Fig. 8: Other autophagy-deficient mutants are also defective in assimilating aspartate into macromolecules under nitrogen starvation.
a Schematic of the experimental design. b Estimation of intracellular aspartate concentration. Three independent replicates. c Uptake of [U-14C]-aspartate. Seven independent replicates for WT and atg1Δ, and eight for atg8Δ and pep4Δprb1Δ. d Incorporation of equivalents of [U-14C]-aspartate (aspartate and its derivatives) into macromolecules. Five independent replicates for WT and atg1Δ, and six for atg8Δ and pep4Δprb1Δ. e Incorporation of total aspartate equivalents into macromolecules. Five independent replicates for WT and atg1Δ, and six for atg8Δ and pep4Δprb1Δ. f Incorporation of equivalents of [U-14C]-aspartate into proteins. Five independent replicates for WT and atg1Δ, and six for atg8Δ and pep4Δprb1Δ. g Incorporation of total aspartate equivalents into proteins. Five independent replicates for WT and atg1Δ, and six for atg8Δ and pep4Δprb1Δ. h Incorporation of equivalents of [U-14C]-aspartate into nucleic acids. Two independent replicates. i Incorporation of total aspartate equivalents into nucleic acids. Two independent replicates. P values were calculated using unpaired two-sided Student’s t test assuming equal variances. Data are presented as mean ± standard deviation for b–g and mean only for h and i.
