MOVSESJAN, Karina, V. SANNINO, Ondrej BELÁŇ, Jarmila MLČOUŠKOVÁ, Mário ŠPÍREK, V. COSTANZO a Lumír KREJČÍ. Fanconi-Anemia-Associated Mutations Destabilize RAD51 Filaments and Impair Replication Fork Protection. Cell Reports. CAMBRIDGE: Cell Press, 2017, roč. 21, č. 2, s. 333-340. ISSN 2211-1247. Dostupné z: https://dx.doi.org/10.1016/j.celrep.2017.09.062. |
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@article{1395559, author = {Movsesjan, Karina and Sannino, V. and Beláň, Ondrej and Mlčoušková, Jarmila and Špírek, Mário and Costanzo, V. and Krejčí, Lumír}, article_location = {CAMBRIDGE}, article_number = {2}, doi = {http://dx.doi.org/10.1016/j.celrep.2017.09.062}, keywords = {Fanconi anemia}, language = {eng}, issn = {2211-1247}, journal = {Cell Reports}, title = {Fanconi-Anemia-Associated Mutations Destabilize RAD51 Filaments and Impair Replication Fork Protection}, volume = {21}, year = {2017} }
TY - JOUR ID - 1395559 AU - Movsesjan, Karina - Sannino, V. - Beláň, Ondrej - Mlčoušková, Jarmila - Špírek, Mário - Costanzo, V. - Krejčí, Lumír PY - 2017 TI - Fanconi-Anemia-Associated Mutations Destabilize RAD51 Filaments and Impair Replication Fork Protection JF - Cell Reports VL - 21 IS - 2 SP - 333-340 EP - 333-340 PB - Cell Press SN - 22111247 KW - Fanconi anemia N2 - Fanconi anemia (FA) is a genetic disorder characterized by a defect in DNA interstrand crosslink (ICL) repair, chromosomal instability, and a predisposition to cancer. Recently, two RAD51 mutations were reported to cause an FA-like phenotype. Despite the tight association of FA/HR proteins with replication fork (RF) stabilization during normal replication, it remains unknown how FA-associated RAD51 mutations affect replication beyond ICL lesions. Here, we report that these mutations fail to protect nascent DNA from MRE11-mediated degradation during RF stalling in Xenopus laevis egg extracts. Reconstitution of DNA protection in vitro revealed that the defect arises directly due to altered RAD51 properties. Both mutations induce pronounced structural changes and RAD51 filament destabilization that is not rescued by prevention of ATP hydrolysis due to aberrant ATP binding. Our results further interconnect the FA pathway with DNA replication and provide mechanistic insight into the role of RAD51 in recombination-independent mechanisms of genome maintenance. ER -
MOVSESJAN, Karina, V. SANNINO, Ondrej BELÁŇ, Jarmila MLČOUŠKOVÁ, Mário ŠPÍREK, V. COSTANZO a Lumír KREJČÍ. Fanconi-Anemia-Associated Mutations Destabilize RAD51 Filaments and Impair Replication Fork Protection. \textit{Cell Reports}. CAMBRIDGE: Cell Press, 2017, roč.~21, č.~2, s.~333-340. ISSN~2211-1247. Dostupné z: https://dx.doi.org/10.1016/j.celrep.2017.09.062.
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