Yeast (Saccharomyces Cerevisiae): Difference between revisions

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 * As a eukaryote, ''S.&nbsp;cerevisiae'' shares the complex internal cell structure of plants and animals without the high percentage of non-coding DNA that can confound research in higher eukaryotes.
 * ''S.&nbsp;cerevisiae'' research is a strong economic driver, at least initially, as a result of its established use in industry.
+===In the study of aging===
+For more than five decades ''S. cerevisiae'' has been studied as a model organism to better understand aging and has contributed to the identification of more mammalian genes affecting aging than any other model organism.<ref name="Replicative">{{cite journal | vauthors = Longo VD, Shadel GS, Kaeberlein M, Kennedy B | title = Replicative and chronological aging in Saccharomyces cerevisiae | journal = Cell Metab. | volume = 16 | issue = 1 | pages = 18–31 | year = 2012 | pmid = 22768836 | pmc = 3392685 | doi = 10.1016/j.cmet.2012.06.002 }}</ref> 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 (RLS), which measures the number of times a cell divides, and Chronological Life Span (CLS), which measures how long a cell can survive in a non-dividing stasis state.<ref name="Replicative" /> 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.<ref name="Recent">{{cite journal | vauthors = Kaeberlein M, Burtner CR, Kennedy BK | title = Recent developments in yeast aging | journal = PLOS Genet. | volume = 3 | issue = 5 | pages = 655–60 | year = 2007 | pmid = 17530929 | pmc = 1877880 | doi = 10.1371/journal.pgen.0030084 | doi-access = free }}</ref> 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 circle]]s, which are thought to be one of the causes of senescence in yeast.<ref name="Recent" /> The effects of dietary restriction may be the result of a decreased signaling in the TOR cellular pathway.<ref name="Replicative" /> This pathway modulates the cell's response to nutrients, and mutations that decrease TOR activity were found to increase CLS and RLS.<ref name="Replicative" /><ref name="Recent" /> This has also been shown to be the case in other animals.<ref name="Replicative" /><ref name="Recent" /> A yeast mutant lacking the genes {{visible anchor|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.<ref>{{cite journal | vauthors = Wei M, Fabrizio P, Hu J, Ge H, Cheng C, Li L, Longo VD | title = Life span extension by calorie restriction depends on Rim15 and transcription factors downstream of Ras/PKA, Tor, and Sch9 | journal = PLOS Genet. | volume = 4 | issue = 1 | pages = 139–49 | year = 2008 | pmid = 18225956 | pmc = 2213705 | doi = 10.1371/journal.pgen.0040013 | doi-access = free }}</ref><ref>{{cite web |title=10-Fold Life Span Extension Reported |url=http://www.usc.edu/uscnews/stories/14716.html |publisher=University of Southern California |url-status=dead |archive-url=https://web.archive.org/web/20160304070340/http://www.usc.edu/uscnews/stories/14716.html |archive-date=2016-03-04}}</ref>
+Mother cells give rise to progeny buds by mitotic divisions, but undergo replicative [[Ageing|aging]] over successive generations and ultimately die. However, when a mother cell undergoes [[meiosis]] and [[gametogenesis]], [[Maximum life span|lifespan]] is reset.<ref>{{cite journal | vauthors = Unal E, Kinde B, Amon A | title = Gametogenesis eliminates age-induced cellular damage and resets life span in yeast | journal = Science | volume = 332 | issue = 6037 | pages = 1554–57 | year = 2011 | pmid = 21700873 | pmc = 3923466 | doi = 10.1126/science.1204349 | bibcode = 2011Sci...332.1554U }}</ref> The replicative potential of [[gametes]] ([[spores]]) formed by aged cells is the same as gametes formed by young cells, indicating that age-associated damage is removed by meiosis from aged mother cells. This observation suggests that during meiosis removal of age-associated damages leads to [[Rejuvenation (aging)|rejuvenation]]. However, the nature of these damages remains to be established.
+During starvation of non-replicating ''S. cerevisiae'' cells, [[reactive oxygen species]] increase leading to the accumulation of [[DNA oxidation|DNA damages]] such as apurinic/apyrimidinic sites and double-strand breaks.<ref name="pmid20223252">{{cite journal |vauthors=Steinboeck F, Hubmann M, Bogusch A, Dorninger P, Lengheimer T, Heidenreich E |title=The relevance of oxidative stress and cytotoxic DNA lesions for spontaneous mutagenesis in non-replicating yeast cells |journal=Mutat. Res. |volume=688 |issue=1–2 |pages=47–52 |date=June 2010 |pmid=20223252 |doi=10.1016/j.mrfmmm.2010.03.006}}</ref>  Also in non-replicating cells the ability to [[DNA repair|repair]] endogenous double-strand breaks declines during chronological [[ageing|aging]].<ref name="pmid30410502">{{cite journal |vauthors=Pongpanich M, Patchsung M, Mutirangura A |title=Pathologic Replication-Independent Endogenous DNA Double-Strand Breaks Repair Defect in Chronological Aging Yeast |journal=Front Genet |volume=9 |pages=501 |date=2018 |pmid=30410502 |pmc=6209823 |doi=10.3389/fgene.2018.00501|doi-access=free }}</ref>
 == See Also ==