PFK2 deletion in S. cerevisiae shifts central carbon metabolism away from fermentation and toward respiration and biosynthesis. The abstract reports stronger physiological and flux changes for pfk2Δ than for pfk1Δ.
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PFK2 deletion in Saccharomyces cerevisiae
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PFK2 deletion, pfk2Δ strain
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In Saccharomyces cerevisiae, PFK2 deletion causes more severe central carbon metabolism defects than PFK1 deletion.
The pfk2Δ strain exhibited more severe defects than pfk1Δ.
Flux balance analysis indicates that PFK2 deletion increases carbon flux to the TCA cycle and elevates respiration-associated carbon flux relative to PFK1 deletion.
Flux balance analysis (FBA) revealed a markedly increased carbon flux to the tricarboxylic acid cycle (TCA) in the pfk2Δ strain, with respiration-associated carbon flux elevated 1.5-fold compared to the pfk1Δ strain.
PFK2 deletion reduces maximum specific growth rate more strongly than PFK1 deletion in Saccharomyces cerevisiae.
Its maximum specific growth rate was reduced by approximately 54 % in pfk2Δ and by about 15 % in pfk1Δ, both relative to the reference strain.
Both PFK1 and PFK2 deletion increase acetate accumulation in Saccharomyces cerevisiae, with a larger increase in pfk2Δ.
Both deletion strains accumulated higher acetate levels compared to the reference strain, increasing by 25.4 % in the pfk1Δ strain and 82 % in the pfk2Δ strain.
PFK2 deletion decreases ethanol production more strongly than PFK1 deletion in Saccharomyces cerevisiae.
Ethanol production decreased by 36 % and 82 % in pfk1Δ strain and pfk2Δ strain, respectively, relative to the reference strain.
PFK2 deletion enhances acetyl-CoA-derived product formation and increases free fatty acid titer in Saccharomyces cerevisiae.
Deletion of PFK2 enhanced acetyl-CoA-derived product formation, with free fatty acid (FFA) titers increasing from 412 mg L^-1 to 517 mg L^-1 (a 33.3 % increase).
PFK2 functions as a key regulatory node that redirects carbon flux from fermentation toward respiration and biosynthesis in Saccharomyces cerevisiae.
These findings establish PFK2 as a key regulatory node redirecting carbon flux from fermentation toward respiration and biosynthesis.
Transcriptomic profiling shows upregulation of respiration-related genes in the PFK2 deletion strain relative to the reference strain.
Transcriptomic profiling showed significant upregulation of respiration-related genes in the pfk2Δ strain compared to the reference strain.