MUS81 promotes common fragile site expression

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

MUS81 promotes common fragile site expression. / Ying, Songmin; Minocherhomji, Sheroy; Chan, Kok Lung; Palmai-Pallag, Timea; Chu, Wai Kit; Wass, Theresa Adeline; Mankouri, Hocine W; Liu, Ying; Hickson, Ian D.

In: Nature Cell Biology, Vol. 15, No. 8, 08.2013, p. 1001-1007.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Ying, S, Minocherhomji, S, Chan, KL, Palmai-Pallag, T, Chu, WK, Wass, TA, Mankouri, HW, Liu, Y & Hickson, ID 2013, 'MUS81 promotes common fragile site expression', Nature Cell Biology, vol. 15, no. 8, pp. 1001-1007. https://doi.org/10.1038/ncb2773

APA

Ying, S., Minocherhomji, S., Chan, K. L., Palmai-Pallag, T., Chu, W. K., Wass, T. A., Mankouri, H. W., Liu, Y., & Hickson, I. D. (2013). MUS81 promotes common fragile site expression. Nature Cell Biology, 15(8), 1001-1007. https://doi.org/10.1038/ncb2773

Vancouver

Ying S, Minocherhomji S, Chan KL, Palmai-Pallag T, Chu WK, Wass TA et al. MUS81 promotes common fragile site expression. Nature Cell Biology. 2013 Aug;15(8):1001-1007. https://doi.org/10.1038/ncb2773

Author

Ying, Songmin ; Minocherhomji, Sheroy ; Chan, Kok Lung ; Palmai-Pallag, Timea ; Chu, Wai Kit ; Wass, Theresa Adeline ; Mankouri, Hocine W ; Liu, Ying ; Hickson, Ian D. / MUS81 promotes common fragile site expression. In: Nature Cell Biology. 2013 ; Vol. 15, No. 8. pp. 1001-1007.

Bibtex

@article{ca2d8cee375b4b3fb27a5a77b672cc2a,
title = "MUS81 promotes common fragile site expression",
abstract = "Fragile sites are chromosomal loci with a propensity to form gaps or breaks during early mitosis, and their instability is implicated as being causative in certain neurological disorders and cancers. Recent work has demonstrated that the so-called common fragile sites (CFSs) often impair the faithful disjunction of sister chromatids in mitosis. However, the mechanisms by which CFSs express their fragility, and the cellular factors required to suppress CFS instability, remain largely undefined. Here, we report that the DNA structure-specific nuclease MUS81-EME1 localizes to CFS loci in early mitotic cells, and promotes the cytological appearance of characteristic gaps or breaks observed at CFSs in metaphase chromosomes. These data indicate that CFS breakage is an active, MUS81-EME1-dependent process, and not a result of inadvertent chromatid rupturing during chromosome condensation. Moreover, CFS cleavage by MUS81-EME1 promotes faithful sister chromatid disjunction. Our findings challenge the prevailing view that CFS breakage is a nonspecific process that is detrimental to cells, and indicate that CFS cleavage actually promotes genome stability.",
author = "Songmin Ying and Sheroy Minocherhomji and Chan, {Kok Lung} and Timea Palmai-Pallag and Chu, {Wai Kit} and Wass, {Theresa Adeline} and Mankouri, {Hocine W} and Ying Liu and Hickson, {Ian D}",
year = "2013",
month = aug,
doi = "10.1038/ncb2773",
language = "English",
volume = "15",
pages = "1001--1007",
journal = "Nature Cell Biology",
issn = "1465-7392",
publisher = "nature publishing group",
number = "8",

}

RIS

TY - JOUR

T1 - MUS81 promotes common fragile site expression

AU - Ying, Songmin

AU - Minocherhomji, Sheroy

AU - Chan, Kok Lung

AU - Palmai-Pallag, Timea

AU - Chu, Wai Kit

AU - Wass, Theresa Adeline

AU - Mankouri, Hocine W

AU - Liu, Ying

AU - Hickson, Ian D

PY - 2013/8

Y1 - 2013/8

N2 - Fragile sites are chromosomal loci with a propensity to form gaps or breaks during early mitosis, and their instability is implicated as being causative in certain neurological disorders and cancers. Recent work has demonstrated that the so-called common fragile sites (CFSs) often impair the faithful disjunction of sister chromatids in mitosis. However, the mechanisms by which CFSs express their fragility, and the cellular factors required to suppress CFS instability, remain largely undefined. Here, we report that the DNA structure-specific nuclease MUS81-EME1 localizes to CFS loci in early mitotic cells, and promotes the cytological appearance of characteristic gaps or breaks observed at CFSs in metaphase chromosomes. These data indicate that CFS breakage is an active, MUS81-EME1-dependent process, and not a result of inadvertent chromatid rupturing during chromosome condensation. Moreover, CFS cleavage by MUS81-EME1 promotes faithful sister chromatid disjunction. Our findings challenge the prevailing view that CFS breakage is a nonspecific process that is detrimental to cells, and indicate that CFS cleavage actually promotes genome stability.

AB - Fragile sites are chromosomal loci with a propensity to form gaps or breaks during early mitosis, and their instability is implicated as being causative in certain neurological disorders and cancers. Recent work has demonstrated that the so-called common fragile sites (CFSs) often impair the faithful disjunction of sister chromatids in mitosis. However, the mechanisms by which CFSs express their fragility, and the cellular factors required to suppress CFS instability, remain largely undefined. Here, we report that the DNA structure-specific nuclease MUS81-EME1 localizes to CFS loci in early mitotic cells, and promotes the cytological appearance of characteristic gaps or breaks observed at CFSs in metaphase chromosomes. These data indicate that CFS breakage is an active, MUS81-EME1-dependent process, and not a result of inadvertent chromatid rupturing during chromosome condensation. Moreover, CFS cleavage by MUS81-EME1 promotes faithful sister chromatid disjunction. Our findings challenge the prevailing view that CFS breakage is a nonspecific process that is detrimental to cells, and indicate that CFS cleavage actually promotes genome stability.

U2 - 10.1038/ncb2773

DO - 10.1038/ncb2773

M3 - Journal article

C2 - 23811685

VL - 15

SP - 1001

EP - 1007

JO - Nature Cell Biology

JF - Nature Cell Biology

SN - 1465-7392

IS - 8

ER -

ID: 47685416