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

SUMO-targeted ubiquitin ligase, Rad60, and Nse2 SUMO ligase suppress spontaneous Top1-mediated DNA damage and genome instability

Autor: John A. Tainer, Johanna Heideker, J. Jefferson P. Perry, John Prudden, Michael N. Boddy

Publikováno v: PLoS genetics, vol 7, iss 3
PLoS Genetics
PLoS Genetics, Vol 7, Iss 3, p e1001320 (2011)

Through as yet undefined proteins and pathways, the SUMO-targeted ubiquitin ligase (STUbL) suppresses genomic instability by ubiquitinating SUMO conjugated proteins and driving their proteasomal destruction. Here, we identify a critical function for

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e540a5098091573028559e383aa42b75
https://escholarship.org/uc/item/99z667n8

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

Interactions among Polycomb Domains Are Guided by Chromosome Architecture

Autor: Bas Tolhuis, Ron M. Kerkhoven, Ludo Pagie, Hans Teunissen, Marleen Blom, Wouter de Laat, Maarten van Lohuizen, Marja Nieuwland, Marieke Simonis, Bas van Steensel

Publikováno v: PLoS Genetics
PLoS Genetics, 7(3). Public Library of Science
PLoS Genetics, Vol 7, Iss 3, p e1001343 (2011)

Polycomb group (PcG) proteins bind and regulate hundreds of genes. Previous evidence has suggested that long-range chromatin interactions may contribute to the regulation of PcG target genes. Here, we adapted the Chromosome Conformation Capture on Ch

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0b0b899db48fd3d029350b832c75629d
http://europepmc.org/articles/PMC3063757

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