig.…”

Section: Discussionmentioning

confidence: 99%

Protein composition of the muscle mitochondrial reticulum during postnatal development

Kim

Yang

Katti

2019

The Journal of Physiology

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Key pointsr Muscle mitochondrial networks changed from a longitudinal, fibre parallel orientation to a perpendicular configuration during postnatal development.r Mitochondrial dynamics, mitophagy and calcium uptake proteins were abundant during early postnatal development.r Mitochondrial biogenesis and oxidative phosphorylation proteins were upregulated throughout muscle development.r Postnatal muscle mitochondrial network formation is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.Abstract Striated muscle mitochondria form connected networks capable of rapid cellular energy distribution. However, the mitochondrial reticulum is not formed at birth and the mechanisms driving network development remain unclear. In the present study, we aimed to establish the network formation timecourse and protein expression profile during postnatal development of the murine muscle mitochondrial reticulum. Two-photon microscopy was used to observe mitochondrial network orientation in tibialis anterior (TA) muscles of live mice at postnatal days (P) 1, 7, 14, 21 and 42, respectively. All muscle fibres maintained a longitudinal, fibre parallel mitochondrial network orientation early in development (P1-7). Mixed networks were most common at P14 but, by P21, almost all fibres had developed the perpendicular mitochondrial orientation observed in mature, glycolytic fibres. Tandem mass tag proteomics were then applied to examine changes in 6869 protein abundances in developing TA muscles. Mitochondrial proteins increased by 32% from P1 to P42. In addition, both nuclear-and mitochondrial-DNA encoded oxidative phosphorylation (OxPhos) components were increased during development, whereas OxPhos assembly factors decreased. Although mitochondrial dynamics and mitophagy were induced at P1-7, mitochondrial biogenesis was enhanced after P14. Moreover, calcium signalling Y. Kim and others J Physiol 597.10 proteins and the mitochondrial calcium uniporter had the highest expression early in postnatal development. In conclusion, mitochondrial networks transform from a fibre parallel to perpendicular orientation during the second and third weeks after birth in murine glycolytic skeletal muscle. This structural transition is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.

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“…The bisected fly hemithoraces were processed for immunohistochemical analysis as described previously (Rai et al 2014). Following blocking, samples were treated differently depending on the type of analysis required.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of miRNA-9 Generates Muscle Hypercontraction Through Translational Repression of Troponin-T inDrosophila melanogasterIndirect Flight Muscles

Katti

Thimmaya

Madan

et al. 2017

G3 Genes|Genomes|Genetics

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MicroRNAs (miRNAs) are small noncoding endogenous RNAs, typically 21–23 nucleotides long, that regulate gene expression, usually post-transcriptionally, by binding to the 3′-UTR of target mRNA, thus blocking translation. The expression of several miRNAs is significantly altered during cardiac hypertrophy, myocardial ischemia, fibrosis, heart failure, and other cardiac myopathies. Recent studies have implicated miRNA-9 (miR-9) in myocardial hypertrophy. However, a detailed mechanism remains obscure. In this study, we have addressed the roles of miR-9 in muscle development and function using a genetically tractable model system, the indirect flight muscles (IFMs) of Drosophila melanogaster. Bioinformatics analysis identified 135 potential miR-9a targets, of which 27 genes were associated with Drosophila muscle development. Troponin-T (TnT) was identified as major structural gene target of miR-9a. We show that flies overexpressing miR-9a in the IFMs have abnormal wing position and are flightless. These flies also exhibit a loss of muscle integrity and sarcomeric organization causing an abnormal muscle condition known as “hypercontraction.” Additionally, miR-9a overexpression resulted in the reduction of TnT protein levels while transcript levels were unaffected. Furthermore, muscle abnormalities associated with miR-9a overexpression were completely rescued by overexpression of TnT transgenes which lacked the miR-9a binding site. These findings indicate that miR-9a interacts with the 3′-UTR of the TnT mRNA and downregulates the TnT protein levels by translational repression. The reduction in TnT levels leads to a cooperative downregulation of other thin filament structural proteins. Our findings have implications for understanding the cellular pathophysiology of cardiomyopathies associated with miR-9 overexpression.

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Drosophila Erect wing (Ewg) controls mitochondrial fusion during muscle growth and maintenance by regulation of the Opa1-like gene

Cited by 35 publications

References 73 publications

E2F function in muscle growth is necessary and sufficient for viability in Drosophila

E2F function in muscle growth is necessary and sufficient for viability in Drosophila

Protein composition of the muscle mitochondrial reticulum during postnatal development

Overexpression of miRNA-9 Generates Muscle Hypercontraction Through Translational Repression of Troponin-T inDrosophila melanogasterIndirect Flight Muscles

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