Excerpt 1): “Our findings have challenged the notion of the aggregation process as a passive consequence of accumulating misfolded proteins,” says Stowers Investigator Rong Li, Ph.D., who led the study. Using budding yeast Saccharomyces cerevisae, a frequently used laboratory model in aging research, Stowers scientists experimentally used heat and other forms of stress to induce misfolded proteins to clump together.”
My comment: Saccharomyces cerevisae is one of the model organisms that links nutrient-dependent cell type differention to pheromone-controlled behavior via the RNA-mediated events we detailed in the context of molecular genetics in our 1996 review: From Fertilization to Adult Sexual Behavior “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).”
Since then, other serious scientists have detailed how thermodynamic cycles of protein biosynthesis and degradation are epigenetically effected. The epigenetic landscape has been repeatedly linked to the physical landscape of DNA in the organized genomes of species from yeasts to primates via RNA-mediated amino acid substitutions that differentiate cell types. Evolutionary theorists, however, still claim that misfolded proteins link mutations to natural selection and the evolution of biodiversity.
Excerpt 2): “Proteins that fail to fold correctly cannot perform their biological functions and are potentially toxic to cells.”
My comment: It does not matter where the potentially toxic proteins are found, mutations are not beneficial. What these researchers now show is that 1) protein aggregation is regulated and 2) it requires active translation. Also, 3) the potentially toxic proteins are not typically transferred to progeny.
Excerpt 3): Li and her colleagues also determined that the association of aggregates with mitochondria gradually declines in the mother budding yeast cells with advanced replicative age, likely contributing to their diminished ability to rejuvenate through asymmetric cell division.
My comment: This links the nutrient-dependent pheromone-controlled misfolded proteins to reproductive senescence, which extends across species to human female reproductive senescence via the conserved molecular mechanisms of epigenetically-effected cell type differentiation in species from microbes to man.