Abstract
Yeast colony population passes through several developmental phases. Relatively young but already chronologically ageing colonies start to starve and become stressed.
Specific signals and pathways then contribute to development of two major populations of U (in upper layers) and L (in lower layers) cells (Mol Cell 46:436, 2012). Stress resistant U cells enhance longevity by activating of unique metabolism controlled by unusual combination of regulatory pathways (e.g.
TOR and GCN4), reducing respiration and activating autophagy. Starving L cells deepen the stressed phenotype of their ancestors and activate degradative mechanisms that could release amino acids and sugars.
These compounds can serve to U cells as nutrients together with nutrients provided by autophagy and those from cells undergoing PCD (J Cell Biol 169:711, 2005). Characteristics of both cell-types indicate an existence of nutrient flow (with glutamine and ammonia as the most important players) in favor of feeding of U cells at the expense of L cells.
This nutrient flow together with other yeast cell characteristics resembles metabolic exchange identified in tumor affected organism, implying a parallel between U cells and tumor cells and between L cells and other mammalian cells manifesting cachexia