S. cerevisiae has been highly studied as a model organism to better understand aging for more than five decades and has contributed to the identification of more mammalian genes affecting aging than any other model organism. Some of the topics studied using yeast are calorie restriction, as well as in genes and cellular pathways involved in senescence. The two most common methods of measuring aging in yeast are Replicative Life Span, which measures the number of times a cell divides, and Chronological Life Span, which measures how long a cell can survive in a non-dividing stasis state. Limiting the amount of glucose or amino acids in the growth medium has been shown to increase RLS and CLS in yeast as well as other organisms. At first, this was thought to increase RLS by up-regulating the sir2 enzyme, however it was later discovered that this effect is independent of sir2. Over-expression of the genes sir2 and fob1 has been shown to increase RLS by preventing the accumulation of extrachromosomal rDNA circles, which are thought to be one of the causes of senescence in yeast. The effects of dietary restriction may be the result of a decreased signaling in the TOR cellular pathway. This pathway modulates the cell's response to nutrients, and mutations that decrease TOR activity were found to increase CLS and RLS. This has also been shown to be the case in other animals. A yeast mutant lacking the genes sch9 and ras2 has recently been shown to have a tenfold increase in chronological lifespan under conditions of calorie restriction and is the largest increase achieved in any organism.