article · 15/04/2016
ESCRT III repairs nuclear envelope ruptures during cell migration to limit DNA damage and cell death
Résumé
In eukaryotic cells, the nuclear envelope separates the genomic DNA from the cytoplasmic space and regulates protein trafficking between the two compartments. This barrier is only transiently dissolved during mitosis. Here, we found that it also opened at high frequency in migrating mammalian cells during interphase, which allowed nuclear proteins to leak out and cytoplasmic proteins to leak in. This transient opening was caused by nuclear deformation and was rapidly repaired in an ESCRT (endosomal sorting complexes required for transport)-dependent manner. DNA double-strand breaks coincided with nuclear envelope opening events. As a consequence, survival of cells migrating through confining environments depended on efficient nuclear envelope and DNA repair machineries. Nuclear envelope opening in migrating leukocytes could have potentially important consequences for normal and pathological immune responses.
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Raab, M., Gentili, M., de Belly, H., Thiam, H.-R., Vargas, P., Jimenez, A.-J., Lautenschlaeger, F., Voituriez, R., Lennon-Dumenil, A.-M., Manel, N., & Piel, M. (2016). ESCRT III repairs nuclear envelope ruptures during cell migration to limit DNA damage and cell death. SCIENCE, 352(6283). https://doi.org/10.1126/science.aad7611@article{Raab2016_175,
author = {Raab, M. and Gentili, M. and de Belly, H. and Thiam, H. R. and Vargas, P. and Jimenez, A. J. and Lautenschlaeger, F. and Voituriez, Raphael and Lennon-Dumenil, A. M. and Manel, N. and Piel, M.},
year = {2016},
month = {4},
title = {ESCRT III repairs nuclear envelope ruptures during cell migration to limit DNA damage and cell death},
journal = {SCIENCE},
volume = {352},
number = {6283},
abstract = {In eukaryotic cells, the nuclear envelope separates the genomic DNA from the cytoplasmic space and regulates protein trafficking between the two compartments. This barrier is only transiently dissolved during mitosis. Here, we found that it also opened at high frequency in migrating mammalian cells during interphase, which allowed nuclear proteins to leak out and cytoplasmic proteins to leak in. This transient opening was caused by nuclear deformation and was rapidly repaired in an ESCRT (endosomal sorting complexes required for transport)-dependent manner. DNA double-strand breaks coincided with nuclear envelope opening events. As a consequence, survival of cells migrating through confining environments depended on efficient nuclear envelope and DNA repair machineries. Nuclear envelope opening in migrating leukocytes could have potentially important consequences for normal and pathological immune responses.},
url = {http://www.dx.doi.org/10.1126/science.aad7611},
doi = {10.1126/science.aad7611},
issn = {0036-8075},
}TY - JOUR
AU - Raab, M.
AU - Gentili, M.
AU - de Belly, H.
AU - Thiam, H. R.
AU - Vargas, P.
AU - Jimenez, A. J.
AU - Lautenschlaeger, F.
AU - Voituriez, Raphael
AU - Lennon-Dumenil, A. M.
AU - Manel, N.
AU - Piel, M.
PY - 2016
DA - 2016/04/15
TI - ESCRT III repairs nuclear envelope ruptures during cell migration to limit DNA damage and cell death
JO - SCIENCE
VL - 352
IS - 6283
SN - 0036-8075
AB - In eukaryotic cells, the nuclear envelope separates the genomic DNA from the cytoplasmic space and regulates protein trafficking between the two compartments. This barrier is only transiently dissolved during mitosis. Here, we found that it also opened at high frequency in migrating mammalian cells during interphase, which allowed nuclear proteins to leak out and cytoplasmic proteins to leak in. This transient opening was caused by nuclear deformation and was rapidly repaired in an ESCRT (endosomal sorting complexes required for transport)-dependent manner. DNA double-strand breaks coincided with nuclear envelope opening events. As a consequence, survival of cells migrating through confining environments depended on efficient nuclear envelope and DNA repair machineries. Nuclear envelope opening in migrating leukocytes could have potentially important consequences for normal and pathological immune responses.
DO - 10.1126/science.aad7611
UR - http://www.dx.doi.org/10.1126/science.aad7611
ER -