ArticleGenetics2008
The telotype defines the telomere state in Saccharomyces cerevisiae and is inherited as a dominant non-Mendelian characteristic in cells lacking telomerase.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Global Gene Expression of Post-Senescent Telomerase-NegativeJournal of fungi (Basel, Switzerland) · 2023Article
- To Fix or Not to Fix: Maintenance of Chromosome Ends Versus Repair of DNA Double-Strand Breaks.Cells · 2022Review
- Aneuploidy as a mechanism of adaptation to telomerase insufficiency.Current genetics · 2016Article
- The telomerase reverse transcriptase subunit from the dimorphic fungus Ustilago maydis.PloS one · 2014Article
- Saccharomyces cerevisiae as a Model to Study Replicative Senescence Triggered by Telomere Shortening.Frontiers in oncology · 2013Article
- The telomere syndromes.Nature reviews. Genetics · 2012Review
- Reversibility of replicative senescence in Saccharomyces cerevisiae: effect of homologous recombination and cell cycle checkpoints.DNA repair · 2012Article
- Modulation of telomeres in alternative lengthening of telomeres type I like human cells by the expression of werner protein and telomerase.Journal of oncology · 2012Article
- Short telomeres are sufficient to cause the degenerative defects associated with aging.American journal of human genetics · 2009Article
- Telomere maintenance and survival in saccharomyces cerevisiae in the absence of telomerase and RAD52.Genetics · 2009Article
- Telomere recombination accelerates cellular aging in Saccharomyces cerevisiae.PLoS genetics · 2009Article
- Telomere heterogeneity: taking advantage of stochastic events.FEBS letters · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Telomeres are an unusual component of the genome because they do not encode genes, but their structure and cellular maintenance machinery (which we define as "telotype") are essential for chromosome stability. Cells can switch between different phenotypic states. One such example is when they switch from maintenance mediated by telomerase (TERT telotype) to one of the two alternative mechanisms of telomere preservation (ALT I and ALT II telotype). The nature of this switch is largely unknown. Reintroduction of telomerase into ALT II, but not ALT I, yeast led to the loss of their ability to survive a second round of telomerase withdrawal. Mating-based genetic analysis of ALT I and II revealed that both types of telomerase-independent telomere maintenance are inherited as a non-Mendelian trait dominant over senescence (SEN telotype). Additionally, inheritance of ALT I and ALT II did not depend on either the mitochondrial genome or a prion-based mechanism. Type I, but not type II, survivor cells exhibited impaired gene silencing, potentially connecting the switch to the ALT telotype epigenetic changes. These data provide evidence that nonprion epigenetic-like mechanisms confer flexibility on cells as a population to adjust to the life-threatening situation of telomerase loss, allowing cells to switch from TERT to ALT telotypes that can sustain viable populations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.