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

Author:

Závodník Michal12ORCID,Pavlištová Veronika13,Machelová Adéla13,Lyčka Martin13,Mozgová Iva45ORCID,Caklová Karolína3,Dvořáčková Martina13ORCID,Fajkus Jiří123ORCID

Affiliation:

1. Mendel Centre for Plant Genomics and Proteomics, CEITEC Masaryk University Brno CZ‐62500 Czech Republic

2. Department of Cell Biology and Radiobiology Institute of Biophysics of the Czech Academy of Sciences, v.v.i. Brno CZ‐61265 Czech Republic

3. Laboratory of Functional Genomics and Proteomics, NCBR, Faculty of Science Masaryk University Brno CZ‐61137 Czech Republic

4. Biology Centre, Czech Academy of Sciences, Institute of Plant Molecular Biology České Budějovice Czech Republic

5. University of South Bohemia Faculty of Science České Budějovice Czech Republic

Abstract

SUMMARYDeficiency 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.

Funder

Grantová Agentura České Republiky

Publisher

Wiley

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