Mouse HORMAD1 and HORMAD2, two conserved meiotic chromosomal proteins, are depleted from synapsed chromosome axes with the help of TRIP13 AAA-ATPase

Autor: Christian R. Eckmann, Verawan Boonsanay, Scott Keeney, Lukasz Wojtasz, Howard J. Cooke, Michael J. McKay, Katrin Daniel, Maria Jasin, Ignasi Roig, Huiling Xu, Attila Tóth, Ewelina Bolcun-Filas

Publikováno v: Recercat: Dipósit de la Recerca de Catalunya
Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
PLoS Genetics
PLoS Genetics, Vol 5, Iss 10, p e1000702 (2009)
Dipòsit Digital de Documents de la UAB
Universitat Autònoma de Barcelona
Recercat. Dipósit de la Recerca de Catalunya
instname
Wojtasz, L, Daniel, K, Roig, I, Bolcun-Filas, E, Xu, H, Boonsanay, V, Eckmann, C R, Cooke, H J, Jasin, M, Keeney, S, McKay, M J & Toth, A 2009, ' Mouse HORMAD1 and HORMAD2, two conserved meiotic chromosomal proteins, are depleted from synapsed chromosome axes with the help of TRIP13 AAA-ATPase ', PLoS Genetics, vol. 5, no. 10, pp. e1000702 . https://doi.org/10.1371/journal.pgen.1000702

Meiotic crossovers are produced when programmed double-strand breaks (DSBs) are repaired by recombination from homologous chromosomes (homologues). In a wide variety of organisms, meiotic HORMA-domain proteins are required to direct DSB repair toward

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4119a892ab132b39dc47cb75d6476744
http://hdl.handle.net/2072/400342

The SUMO isopeptidase Ulp2p is required to prevent recombination-induced chromosome segregation lethality following DNA replication stress

Autor: Jeff Bachant, Ming-Ta Lee, Abla A. Bakir, Kristen N. Nguyen

Publikováno v: PLoS Genetics, Vol 7, Iss 3, p e1001355 (2011)
PLoS Genetics

SUMO conjugation is a key regulator of the cellular response to DNA replication stress, acting in part to control recombination at stalled DNA replication forks. Here we examine recombination-related phenotypes in yeast mutants defective for the SUMO

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b3de0802c82873d03554758417eea742
http://europepmc.org/articles/PMC3069114?pdf=render

New functions of Ctf18-RFC in preserving genome stability outside its role in sister chromatid cohesion

Autor: Danae Schulz, Robert S. Lahue, Catherine H. Freudenreich, Lionel Gellon, Lauren Verra, David F. Razidlo, Olive Gleeson

Publikováno v: PLoS Genetics, Vol 7, Iss 2, p e1001298 (2011)
PLoS Genetics

Expansion of DNA trinucleotide repeats causes at least 15 hereditary neurological diseases, and these repeats also undergo contraction and fragility. Current models to explain this genetic instability invoke erroneous DNA repair or aberrant replicati

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5946026ed0ce8da8a90eb562592e8e98
http://europepmc.org/articles/PMC3037408?pdf=render

The meiotic recombination checkpoint suppresses NHK-1 kinase to prevent reorganisation of the oocyte nucleus in Drosophila

Autor: C. Fiona Cullen, Manuel Breuer, Oscar M. Lancaster, Hiroyuki Ohkura, Takashi Ito

Publikováno v: PLoS Genetics, Vol 6, Iss 10, p e1001179 (2010)
PLoS Genetics
Lancaster, O M, Breuer, M, Cullen, C F, Ito, T & Ohkura, H 2010, ' The Meiotic Recombination Checkpoint Suppresses NHK-1 Kinase to Prevent Reorganisation of the Oocyte Nucleus in Drosophila ', PLoS Genetics, vol. 6, no. 10, e1001179, pp.-. https://doi.org/10.1371/journal.pgen.1001179

The meiotic recombination checkpoint is a signalling pathway that blocks meiotic progression when the repair of DNA breaks formed during recombination is delayed. In comparison to the signalling pathway itself, however, the molecular targets of the c

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a86a206051ff7465e4bf53f43898fbc5
http://europepmc.org/articles/PMC2965759?pdf=render

The Baker's Yeast Diploid Genome Is Remarkably Stable in Vegetative Growth and Meiosis

Autor: Andreas Schlattl, Nicolas Delhomme, Wu Wei, Jan O. Korbel, Lars M. Steinmetz, Zhenglong Gu, K. T. Nishant, Eric Alani, Eugenio Mancera, Xin Ma, Carlos Bustamante, Juan Lucas Argueso

Publikováno v: PLoS Genetics
PLoS Genetics, Vol 6, Iss 9, p e1001109 (2010)

Accurate estimates of mutation rates provide critical information to analyze genome evolution and organism fitness. We used whole-genome DNA sequencing, pulse-field gel electrophoresis, and comparative genome hybridization to determine mutation rates

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3a50ff473ceddabb75ffd3b538c1512c
http://europepmc.org/articles/PMC2936533