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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

Mio is not necessary for normal expression of structural genes in adult fly muscle.Expression of Actin 88F (Act88F, n = 8), Myosin Heavy Chain (MHC, n = 11), and Myosin light chain-2 (Mlc-2, n = 8) was measured by performing quantitative PCR on thorax cDNA from 5–7 day old Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR flies and compared to Mef2-Gal4>GFP controls. mRNA levels of Mef2-Gal4>GFP controls were set to 1.0 and mRNA levels of Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR animals were then normalized to their respective control. Values represent mean±SEM. *p<0.05 by One-way ANOVA with post hoc Tukey test.
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pone.0136504.g007: Mio is not necessary for normal expression of structural genes in adult fly muscle.Expression of Actin 88F (Act88F, n = 8), Myosin Heavy Chain (MHC, n = 11), and Myosin light chain-2 (Mlc-2, n = 8) was measured by performing quantitative PCR on thorax cDNA from 5–7 day old Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR flies and compared to Mef2-Gal4>GFP controls. mRNA levels of Mef2-Gal4>GFP controls were set to 1.0 and mRNA levels of Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR animals were then normalized to their respective control. Values represent mean±SEM. *p<0.05 by One-way ANOVA with post hoc Tukey test.

Mentions: To test this hypothesis, we measured the mRNA levels of an indirect flight muscle-specific actin gene (Act88F), Myosin heavy chain (Mhc), and Myosin light chain-2 (Mlc-2), genes important for muscle development and assembly that when mutated cause a similar altered myofibril phenotype as seen in our Mio-deficient animals [21, 33–35]. Interestingly, no consistent differences in the expression of these genes were observed in Mio-RNAi adults (Fig 7). Together, these data suggest that Mio does not function to regulate the expression of genes required for myofibril assembly, but may be important for normal metabolic homeostasis of muscle cells throughout the life cycle of the animal.


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)

Mio is not necessary for normal expression of structural genes in adult fly muscle.Expression of Actin 88F (Act88F, n = 8), Myosin Heavy Chain (MHC, n = 11), and Myosin light chain-2 (Mlc-2, n = 8) was measured by performing quantitative PCR on thorax cDNA from 5–7 day old Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR flies and compared to Mef2-Gal4>GFP controls. mRNA levels of Mef2-Gal4>GFP controls were set to 1.0 and mRNA levels of Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR animals were then normalized to their respective control. Values represent mean±SEM. *p<0.05 by One-way ANOVA with post hoc Tukey test.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0136504.g007: Mio is not necessary for normal expression of structural genes in adult fly muscle.Expression of Actin 88F (Act88F, n = 8), Myosin Heavy Chain (MHC, n = 11), and Myosin light chain-2 (Mlc-2, n = 8) was measured by performing quantitative PCR on thorax cDNA from 5–7 day old Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR flies and compared to Mef2-Gal4>GFP controls. mRNA levels of Mef2-Gal4>GFP controls were set to 1.0 and mRNA levels of Mef2-Gal4>MiodsRNA and Mef2-Gal4>Mio-IR animals were then normalized to their respective control. Values represent mean±SEM. *p<0.05 by One-way ANOVA with post hoc Tukey test.
Mentions: To test this hypothesis, we measured the mRNA levels of an indirect flight muscle-specific actin gene (Act88F), Myosin heavy chain (Mhc), and Myosin light chain-2 (Mlc-2), genes important for muscle development and assembly that when mutated cause a similar altered myofibril phenotype as seen in our Mio-deficient animals [21, 33–35]. Interestingly, no consistent differences in the expression of these genes were observed in Mio-RNAi adults (Fig 7). Together, these data suggest that Mio does not function to regulate the expression of genes required for myofibril assembly, but may be important for normal metabolic homeostasis of muscle cells throughout the life cycle of the animal.

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