Abstract
A FAS solution to a DEAD case.
Highlights
They traced the problem to a failure to degrade the mRNA of pdh, encoding pyruvate dehydrogenase (PDH), which in aerobic conditions produces acetyl-CoA, a hub metabolite and FASII precursor (Fig 1). pdh mRNA accumulated in the cshA mutant compared to wild type (WT), reasonably predicting that acetyl-CoA pools were increased
Acetyl-CoA competes with branched-chain acyl-CoA, the precursors for branchedchain fatty acids (BCFA), which fluidify membranes [4]. This SCFA to BCFA ratio is critical to membrane fluidity
Less PDH in tested suppressor mutants restored this ratio to that of the WT, so that the membrane would regain fluidity. This highly documented study identifies pdh mRNA as the essential degradosome target for cold survival, and highlights the intimate connection between membrane state and central metabolism via acetyl-CoA
Summary
Citation: Gruss A (2020) A FAS solution to a DEAD case. PLoS Genet 16(7): e1008842. https://doi.org/ 10.1371/journal.pgen.1008842 Editor: Carmen Buchreiser, French National Centre for Scientific Research, FRANCE Funding: Work in AG group is supported by funding from the Fondation pour la Recherche Medicale (DBF20161136769) and the French Agence Nationale de la Recherche (StaphEscape project ANR-13001038). Competing interests: The author has declared that no competing interests exist.
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