Homologous recombination repair intermediates promote efficient de novo telomere addition at DNA double-strand breaks

Abstract The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death. However, it is unclear how de novo telomere addition (dnTA) is regulated at DN...

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Published in:Nucleic acids research Vol. 48; no. 3; pp. 1271 - 1284
Main Authors: Davé, Anoushka, Pai, Chen-Chun, Durley, Samuel C, Hulme, Lydia, Sarkar, Sovan, Wee, Boon-Yu, Prudden, John, Tinline-Purvis, Helen, Cullen, Jason K, Walker, Carol, Watson, Adam, Carr, Antony M, Murray, Johanne M, Humphrey, Timothy C
Format: Journal Article
Language:English
Published: England Oxford University Press 20.02.2020
Subjects:
Chromosomes, Fungal - genetics
DNA Breaks, Double-Stranded
DNA Helicases - genetics
DNA-Binding Proteins - genetics
Exodeoxyribonucleases - genetics
Gene Expression Regulation, Fungal - genetics
Genome Integrity, Repair and
Genome, Fungal - genetics
Genomic Instability - genetics
Loss of Heterozygosity - genetics
Rad51 Recombinase - genetics
Recombinational DNA Repair - genetics
Schizosaccharomyces - genetics
Schizosaccharomyces pombe Proteins - genetics
Telomere - genetics
ISSN:0305-1048, 1362-4962, 1362-4962
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Abstract Abstract The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death. However, it is unclear how de novo telomere addition (dnTA) is regulated at DNA double-strand breaks (DSBs). Here, using a non-essential minichromosome in fission yeast, we identify roles for the HR factors Rqh1 helicase, in concert with Rad55, in suppressing dnTA at or near a DSB. We find the frequency of dnTA in rqh1Δ rad55Δ cells is reduced following loss of Exo1, Swi5 or Rad51. Strikingly, in the absence of the distal homologous chromosome arm dnTA is further increased, with nearly half of the breaks being healed in rqh1Δ rad55Δ or rqh1Δ exo1Δ cells. These findings provide new insights into the genetic context of highly efficient dnTA within HR intermediates, and how such events are normally suppressed to maintain genome stability.
AbstractList The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death. However, it is unclear how de novo telomere addition (dnTA) is regulated at DNA double-strand breaks (DSBs). Here, using a non-essential minichromosome in fission yeast, we identify roles for the HR factors Rqh1 helicase, in concert with Rad55, in suppressing dnTA at or near a DSB. We find the frequency of dnTA in rqh1Δ rad55Δ cells is reduced following loss of Exo1, Swi5 or Rad51. Strikingly, in the absence of the distal homologous chromosome arm dnTA is further increased, with nearly half of the breaks being healed in rqh1Δ rad55Δ or rqh1Δ exo1Δ cells. These findings provide new insights into the genetic context of highly efficient dnTA within HR intermediates, and how such events are normally suppressed to maintain genome stability.
Abstract The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death. However, it is unclear how de novo telomere addition (dnTA) is regulated at DNA double-strand breaks (DSBs). Here, using a non-essential minichromosome in fission yeast, we identify roles for the HR factors Rqh1 helicase, in concert with Rad55, in suppressing dnTA at or near a DSB. We find the frequency of dnTA in rqh1Δ rad55Δ cells is reduced following loss of Exo1, Swi5 or Rad51. Strikingly, in the absence of the distal homologous chromosome arm dnTA is further increased, with nearly half of the breaks being healed in rqh1Δ rad55Δ or rqh1Δ exo1Δ cells. These findings provide new insights into the genetic context of highly efficient dnTA within HR intermediates, and how such events are normally suppressed to maintain genome stability.
The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death. However, it is unclear how de novo telomere addition (dnTA) is regulated at DNA double-strand breaks (DSBs). Here, using a non-essential minichromosome in fission yeast, we identify roles for the HR factors Rqh1 helicase, in concert with Rad55, in suppressing dnTA at or near a DSB. We find the frequency of dnTA in rqh1Δ rad55Δ cells is reduced following loss of Exo1, Swi5 or Rad51. Strikingly, in the absence of the distal homologous chromosome arm dnTA is further increased, with nearly half of the breaks being healed in rqh1Δ rad55Δ or rqh1Δ exo1Δ cells. These findings provide new insights into the genetic context of highly efficient dnTA within HR intermediates, and how such events are normally suppressed to maintain genome stability.The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive loss of heterozygosity, genetic disease, or cell death. However, it is unclear how de novo telomere addition (dnTA) is regulated at DNA double-strand breaks (DSBs). Here, using a non-essential minichromosome in fission yeast, we identify roles for the HR factors Rqh1 helicase, in concert with Rad55, in suppressing dnTA at or near a DSB. We find the frequency of dnTA in rqh1Δ rad55Δ cells is reduced following loss of Exo1, Swi5 or Rad51. Strikingly, in the absence of the distal homologous chromosome arm dnTA is further increased, with nearly half of the breaks being healed in rqh1Δ rad55Δ or rqh1Δ exo1Δ cells. These findings provide new insights into the genetic context of highly efficient dnTA within HR intermediates, and how such events are normally suppressed to maintain genome stability.
Author Sarkar, Sovan
Hulme, Lydia
Wee, Boon-Yu
Prudden, John
Pai, Chen-Chun
Cullen, Jason K
Tinline-Purvis, Helen
Davé, Anoushka
Murray, Johanne M
Walker, Carol
Humphrey, Timothy C
Durley, Samuel C
Watson, Adam
Carr, Antony M
AuthorAffiliation 1 CRUK/MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford , Oxford OX3 7DQ, UK
2 Genome Damage and Stability Centre, School of Life Sciences, University of Sussex , Sussex BN1 9RQ, UK
3 QIMR Berghofer Medical Research Institute , Brisbane 4006, Australia
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Snippet Abstract The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause...
The healing of broken chromosomes by de novo telomere addition, while a normal developmental process in some organisms, has the potential to cause extensive...
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StartPage 1271
SubjectTerms Chromosomes, Fungal - genetics
DNA Breaks, Double-Stranded
DNA Helicases - genetics
DNA-Binding Proteins - genetics
Exodeoxyribonucleases - genetics
Gene Expression Regulation, Fungal - genetics
Genome Integrity, Repair and
Genome, Fungal - genetics
Genomic Instability - genetics
Loss of Heterozygosity - genetics
Rad51 Recombinase - genetics
Recombinational DNA Repair - genetics
Schizosaccharomyces - genetics
Schizosaccharomyces pombe Proteins - genetics
Telomere - genetics
Title Homologous recombination repair intermediates promote efficient de novo telomere addition at DNA double-strand breaks
URI https://www.ncbi.nlm.nih.gov/pubmed/31828313
https://www.proquest.com/docview/2325299978
https://pubmed.ncbi.nlm.nih.gov/PMC7026635
Volume 48
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