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.
Spirogyra sp. Link was found to be parasitized by filamentous fungi tentatively identified as Saprolegnia asterophora de Bary and Pythium gracile Schenk, in field samples and when maintained in unaltered pond water in an 18 h fluorescent light–6 h dark regime at 18 ± 2°C. Collections were made periodically between March 1978, and November 1979, from a pond in Mill Seek Sanctuary near Oyster Bay, Nassau Co., Long Island, New York. Initially, less than 1% of the total field population of Spirogyra sp. was infected by either fungal parasite with Saprolegnia asterophora being the dominant parasite present generally alone in most samples or present in 80–95% of the total number of infected algal filaments when occurring concurrently with P. gracile. However, in the laboratory, approximately 100% of the Spirogyra sp. filaments in any given sample became infected by Saprolegnia asterophora and/or P. gracile within a 1—2 wk and 3–4 wk period, respectively, with vegetative hyphae involved in the spread of infection to neighboring algal filaments. Infection of algal filaments occurred at random points with cell to cell hyphal extension within the filament causing disruption of host cells. Development of S. asterophora, and possibly P. gracile, sexual reproductive structures was common in relation with the host with asexual sporangial production not observed. Saprolegnia asterophora and P. gracile were cultured on glucose, yeast extract, malt extract (GYM) medium from infected Spirogyra sp. filaments, with infection of healthy algal filaments using these cultures by Saprolegnia asterophora, but not by P. gracile, induced in the laboratory. Growth responses and tropic responses of the fungi to the algal host could not be demonstrated.
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