New paper from the Cejka lab published in Nature Communications
on Thursday, October 11, 2018
When DNA gets broken, cells can utilize two main repair pathways. The first mechanism simply patches the two broken ends together at the cost of mutations in the vicinity of the break site. The second process, termed homologous recombination, is using a sister chromatid (a DNA molecule with the same sequence information) as a temple for repair. Homologous recombination is therefore a more accurate repair pathway, which can however only be utilized the S-G2 phase of the cell cycle when sister chromatids are available.
In the study, entitled "Regulatory control of DNA end resection by Sae2 phosphorylation", the scientists reveal how phosphorylation of a protein called Sae2 regulates the initiation of the homologous recombination pathway. A process called DNA end resection, which initiates and commits the DNA repair to the homologous recombination machinery, is only allowed when Sae2 is phosphorylated.
The publication resulted from a collaboration between IRB Bellinzona, University of Sussex (UK), National Institutes of Health (USA), Friedrich Miescher Institute (FMI - Basel, CH) and ETH Zurich (CH).
The figure shows a comparison of multimeric inactive Sae2 (left) and phosphorylated active Sae2 protein (right).
Cannavo, E., D. Johnson, S. N. Andres, V. M. Kissling, J. K. Reinert, V. Garcia, D. A. Erie, D. Hess, N. H. Thoma, R. I. Enchev, M. Peter, R. S. Williams, M. J. Neale and P. Cejka
Nat Commun. 2018; 9:4016.