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Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
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ACSS2 involved in acetyl-CoA synthesis regulates skeletal muscle function.

Mekala Gunasekaran1, Gloriana Campos1, Natalya M Wells1

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Acyl-coenzyme A synthetase short-chain family member-2 (ACSS2) is crucial for skeletal muscle function. Its deficiency in mice and flies leads to muscle atrophy, metabolic issues, and impaired motor function, highlighting its role in muscle health.

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ACSS2cholesterol metabolismmuscle development

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Acyl-coenzyme A synthetase short-chain family member-2 (ACSS2) converts acetate to acetyl-CoA, impacting cholesterol metabolism.
  • Cholesterol metabolism is increasingly linked to skeletal muscle function and disease.
  • Muscular dystrophy has been associated with HMGCR, a key enzyme in cholesterol synthesis.

Purpose of the Study:

  • To investigate the role of ACSS2 in skeletal muscle function.
  • To explore the consequences of ACSS2 deficiency in mouse and fly models.

Main Methods:

  • Studied Acss2 knockout mice (Acss2-/-) and AcCoA knockdown in Drosophila.
  • Analyzed skeletal muscle morphology, lipid accumulation, NADH levels, and myoblast differentiation in mice.
  • Assessed exercise-induced fatigue in mice, including effects of ATP-citrate lyase (ACLY) inhibition.
  • Evaluated body size and locomotor activity in Drosophila.

Main Results:

  • Acss2-/- mice exhibited skeletal muscle atrophy, lipid accumulation, and reduced NADH levels.
  • Myoblasts from Acss2-/- mice showed precocious differentiation.
  • Acss2-/- mice experienced exercise-induced fatigue, worsened by ACLY inhibition.
  • AcCoA knockdown in flies resulted in reduced body size and locomotor defects.

Conclusions:

  • ACSS2 is vital for maintaining skeletal muscle morphology, metabolism, and function.
  • ACSS2 deficiency leads to significant muscle defects and motor impairments.
  • ACSS2 warrants further investigation as a potential factor in muscle diseases linked to cholesterol metabolism.