Imperial College London

ProfessorLuisAragon Alcaide

Faculty of MedicineInstitute of Clinical Sciences

Professor of Genetics
 
 
 
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Contact

 

+44 (0)20 3313 8013luis.aragon

 
 
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Location

 

CRB (Clinical Research Building)Hammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@phdthesis{Patel:2014,
author = {Patel, A},
title = {The role of the sister chromatid during repair of a DNA double-strand break},
year = {2014}
}

RIS format (EndNote, RefMan)

TY  - THES
AB - Chromosomal breaks are extremely cytotoxic and can occur during normal cell metabolism, and after exposure to exogenous DNA damaging agents. Double strand breaks (DSBs) are repaired to maintain and restore genetic integrity, principally through two major pathways: homologous recombination (HR) and non-homologous end-joining (NHEJ). HR can be error-free when sister chromatids are used as a template for repair, and is initiated by nucleolytic resection of the DSB. Cyclin-dependent kinase 1 (Cdk1) activity is crucial to promote HR. As Cdk1 activity and the sister chromatid are only present during certain cell division cycle stages, this study investigated whether in addition to Cdk1 activity the presence of an intact sister chromatid is a requirement to initiate HR. Conditional alleles that arrest the cell division cycle with separated sister chromatids and high Cdk1 activity were constructed in budding yeast and used to investigate this possibility. This study has found that HR occurs with segregated sister chromatids during telophase, at a time when mitotic Cdk1 activity is high. HR is also less efficient during metaphase if microtubule function is impaired. Overall, the availability of the sister chromatid is not an additional requirement to mitotic Cdk1 activity to promote DSB repair with the HR pathway.
AU - Patel,A
PY - 2014///
TI - The role of the sister chromatid during repair of a DNA double-strand break
ER -