Download PDF by Michael Breitenbach, S. Michal Jazwinski, Peter Laun: Aging Research in Yeast
By Michael Breitenbach, S. Michal Jazwinski, Peter Laun
This quantity contains contributions by means of the prime specialists within the box of yeast getting older. Budding yeast (Saccharomyces cerevisiae) and different fungal organisms offer versions for getting older study which are suitable to organismic getting older and to the getting older tactics taking place within the human physique. Replicative getting older, during which purely the mum cellphone a while whereas the daughter mobile resets the clock to 0 is a version for the getting older of stem mobilephone populations in people, whereas chronological getting older (measured via survival in desk bound section) is a version for the getting older techniques in postmitotic cells (for example, neurons of the brain). such a lot mechanisms of getting older are studied in yeast. between them, this publication discusses: mitochondrial theories of getting older, emphasizing oxidative rigidity and retrograde responses; the function of autophagy and mitophagy; the connection of apoptosis to getting older methods; the position of uneven segregation of wear in replicative getting older; the position of replication pressure; and the function of the cytoskeleton in getting older. glossy tools of yeast genetics and genomics are defined that may be used to go looking for aging-specific capabilities in a genome-wide independent style. The similarities within the pathology of senescence (studied in yeast) and of melanoma cells, together with genome instability, are examined.
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Progression through the cell cycle is regulated by coordinated gene expression under the control of a small number of transcription regulators which are sequentially activated (Burhans and Heintz 2009). Different ROS lead to cell cycle arrest at different checkpoints, mostly at G1 or late S/G2. The response is through stress signalling and inhibition of gene expression that is required for cell cycle progression (Burhans and Heintz 2009). Treatment with H2 O2 leads to cell cycle arrest in G2 and this is dependent on the Rad9p-dependent DNA damage checkpoint pathway (Flattery-O’Brien and Dawes 1998).
Similar adaptation to H2 O2 also occurs when anaerobically grown cells are exposed to oxygen for a short time (Beckhouse et al. 2008). Although inhibition of glutathione metabolism has been reported to reduce adaptation, we have not found loss of adaptation in the mutants that are unable to synthesise glutathione. Yap1p and Yap2p were shown to play a role in adaptation to H2 O2 but not to O•− 2 in a previous study (Stephen et al. 1995). The critical role of Yap1p and of NADPH generation systems could indicate that adaptation is due to mainly to activation of Yap1p, and that it is maintained in the cell as long as Yap1p remains activated after an initial oxidative insult.
2000). The phosphorylated Msn2/4p transcription factors are localized in the cytoplasm during optimal growth conditions (Beck and Hall 1999; Gorner et al. 1998). Under stress conditions, they are imported into the nucleus and the nuclear export is dependent on the Msn5p nuclear export factor (Durchschlag et al. 2004). Although it is still a puzzle how the oxidative stress signal is received and triggers the nucelo-cytoplasmic trafficking of Msn2/4, it has been shown that both cytoplasmic thioredoxins, Trx1p and Trx2p, are essential for nuclear accumulation of Msn2/4 under H2 O2 treatment and the oxidised thioredoxins are essential for signaling the presence of H2 O2 (Boisnard et al.
Aging Research in Yeast by Michael Breitenbach, S. Michal Jazwinski, Peter Laun