KU70 and CAF-1 in Arabidopsis: Divergent roles in rDNA stability and telomere homeostasis

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Publikace nespadá pod Ekonomicko-správní fakultu, ale pod Středoevropský technologický institut. Oficiální stránka publikace je na webu muni.cz.
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ZÁVODNÍK Michal PAVLIŠTOVÁ Veronika MACHELOVÁ Adéla LYČKA Martin MOZGOVA Iva CAKLOVÁ Karolína DVOŘÁČKOVÁ Martina FAJKUS Jiří

Rok publikování 2024
Druh Článek v odborném periodiku
Časopis / Zdroj Plant Journal
Fakulta / Pracoviště MU

Středoevropský technologický institut

Citace
www https://onlinelibrary.wiley.com/doi/10.1111/tpj.16718
Doi http://dx.doi.org/10.1111/tpj.16718
Klíčová slova Arabidopsis thaliana; CAF-1; FAS1; ALT; KU70; telomeres; 45S rDNA; genome instability
Popis Deficiency in chromatin assembly factor-1 (CAF-1) in plants through dysfunction of its components, FASCIATA1 and 2 (FAS1, FAS2), leads to the specific and progressive loss of rDNA and telomere repeats in plants. This loss is attributed to defective repair mechanisms for the increased DNA breaks encountered during replication, a consequence of impaired replication-dependent chromatin assembly. In this study, we explore the role of KU70 in these processes. Our findings reveal that, although the rDNA copy number is reduced in ku70 mutants when compared with wild-type plants, it is not markedly affected by diverse KU70 status in fas1 mutants. This is consistent with our previous characterisation of rDNA loss in fas mutants as a consequence part of the single-strand annealing pathway of homology-dependent repair. In stark contrast to rDNA, KU70 dysfunction fully suppresses the loss of telomeres in fas1 plants and converts telomeres to their elongated and heterogeneous state typical for ku70 plants. We conclude that the alternative telomere lengthening pathway, known to be activated in the absence of KU70, overrides progressive telomere loss due to CAF-1 dysfunction.
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