A comprehensive mapping of the proteome and transcriptome during the complete replicative lifespan of budding yeast predicted an increased abundance of the protein biogenesis machinery is most causal for aging.
The major cytosolic yeast peroxiredoxin Tsa1 controls aging and H2O2-resistance by inhibiting protein kinase A through a conserved cysteine in the catalytic subunit activation loop and not by scavenging H2O2.
By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.
In mitotically aging yeast cells, the cytosol acidifies, the distances between the organellar membranes decrease dramatically, but crowding on the scale of the average size protein is relatively stable.
Biochemical tags can be easily knocked into endogenous genes in mammalian stem cells using optimised and scalable protocols that will enable annotation of protein levels, localisation and interaction partners.