Editors' ChoiceMicrobiology

Bacteria stop fermentation with lactic acid

Sci. Signal.  06 Dec 2016:
Vol. 9, Issue 457, pp. ec288
DOI: 10.1126/scisignal.aal5141

Many species of yeast favor glucose so strongly as a carbon source that even trace amounts of glucose in their growth medium suppresses their ability to use other carbon sources, a phenotype called glucose-associated repression. A prion-mediated response referred to as [GAR+] enables yeast to use nonfermentable carbon sources, such as glycerol, in the presence of glucose. This prion-based metabolic switch may be a mechanism by which bacterial contamination stalls fermentation of wines and beers. Garcia et al. found that bacterially produced lactic acid triggers the [GAR+] phenotype. The presence of sterile conditioned medium from cultures of the [GAR+]-inducing bacteria Staphylococcus gallinarum and Listeria innocua enabled the yeast Saccharomyces cerevisiae to grow on medium containing glycerol and glucosamine (GLY+GlcN), a medium that mimics conditions in which trace amounts of glucose suppress glycerol metabolism. The active fractions of the bacteria-conditioned media contained high concentrations of lactic acid, and addition of either the L- or D- isomer of lactic acid enabled yeast to grow on GLY+GlcN media. After crossing yeast that had been induced by lactic acid to grow on GLY+GlcN with naïve yeast, offspring were assayed for the [GAR+] phenotype in the absence of lactic acid. They showed a pattern of inheritance of growth on GLY+GlcN consistent with prion inheritance, and the ability to grow on the medium persisted stably over at least 75 generations. [GAR+] depends on the chaperone heat shock protein 70 (Hsp70), and transformation of lactic-acid induced yeast cells growing on GLY+GlcN with a plasmid containing a dominant-negative variant of hsp70 resulted in the strains that could not grow on GLY+GlcN even after they had lost the plasmid. Yeast strains with deleted JEN1, a transporter involved in active transport of lactic acid, or deleted genes encoding lactic acid dehydrogenases and transhydrogenases could still be induced with lactic acid to grow on GLY+GlcN. However, deletion of SOK2, which encodes a transcription factor required for passive transport of lactic acid, resulted in yeast that did not grow on GLY+GlcN in the presence of lactic acid. Because many bacteria produce lactic acid and reversal of glucose-associated repression also occurred in response to lactic acid in the divergent yeast Dekkera bruxellensis, these results suggested that lactic acid may be a conserved mechanism of bacterial-to-eukaryote signaling. However, Tuite notes that not all lactic acid–producing bacteria induce the [GAR+] phenotype in S. cerevisiae, that not all [GAR+] inducers are known to produce lactic acid, and that certain strains of bacteria induce the phenotype in S. cerevisiae but not D. bruxellensis, suggesting that additional species-specific factors may govern this type of interaction in nature.

D. M. Garcia, D. Dietrich, J. Clardy, D. F. Jarosz, A common bacterial metabolite elicits prion-based bypass of glucose repression. eLife 5, e17978 (2016). [Online Journal]

M. F. Tuite, An acid tale of prion formation. eLife 5, e22256 (2016). [PubMed]

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