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Abstract
Loss of DNA polymerase theta (Polθ) in the two-spotted spider mite enhances homology-directed repair efficiency.
- SYNCAS-mediated genome editing in Tetranychus urticae may vary in efficiency due to competition between DNA repair pathways.
- The absence of DNA polymerase theta redirects repair mechanisms almost entirely toward homology-directed repair.
- No detectable impact on DNA repair was observed with the loss of Ligase IV.
- Polθ-deficient strains show increased incorporation of repair templates, even with distant mutations.
- Inserting larger DNA fragments is more successful in Polθ-deficient strains.
- Disruption of Polθ results in only a modest fitness cost, suggesting potential for future genome engineering.
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