Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C

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

Standard

Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C. / Garvanska, Dimitriya H; Larsen, Marie Sofie Yoo; Nilsson, Jakob.

In: Biology Open, Vol. 5, 02.09.2016, p. 1441-1448.

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

Harvard

Garvanska, DH, Larsen, MSY & Nilsson, J 2016, 'Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C', Biology Open, vol. 5, pp. 1441-1448. https://doi.org/10.1242/bio.020842

APA

Garvanska, D. H., Larsen, M. S. Y., & Nilsson, J. (2016). Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C. Biology Open, 5, 1441-1448. https://doi.org/10.1242/bio.020842

Vancouver

Garvanska DH, Larsen MSY, Nilsson J. Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C. Biology Open. 2016 Sep 2;5:1441-1448. https://doi.org/10.1242/bio.020842

Author

Garvanska, Dimitriya H ; Larsen, Marie Sofie Yoo ; Nilsson, Jakob. / Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C. In: Biology Open. 2016 ; Vol. 5. pp. 1441-1448.

Bibtex

@article{691916bf043246048fcdec9220642720,
title = "Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C",
abstract = "The spindle assembly checkpoint (SAC) inhibits the anaphase-promoting complex/cyclosome (APC/C) in response to unattached kinetochores by generating a diffusible inhibitor termed the mitotic checkpoint complex (MCC). At metaphase, rapid activation of the APC/C requires removal of the MCC, a process that has been shown to depend on the APC/C E2 enzymes, UBE2C and UBE2S. Here we investigate the in vivo role of the APC/C E2 enzymes in SAC silencing using CRISPR/Cas9 genetically engineered HCT116 UBE2C or UBE2S null cell lines. Using live cell assays, we show that UBE2C and UBE2S make a minor contribution to SAC silencing in HCT116 cells. Strikingly in cells specifically lacking UBE2C, we observe a strong synergistic inhibition of mitotic progression when we stabilize the MCC on the APC/C by depleting APC15, potentially reflecting increased competition between the MCC and the remaining initiating E2 enzyme UBE2D. In conclusion, we provide in vivo insight into the APC/C E2 module and its interplay with SAC silencing components.",
author = "Garvanska, {Dimitriya H} and Larsen, {Marie Sofie Yoo} and Jakob Nilsson",
note = "{\textcopyright} 2016. Published by The Company of Biologists Ltd.",
year = "2016",
month = sep,
day = "2",
doi = "10.1242/bio.020842",
language = "English",
volume = "5",
pages = "1441--1448",
journal = "Biology Open",
issn = "2046-6390",
publisher = "The Company of Biologists Ltd.",

}

RIS

TY - JOUR

T1 - Synergistic inhibition of the APC/C by the removal of APC15 in HCT116 cells lacking UBE2C

AU - Garvanska, Dimitriya H

AU - Larsen, Marie Sofie Yoo

AU - Nilsson, Jakob

N1 - © 2016. Published by The Company of Biologists Ltd.

PY - 2016/9/2

Y1 - 2016/9/2

N2 - The spindle assembly checkpoint (SAC) inhibits the anaphase-promoting complex/cyclosome (APC/C) in response to unattached kinetochores by generating a diffusible inhibitor termed the mitotic checkpoint complex (MCC). At metaphase, rapid activation of the APC/C requires removal of the MCC, a process that has been shown to depend on the APC/C E2 enzymes, UBE2C and UBE2S. Here we investigate the in vivo role of the APC/C E2 enzymes in SAC silencing using CRISPR/Cas9 genetically engineered HCT116 UBE2C or UBE2S null cell lines. Using live cell assays, we show that UBE2C and UBE2S make a minor contribution to SAC silencing in HCT116 cells. Strikingly in cells specifically lacking UBE2C, we observe a strong synergistic inhibition of mitotic progression when we stabilize the MCC on the APC/C by depleting APC15, potentially reflecting increased competition between the MCC and the remaining initiating E2 enzyme UBE2D. In conclusion, we provide in vivo insight into the APC/C E2 module and its interplay with SAC silencing components.

AB - The spindle assembly checkpoint (SAC) inhibits the anaphase-promoting complex/cyclosome (APC/C) in response to unattached kinetochores by generating a diffusible inhibitor termed the mitotic checkpoint complex (MCC). At metaphase, rapid activation of the APC/C requires removal of the MCC, a process that has been shown to depend on the APC/C E2 enzymes, UBE2C and UBE2S. Here we investigate the in vivo role of the APC/C E2 enzymes in SAC silencing using CRISPR/Cas9 genetically engineered HCT116 UBE2C or UBE2S null cell lines. Using live cell assays, we show that UBE2C and UBE2S make a minor contribution to SAC silencing in HCT116 cells. Strikingly in cells specifically lacking UBE2C, we observe a strong synergistic inhibition of mitotic progression when we stabilize the MCC on the APC/C by depleting APC15, potentially reflecting increased competition between the MCC and the remaining initiating E2 enzyme UBE2D. In conclusion, we provide in vivo insight into the APC/C E2 module and its interplay with SAC silencing components.

U2 - 10.1242/bio.020842

DO - 10.1242/bio.020842

M3 - Journal article

C2 - 27591192

VL - 5

SP - 1441

EP - 1448

JO - Biology Open

JF - Biology Open

SN - 2046-6390

ER -

ID: 166506094