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The Regulation of Muscle Structure and Metabolism by Mio/dChREBP in Drosophila.

Polak GL, Pasqualino A, Docherty JE, Beck SJ, DiAngelo JR - PLoS ONE (2015)

Bottom Line: Decreasing Mio levels using RNAi specifically in muscle results in increased thorax glycogen storage.Myofibril size is also decreased in flies just before emerging from their pupal cases, suggesting a role for Mio in myofibril development.Together, these data indicate a novel role for Mio in controlling muscle structure and metabolism and may provide a molecular link between nutrient availability and muscle function.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Hofstra University, Hempstead, NY, 11549, United States of America.

ABSTRACT
All cells require energy to perform their specialized functions. Muscle is particularly sensitive to the availability of nutrients due to the high-energy requirement for muscle contraction. Therefore the ability of muscle cells to obtain, store and utilize energy is essential for the function of these cells. Mio, the Drosophila homolog of carbohydrate response element binding protein (ChREBP), has recently been identified as a nutrient responsive transcription factor important for triglyceride storage in the fly fat body. However, the function of Mio in muscle is unknown. In this study, we characterized the role of Mio in controlling muscle function and metabolism. Decreasing Mio levels using RNAi specifically in muscle results in increased thorax glycogen storage. Adult Mio-RNAi flies also have a flight defect due to altered myofibril shape and size in the indirect flight muscles as shown by electron microscopy. Myofibril size is also decreased in flies just before emerging from their pupal cases, suggesting a role for Mio in myofibril development. Together, these data indicate a novel role for Mio in controlling muscle structure and metabolism and may provide a molecular link between nutrient availability and muscle function.

No MeSH data available.


Related in: MedlinePlus

Decreasing Mio levels results in abnormal myofibril ultrastructure.Transmission Electron Microscopy of Indirect Flight Muscles of adult Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR females compared to Mef2-Gal4>GFP controls. Panels (A), (B) and (C) show cross sections of the myofibrils; panels (D), (E) and (F) show longitudinal sections of myofibrils. f, myofibril; c, mitochondrion; g, glycogen granules; m, m-line; z, z-line. Scale bar = 0.5μm.
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pone.0136504.g003: Decreasing Mio levels results in abnormal myofibril ultrastructure.Transmission Electron Microscopy of Indirect Flight Muscles of adult Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR females compared to Mef2-Gal4>GFP controls. Panels (A), (B) and (C) show cross sections of the myofibrils; panels (D), (E) and (F) show longitudinal sections of myofibrils. f, myofibril; c, mitochondrion; g, glycogen granules; m, m-line; z, z-line. Scale bar = 0.5μm.

Mentions: The phenotypes observed in many previously identified Drosophila flight mutants have resulted from altered myofibril structure [22]. To test whether loss of Mio results in flight impairment due to altered muscle structure, we made use of Transmission Electron Microscopy (TEM) to visualize the indirect flight muscles (IFM). Micrographs of IFM ultrastructure showed abnormal myofibril assembly in cross sectional views in adult flies where Mio was decreased when compared to their GFP-expressing controls. Cross sections of Mio-RNAi myofibrils revealed normal actin/myosin crystal lattice structure, but the myofibrils themselves failed to retain their circular shape and looked smaller than the control myofibrils (Fig 3A–3C). IFM from Mio-RNAi flies also visually accumulated more glycogen granules around the myofibrils when compared to controls (Fig 3A–3C), consistent with the increased glycogen phenotype observed above. Although cross sections of Mio-RNAi flies showed disrupted myofibril ultrastructure, longitudinal sections revealed normal sarcomere assembly (Fig 3E and 3F) when compared with their respective GFP controls (Fig 3D). In addition, no obvious alterations in mitochondrial morphology were observed in muscles from Mio-RNAi flies (unpublished observations) suggesting that Mio does not regulate mitochondrial structure.


The Regulation of Muscle Structure and Metabolism by Mio/dChREBP in Drosophila.

Polak GL, Pasqualino A, Docherty JE, Beck SJ, DiAngelo JR - PLoS ONE (2015)

Decreasing Mio levels results in abnormal myofibril ultrastructure.Transmission Electron Microscopy of Indirect Flight Muscles of adult Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR females compared to Mef2-Gal4>GFP controls. Panels (A), (B) and (C) show cross sections of the myofibrils; panels (D), (E) and (F) show longitudinal sections of myofibrils. f, myofibril; c, mitochondrion; g, glycogen granules; m, m-line; z, z-line. Scale bar = 0.5μm.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549115&req=5

pone.0136504.g003: Decreasing Mio levels results in abnormal myofibril ultrastructure.Transmission Electron Microscopy of Indirect Flight Muscles of adult Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR females compared to Mef2-Gal4>GFP controls. Panels (A), (B) and (C) show cross sections of the myofibrils; panels (D), (E) and (F) show longitudinal sections of myofibrils. f, myofibril; c, mitochondrion; g, glycogen granules; m, m-line; z, z-line. Scale bar = 0.5μm.
Mentions: The phenotypes observed in many previously identified Drosophila flight mutants have resulted from altered myofibril structure [22]. To test whether loss of Mio results in flight impairment due to altered muscle structure, we made use of Transmission Electron Microscopy (TEM) to visualize the indirect flight muscles (IFM). Micrographs of IFM ultrastructure showed abnormal myofibril assembly in cross sectional views in adult flies where Mio was decreased when compared to their GFP-expressing controls. Cross sections of Mio-RNAi myofibrils revealed normal actin/myosin crystal lattice structure, but the myofibrils themselves failed to retain their circular shape and looked smaller than the control myofibrils (Fig 3A–3C). IFM from Mio-RNAi flies also visually accumulated more glycogen granules around the myofibrils when compared to controls (Fig 3A–3C), consistent with the increased glycogen phenotype observed above. Although cross sections of Mio-RNAi flies showed disrupted myofibril ultrastructure, longitudinal sections revealed normal sarcomere assembly (Fig 3E and 3F) when compared with their respective GFP controls (Fig 3D). In addition, no obvious alterations in mitochondrial morphology were observed in muscles from Mio-RNAi flies (unpublished observations) suggesting that Mio does not regulate mitochondrial structure.

Bottom Line: Decreasing Mio levels using RNAi specifically in muscle results in increased thorax glycogen storage.Myofibril size is also decreased in flies just before emerging from their pupal cases, suggesting a role for Mio in myofibril development.Together, these data indicate a novel role for Mio in controlling muscle structure and metabolism and may provide a molecular link between nutrient availability and muscle function.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Hofstra University, Hempstead, NY, 11549, United States of America.

ABSTRACT
All cells require energy to perform their specialized functions. Muscle is particularly sensitive to the availability of nutrients due to the high-energy requirement for muscle contraction. Therefore the ability of muscle cells to obtain, store and utilize energy is essential for the function of these cells. Mio, the Drosophila homolog of carbohydrate response element binding protein (ChREBP), has recently been identified as a nutrient responsive transcription factor important for triglyceride storage in the fly fat body. However, the function of Mio in muscle is unknown. In this study, we characterized the role of Mio in controlling muscle function and metabolism. Decreasing Mio levels using RNAi specifically in muscle results in increased thorax glycogen storage. Adult Mio-RNAi flies also have a flight defect due to altered myofibril shape and size in the indirect flight muscles as shown by electron microscopy. Myofibril size is also decreased in flies just before emerging from their pupal cases, suggesting a role for Mio in myofibril development. Together, these data indicate a novel role for Mio in controlling muscle structure and metabolism and may provide a molecular link between nutrient availability and muscle function.

No MeSH data available.


Related in: MedlinePlus