ArticleChromosoma2013
A telomerase-independent component of telomere loss in chromatin assembly factor 1 mutants of Arabidopsis thaliana.
Article in Chromosoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Telomerase Interaction Partners-Insight from Plants.International journal of molecular sciences · 2021Article
- G2/M-checkpoint activation in fasciata1 rescues an aberrant S-phase checkpoint but causes genome instability.Plant physiology · 2021Article
- Nuclear Chaperone ASF1 is Required for Gametogenesis in Arabidopsis thaliana.Scientific reports · 2019Article
- The Absence of the Arabidopsis Chaperone Complex CAF-1 Produces Mitotic Chromosome Abnormalities and Changes in the Expression Profiles of Genes Involved in DNA Repair.Frontiers in plant science · 2017Article
- Telomere dynamics in the lower plant Physcomitrella patens.Plant molecular biology · 2015Article
- Homology-dependent repair is involved in 45S rDNA loss in plant CAF-1 mutants.The Plant journal : for cell and molecular biology · 2015Article
- Compromised telomere maintenance in hypomethylated Arabidopsis thaliana plants.Nucleic acids research · 2014Article
- Looking at plant cell cycle from the chromatin window.Frontiers in plant science · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunction of chromatin assembly factor 1 in FASCIATA mutants (fas) of Arabidopsis thaliana results in progressive loss of telomeric DNA. Although replicative telomere shortening is typically associated with incomplete resynthesis of their ends by telomerase, no change in telomerase activity could be detected in vitro in extracts from fas mutants. Besides a possible telomerase malfunction, the telomere shortening in fas mutants could presumably be due to problems with conventional replication of telomeres. To distinguish between the possible contribution of suboptimal function of telomerase in fas mutants under in vivo conditions and problems in conventional telomere replication, we crossed fas and tert (telomerase reverse transcriptase) knockout mutants and analyzed telomere shortening in segregated fas mutants, tert mutants, and double fas tert mutants in parallel. We demonstrate that fas tert knockouts show greater replicative telomere shortening than that observed even in the complete absence of telomerase (tert mutants). While the effect of tert and fas mutations on telomere lengths in double mutants is additive, manifestations of telomere dysfunction in double fas tert mutants (frequency of anaphase bridges, onset of chromosome end fusions, and common involvement of 45S rDNA in chromosome fusion sites) are similar to those in tert mutants. We conclude that in addition to possible impairment of telomerase action, a further mechanism contributes to telomere shortening in fas mutants.
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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.