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Gametogenesis eliminates age-induced cellular damage and resets life span in yeast.
Science. 2011 Jun 24; 332(6037):1554-7
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30 Jun 2011
New Finding
DOI: 10.3410/f.11636958.12697056
This paper provides a clear answer to a logical gap.
Cells from yeast to humans have a replicative life span, and each cell can divide a limited number of times before dying or entering a quiescent state. Yet newborn cells must have somehow reset this replicative life span, otherwise you should have...Continue reading
Cells from yeast to humans have a replicative life span, and each cell can divide a limited number of times before dying or entering a quiescent state. Yet newborn cells must have somehow reset this replicative life span, otherwise you should have...Continue reading
This paper provides a clear answer to a logical gap.
Cells from yeast to humans have a replicative life span, and each cell can divide a limited number of times before dying or entering a quiescent state. Yet newborn cells must have somehow reset this replicative life span, otherwise you should have been born as old as your mother, in essence. In this paper, the authors show that aged yeast cells can reset their age during sporulation (gametogenesis) and further show that the resetting requires IMRE1 and NDT80 genes. Strikingly, transient expression of NDT80 without the gametogenesis process is sufficient to reset the life span. While this certainly provides a big hope that one might be able to manipulate the age of cells, this work also leaves a fascinating philosophical question: if cells have a capability to reset their age, why do they age in the first place?
Cells from yeast to humans have a replicative life span, and each cell can divide a limited number of times before dying or entering a quiescent state. Yet newborn cells must have somehow reset this replicative life span, otherwise you should have been born as old as your mother, in essence. In this paper, the authors show that aged yeast cells can reset their age during sporulation (gametogenesis) and further show that the resetting requires IMRE1 and NDT80 genes. Strikingly, transient expression of NDT80 without the gametogenesis process is sufficient to reset the life span. While this certainly provides a big hope that one might be able to manipulate the age of cells, this work also leaves a fascinating philosophical question: if cells have a capability to reset their age, why do they age in the first place?
Disclosures
None declared
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Yamashita Y: F1000Prime Recommendation of [Unal E et al., Science 2011, 332(6037):1554-7]. In F1000Prime, 30 Jun 2011; DOI: 10.3410/f.11636958.12697056. F1000Prime.com/11636958#eval12697056
01 Jul 2011
New Finding
DOI: 10.3410/f.11636958.12723055
The authors used clever single-cell micromanipulations to show that replicative life span in yeast is reset after gametogenesis through sporulation, in a manner dependent on the transcription factor NDT80. Surprisingly, transient over-expression of NDT80 extended lifespan in both old and young actively...Continue reading
The authors used clever single-cell micromanipulations to show that replicative life span in yeast is reset after gametogenesis through sporulation, in a manner dependent on the transcription factor NDT80. Surprisingly, transient over-expression of NDT80 extended lifespan in both old and young actively growing cells, although not all markers of aging were cleared.
The results raise important insights into which features of aging are causal and set the stage for future studies to pin down the precise role of NDT80 and its targets in lifespan extension.
The results raise important insights into which features of aging are causal and set the stage for future studies to pin down the precise role of NDT80 and its targets in lifespan extension.
Disclosures
None declared
Gasch A: F1000Prime Recommendation of [Unal E et al., Science 2011, 332(6037):1554-7]. In F1000Prime, 01 Jul 2011; DOI: 10.3410/f.11636958.12723055. F1000Prime.com/11636958#eval12723055
09 Sep 2011
New Finding, Novel Drug Target
DOI: 10.3410/f.11636958.14452055
This work of the laboratory of Angelika Amon at MIT (Cambridge, Massachusetts, USA) demonstrates that age-induced cellular damage can be repaired and that rejuvenation is possible by inducing the expression of a transcription factor required for gametogenesis.
All eukaryotic organisms age but, by unknown...Continue reading
All eukaryotic organisms age but, by unknown...Continue reading
This work of the laboratory of Angelika Amon at MIT (Cambridge, Massachusetts, USA) demonstrates that age-induced cellular damage can be repaired and that rejuvenation is possible by inducing the expression of a transcription factor required for gametogenesis.
All eukaryotic organisms age but, by unknown mechanisms, age-induced changes are not transmitted to the progeny. By using the yeast model system, Amon and coworkers show that resetting of replicative life span (number of cell divisions) occurs during gametogenesis (meiosis, sporulation in yeast) and is associated with elimination of aberrant (fragmented) nucleolar structures. Transient expression in vegetative cells of NDT80, a gene required for sporulation encoding a p53-like transcription factor, leads to extension of life span in both aged and young cells.
These results constitute an important step towards the dream of increasing human longevity. The utilization of transcription factors required for gametogenesis is a novel strategy that could complement telomerase-based approaches {1}. The molecular mechanisms involved in aging and rejuvenation, however, remain unknown and at this stage scientists are like a sorcerer's apprentice tackling one of the most important secrets of life without help from the Holy Grail.
All eukaryotic organisms age but, by unknown mechanisms, age-induced changes are not transmitted to the progeny. By using the yeast model system, Amon and coworkers show that resetting of replicative life span (number of cell divisions) occurs during gametogenesis (meiosis, sporulation in yeast) and is associated with elimination of aberrant (fragmented) nucleolar structures. Transient expression in vegetative cells of NDT80, a gene required for sporulation encoding a p53-like transcription factor, leads to extension of life span in both aged and young cells.
These results constitute an important step towards the dream of increasing human longevity. The utilization of transcription factors required for gametogenesis is a novel strategy that could complement telomerase-based approaches {1}. The molecular mechanisms involved in aging and rejuvenation, however, remain unknown and at this stage scientists are like a sorcerer's apprentice tackling one of the most important secrets of life without help from the Holy Grail.
References
1.
Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.
Nature 2011 Jan 6; 7328(469):102-6
PMID: 21113150
Disclosures
None declared
Serrano R: F1000Prime Recommendation of [Unal E et al., Science 2011, 332(6037):1554-7]. In F1000Prime, 09 Sep 2011; DOI: 10.3410/f.11636958.14452055. F1000Prime.com/11636958#eval14452055
18 Oct 2011
New Finding
DOI: 10.3410/f.11636958.14725133
This is a conceptually simple paper with striking results that raise fascinating questions and new avenues of research. I very much agree with the previous evaluators (Ramon Serrano, Audrey Gasch, and Yukiko Yamashita)...Continue reading
This is a conceptually simple paper with striking results that raise fascinating questions and new avenues of research. I very much agree with the previous evaluators (Ramon Serrano, Audrey Gasch, and Yukiko Yamashita) that this is a 'must read' paper.
Disclosures
None declared
Bahler J: F1000Prime Recommendation of [Unal E et al., Science 2011, 332(6037):1554-7]. In F1000Prime, 18 Oct 2011; DOI: 10.3410/f.11636958.14725133. F1000Prime.com/11636958#eval14725133
F1000Prime Recommendations, Dissents and Comments for [Unal E et al., Science 2011, 332(6037):1554-7]. In F1000Prime, 25 May 2013; F1000Prime.com/11636958
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Eukaryotic organisms age, yet detrimental age-associated traits are not passed on to progeny. How life span is reset from one generation to the next is not known. We show that in budding yeast resetting of life span occurs during gametogenesis. Gametes (spores) generated by aged cells show the same replicative potential as gametes generated by young cells. Age-associated damage is no longer detectable in mature gametes. Furthermore, transient induction of a transcription factor essential for later stages of gametogenesis extends the replicative life span of aged cells. Our results indicate that gamete formation brings about rejuvenation by eliminating age-induced cellular damage.
PMID: 21700873
