Profiling the compendium of changes in Saccharomyces cerevisiae due to mutations that alter availability of the main methyl donor S-Adenosylmethionine.

The SAM1 and SAM2 genes encode for S-Adenosylmethionine (AdoMet) synthetase enzymes, with AdoMet serving as the main cellular methyl donor. We have previously shown that independent deletion of these genes alters chromosome stability and AdoMet concentrations in opposite ways in Saccharomyces cerevisiae. To characterize other changes occurring in these mutants, we grew wildtype, sam1Δ/sam1Δ, and sam2Δ/sam2Δ strains in 15 different Phenotypic Microarray plates with different components and measured growth variations.

Profiling The Compendium Of Changes In Due To Mutations That Alter Availability Of The Main Methyl Donor S-Adenosylmethionine.

The and genes encode for S-AdenosylMethionine (AdoMet) synthetase enzymes, with AdoMet serving as the main methyl donor. We have previously shown that independent deletion of these genes alters chromosome stability and AdoMet concentrations in opposite ways in To characterize other changes occurring in these mutants, we grew wildtype, and strains in 15 different Phenotypic Microarray plates with different components, equal to 1440 wells, and measured for growth variations. RNA-Sequencing was also carried out on these strains and differential gene expression determined for each mutant.

Heterozygous Mutations in Aromatic Amino Acid Synthesis Genes Trigger TOR Pathway Activation in .

The highly conserved complexes of Target of Rapamycin (TORC1 and TORC2) are central regulators to many vital cellular processes including growth and autophagy in response to nutrient availability. Previous research has extensively elucidated exogenous nutrient control on TORC1/TORC2; however, little is known about the potential alteration of nutrient pools from mutations in biosynthesis pathways and their impact on Tor pathway activity. Here, we analyze the impacts of heterozygous mutations in aromatic amino acid biosynthesis genes on TOR signaling via differential expression of genes downstream of TORC1 and autophagy induction for TORC1 and TORC2 activity.