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FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells

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FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells. / Pentzold, Constanze; Shah, Shiraz Ali; Hansen, Niels Richard; Le Tallec, Benoit; Seguin-Orlando, Andaine; Debatisse, Michelle; Lisby, Michael; Oestergaard, Vibe Hallundbæk.

I: Nucleic Acids Research, Bind 46, Nr. 3, 2018, s. 1280-1294.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Pentzold, C, Shah, SA, Hansen, NR, Le Tallec, B, Seguin-Orlando, A, Debatisse, M, Lisby, M & Oestergaard, VH 2018, 'FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells', Nucleic Acids Research, bind 46, nr. 3, s. 1280-1294. https://doi.org/10.1093/nar/gkx1260

APA

Pentzold, C., Shah, S. A., Hansen, N. R., Le Tallec, B., Seguin-Orlando, A., Debatisse, M., Lisby, M., & Oestergaard, V. H. (2018). FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells. Nucleic Acids Research, 46(3), 1280-1294. https://doi.org/10.1093/nar/gkx1260

Vancouver

Pentzold C, Shah SA, Hansen NR, Le Tallec B, Seguin-Orlando A, Debatisse M o.a. FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells. Nucleic Acids Research. 2018;46(3):1280-1294. https://doi.org/10.1093/nar/gkx1260

Author

Pentzold, Constanze ; Shah, Shiraz Ali ; Hansen, Niels Richard ; Le Tallec, Benoit ; Seguin-Orlando, Andaine ; Debatisse, Michelle ; Lisby, Michael ; Oestergaard, Vibe Hallundbæk. / FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells. I: Nucleic Acids Research. 2018 ; Bind 46, Nr. 3. s. 1280-1294.

Bibtex

@article{b931505e28954c01adfdf7d5f96cb00a,
title = "FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells",
abstract = "Common Chromosomal Fragile Sites (CFSs) are specific genomic regions prone to form breaks on metaphase chromosomes in response to replication stress. Moreover, CFSs are mutational hotspots in cancer genomes, showing that the mutational mechanisms that operate at CFSs are highly active in cancer cells. Orthologs of human CFSs are found in a number of other mammals, but the extent of CFS conservation beyond the mammalian lineage is unclear. Characterization of CFSs from distantly related organisms can provide new insight into the biology underlying CFSs. Here, we have mapped CFSs in an avian cell line. We find that, overall the most significant CFSs coincide with extremely large conserved genes, from which very long transcripts are produced. However, no significant correlation between any sequence characteristics and CFSs is found. Moreover, we identified putative early replicating fragile sites (ERFSs), which is a distinct class of fragile sites and we developed a fluctuation analysis revealing high mutation rates at the CFS gene PARK2, with deletions as the most prevalent mutation. Finally, we show that avian homologs of the human CFS genes despite their fragility have resisted the general intron size reduction observed in birds suggesting that CFSs have a conserved biological function.",
author = "Constanze Pentzold and Shah, {Shiraz Ali} and Hansen, {Niels Richard} and {Le Tallec}, Benoit and Andaine Seguin-Orlando and Michelle Debatisse and Michael Lisby and Oestergaard, {Vibe Hallundb{\ae}k}",
year = "2018",
doi = "10.1093/nar/gkx1260",
language = "English",
volume = "46",
pages = "1280--1294",
journal = "Nucleic Acids Research",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells

AU - Pentzold, Constanze

AU - Shah, Shiraz Ali

AU - Hansen, Niels Richard

AU - Le Tallec, Benoit

AU - Seguin-Orlando, Andaine

AU - Debatisse, Michelle

AU - Lisby, Michael

AU - Oestergaard, Vibe Hallundbæk

PY - 2018

Y1 - 2018

N2 - Common Chromosomal Fragile Sites (CFSs) are specific genomic regions prone to form breaks on metaphase chromosomes in response to replication stress. Moreover, CFSs are mutational hotspots in cancer genomes, showing that the mutational mechanisms that operate at CFSs are highly active in cancer cells. Orthologs of human CFSs are found in a number of other mammals, but the extent of CFS conservation beyond the mammalian lineage is unclear. Characterization of CFSs from distantly related organisms can provide new insight into the biology underlying CFSs. Here, we have mapped CFSs in an avian cell line. We find that, overall the most significant CFSs coincide with extremely large conserved genes, from which very long transcripts are produced. However, no significant correlation between any sequence characteristics and CFSs is found. Moreover, we identified putative early replicating fragile sites (ERFSs), which is a distinct class of fragile sites and we developed a fluctuation analysis revealing high mutation rates at the CFS gene PARK2, with deletions as the most prevalent mutation. Finally, we show that avian homologs of the human CFS genes despite their fragility have resisted the general intron size reduction observed in birds suggesting that CFSs have a conserved biological function.

AB - Common Chromosomal Fragile Sites (CFSs) are specific genomic regions prone to form breaks on metaphase chromosomes in response to replication stress. Moreover, CFSs are mutational hotspots in cancer genomes, showing that the mutational mechanisms that operate at CFSs are highly active in cancer cells. Orthologs of human CFSs are found in a number of other mammals, but the extent of CFS conservation beyond the mammalian lineage is unclear. Characterization of CFSs from distantly related organisms can provide new insight into the biology underlying CFSs. Here, we have mapped CFSs in an avian cell line. We find that, overall the most significant CFSs coincide with extremely large conserved genes, from which very long transcripts are produced. However, no significant correlation between any sequence characteristics and CFSs is found. Moreover, we identified putative early replicating fragile sites (ERFSs), which is a distinct class of fragile sites and we developed a fluctuation analysis revealing high mutation rates at the CFS gene PARK2, with deletions as the most prevalent mutation. Finally, we show that avian homologs of the human CFS genes despite their fragility have resisted the general intron size reduction observed in birds suggesting that CFSs have a conserved biological function.

U2 - 10.1093/nar/gkx1260

DO - 10.1093/nar/gkx1260

M3 - Journal article

C2 - 29253234

VL - 46

SP - 1280

EP - 1294

JO - Nucleic Acids Research

JF - Nucleic Acids Research

SN - 0305-1048

IS - 3

ER -

ID: 192786172