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CDK targets Sae2 to control DNA-end resection and homologous recombination

Author

Listed:
  • Pablo Huertas

    (The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK)

  • Felipe Cortés-Ledesma

    (Centro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC, Avenida Américo Vespucio s/n, 41092 Sevilla, Spain)

  • Alessandro A. Sartori

    (The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Present address: Institute of Molecular Cancer Research, University of Zurich-Irchel, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.)

  • Andrés Aguilera

    (Centro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC, Avenida Américo Vespucio s/n, 41092 Sevilla, Spain)

  • Stephen P. Jackson

    (The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK)

Abstract

DNA repair: pathways in balance DNA can be repaired by two fundamentally different mechanisms, depending on whether a homologous template is available or not. Given that DNA is duplicated in S phase, homologous recombination is restricted to S and G2 phases of the cell cycle. The activity of cyclin-dependent kinases (CDKs) is also cell-cycle regulated, and the yeast CDK Cdc28 controls DNA resection, an early step of homologous recombination. In this work, Huertas et al. show that the target of Cdc28 in regulating DNA resection is Sae2, a protein with endonuclease activity that was first identified as being required for meiotic recombination. These results support models in which the commitment to DSB resection is highly regulated to ensure that the cell engages the most appropriate DNA repair pathway at the right time, thereby optimizing genome stability.

Suggested Citation

  • Pablo Huertas & Felipe Cortés-Ledesma & Alessandro A. Sartori & Andrés Aguilera & Stephen P. Jackson, 2008. "CDK targets Sae2 to control DNA-end resection and homologous recombination," Nature, Nature, vol. 455(7213), pages 689-692, October.
    • Handle: RePEc:nat:nature:v:455:y:2008:i:7213:d:10.1038_nature07215
    DOI: 10.1038/nature07215
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    Cited by:

    1. Lorenzo Galanti & Martina Peritore & Robert Gnügge & Elda Cannavo & Johannes Heipke & Maria Dilia Palumbieri & Barbara Steigenberger & Lorraine S. Symington & Petr Cejka & Boris Pfander, 2024. "Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    2. Vera M. Kissling & Giordano Reginato & Eliana Bianco & Kristina Kasaciunaite & Janny Tilma & Gea Cereghetti & Natalie Schindler & Sung Sik Lee & Raphaël Guérois & Brian Luke & Ralf Seidel & Petr Cejka, 2022. "Mre11-Rad50 oligomerization promotes DNA double-strand break repair," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    3. Qian Zhu & Jinzhou Huang & Hongyang Huang & Huan Li & Peiqiang Yi & Jake A. Kloeber & Jian Yuan & Yuping Chen & Min Deng & Kuntian Luo & Ming Gao & Guijie Guo & Xinyi Tu & Ping Yin & Yong Zhang & Jun , 2021. "RNF19A-mediated ubiquitination of BARD1 prevents BRCA1/BARD1-dependent homologous recombination," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
    4. Bert Kooij & Fenna J. Wal & Magdalena B. Rother & Wouter W. Wiegant & Pau Creixell & Merula Stout & Brian A. Joughin & Julia Vornberger & Matthias Altmeyer & Marcel A. T. M. Vugt & Michael B. Yaffe & , 2024. "The Fanconi anemia core complex promotes CtIP-dependent end resection to drive homologous recombination at DNA double-strand breaks," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    5. Adrián Campos & Facundo Ramos & Lydia Iglesias & Celia Delgado & Eva Merino & Antonio Esperilla-Muñoz & Jaime Correa-Bordes & Andrés Clemente-Blanco, 2023. "Cdc14 phosphatase counteracts Cdk-dependent Dna2 phosphorylation to inhibit resection during recombinational DNA repair," Nature Communications, Nature, vol. 14(1), pages 1-20, December.

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