Presenters

Soobin AnFollow

Academic department under which the project should be listed

CSM - Molecular and Cellular Biology

Faculty Sponsor Name

Anton Bryantsev

Abstract (300 words maximum)

Sarcopenia is a health condition in the elderly that is associated with degradation of muscle size, mass, and function. It can cause physical disability and, in extreme cases, death. The genetic aspect of sarcopenia is still not well understood. To shed light on sarcopenia mechanisms, we investigated muscle loss in aging fruit flies, Drosophila melanogaster. Our hypothesis was that aging-dependent muscle degradation can be affected by suboptimal functioning of the central nervous system (CNS). We used RNA interference and tissue-specific genetic drivers to induce a selective knockdown (KD) of the julius seizure gene (jus), which is associated with neurological phenotypes. Flies with CNS-specific jus KD (elav>jus KD) demonstrated seizures and paralysis after a brief mechanical stimulation (shaking). We have compared aged elav>jus KD flies, (with (+) and without (-) chronic shaking treatment), with genetically matched controls (elav>+, + /- shaking), as well as muscle-specific jus KD (Mef2>jus KD) flies. The muscle loss was evaluated by quantifying missing muscle fibers in the jump muscle. We found that all groups had some levels of spontaneous fiber loss with age. However, elav>jus KD flies (+/- shaking) had strikingly more lost fibers than control (elav>+, +/- shaking) or Mef2>jus KD flies. Surprisingly, chronic stimulation of seizures and paralysis by shaking was not a contributing factor to the exacerbated muscle loss in elav>jus KD flies. We conclude that even subtle, not apparently noticeable, abnormalities in the functioning of the CNS can stimulate aging-related muscle loss. Our results suggest that genetic causes of sarcopenia are likely to be associated with the genes associated with the CNS functioning.

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Neurological gene jus is associated with aging-related muscle loss in the fly model of sarcopenia.

Sarcopenia is a health condition in the elderly that is associated with degradation of muscle size, mass, and function. It can cause physical disability and, in extreme cases, death. The genetic aspect of sarcopenia is still not well understood. To shed light on sarcopenia mechanisms, we investigated muscle loss in aging fruit flies, Drosophila melanogaster. Our hypothesis was that aging-dependent muscle degradation can be affected by suboptimal functioning of the central nervous system (CNS). We used RNA interference and tissue-specific genetic drivers to induce a selective knockdown (KD) of the julius seizure gene (jus), which is associated with neurological phenotypes. Flies with CNS-specific jus KD (elav>jus KD) demonstrated seizures and paralysis after a brief mechanical stimulation (shaking). We have compared aged elav>jus KD flies, (with (+) and without (-) chronic shaking treatment), with genetically matched controls (elav>+, + /- shaking), as well as muscle-specific jus KD (Mef2>jus KD) flies. The muscle loss was evaluated by quantifying missing muscle fibers in the jump muscle. We found that all groups had some levels of spontaneous fiber loss with age. However, elav>jus KD flies (+/- shaking) had strikingly more lost fibers than control (elav>+, +/- shaking) or Mef2>jus KD flies. Surprisingly, chronic stimulation of seizures and paralysis by shaking was not a contributing factor to the exacerbated muscle loss in elav>jus KD flies. We conclude that even subtle, not apparently noticeable, abnormalities in the functioning of the CNS can stimulate aging-related muscle loss. Our results suggest that genetic causes of sarcopenia are likely to be associated with the genes associated with the CNS functioning.