The <scp>DNA</scp> helicase <scp>RTEL1</scp> is involved in the repair of replicative <scp>DNA</scp> damage independently of the alternative end joining and the <scp>DNA</scp> –protein cross‐link repair pathways in <i>Arabidopsis</i>
Recent studies indicate that the Fe-S DNA helicase RTEL1 plays an important role in replicative DNA repair in plants. Since non-homologous end joining (NHEJ) and DNA-protein cross-link (DPC) repair also protect DNA replication in Arabidopsis, we set out to further define the interactions of RTEL1 and these pathways by analyzing double mutants. Plants with simultaneous defects in the alternative NHEJ factor POLQ and RTEL1 were severely restricted in growth and fertility. While both single mutants showed mitotic anaphase chromosome fragmentation at low frequencies, the simultaneous loss of both factors aggravated the effect by an order of magnitude. In contrast, simultaneous knockout of the classical NHEJ factor KU70 and RTEL1 hardly hampered proliferation and did not lead to any enhancement in chromosome fragmentation. This finding indicates that RTEL1 acts in a parallel pathway to the alternative NHEJ but not classical NHEJ in repairing aberrant replication intermediates. Simultaneous loss of RTEL1 and the protease WSS1A, which is involved in DPC repair, also showed strongly enhanced growth defects, enhanced sensitivity to cross-linking agents and chromosomal aberrations. Thus, RTEL1 is also able to handle aberrant proteinoid DNA replication intermediates but independently of DPC repair.
Authors
- A Dorn (ORCID: https://orcid.org/0000-0002-0749-8425)
- Laura Lechner
- Holger Puchta (ORCID: https://orcid.org/0000-0003-1073-8546)
- Niklas Capdeville (ORCID: https://orcid.org/0000-0001-6512-0466)
- Lara Goldkuhle (ORCID: https://orcid.org/0009-0005-8043-2827)
Institutions
- Karlsruhe Institute of Technology (DE)
Publication Details
- Journal
- The Plant Journal
- Published
- 2026-05-01
- DOI
- https://doi.org/10.1111/tpj.70903
- Primary Topic
- DNA Repair Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00