Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (41)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Page, S. L.
Right arrow Articles by Shaffer, L. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Page, S. L.
Right arrow Articles by Shaffer, L. G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, Vol 5, 1279-1288, Copyright © 1996 by Oxford University Press

ARTICLES

Breakpoint diversity illustrates distinct mechanisms for Robertsonian translocation formation

SL Page, JC Shin, JY Han, KH Choo and LG Shaffer
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.

Robertsonian translocations are the most common chromosomal rearrangements in humans. The vast majority of the ten possible nonhomologous types of Robertsonian translocations ascertained are rob(13q14q) and rob(14q21q). Recombination between homologous sequences on nonhomologous chromosomes has been proposed as a mechanism leading to the preferential formation of rob(13q14q) and rob(14q21q). However, little evidence exists to indicate whether the remaining less common Robertsonian translocations form through a similar mechanism. To better elucidate the mechanisms involved in Robertsonian translocation formation, we have used fluorescence in situ hybridization to localize the breakpoints in 56 nonhomologous Robertsonian translocations. This study revealed highly variable locations of breakpoints in seven types of the less common Robertsonians, while nearly all rob(13q14q) and rob(14q21q) analyzed displayed breakpoints in the same locations. Therefore, this study provides direct evidence that rob(13q14q) and rob(14q21q) form through a specific mechanism, possibly involving homologous recombination, which is distinct from the mechanism(s) that contributes to the formation of the remaining types of Robertsonian translocations.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Genome ResHome page
D. M. Stults, M. W. Killen, H. H. Pierce, and A. J. Pierce
Genomic architecture and inheritance of human ribosomal RNA gene clusters
Genome Res., January 1, 2008; 18(1): 13 - 18.
[Abstract] [Full Text] [PDF]

Home page
 Hum ReprodHome page
K. Moradkhani, J. Puechberty, S. Bhatt, J. Lespinasse, P. Vago, G. Lefort, P. Sarda, S. Hamamah, and F. Pellestor
Rare Robertsonian translocations and meiotic behaviour: sperm FISH analysis of t(13;15) and t(14;15) translocations: A Case Report
Hum. Reprod., December 1, 2006; 21(12): 3193 - 3198.
[Abstract] [Full Text] [PDF]

Home page
 Hum ReprodHome page
K. Moradkhani, J. Puechberty, S. Bhatt, P. Vago, L. Janny, G. Lefort, S. Hamamah, P. Sarda, and F. Pellestor
Meiotic segregation of rare Robertsonian translocations: sperm analysis of three t(14q;22q) cases
Hum. Reprod., May 1, 2006; 21(5): 1166 - 1171.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
S. Garagna, N. Marziliano, M. Zuccotti, J. B. Searle, E. Capanna, and C. A. Redi
Pericentromeric organization at the fusion point of mouse Robertsonian translocation chromosomes
PNAS, January 2, 2001; 98(1): 171 - 175.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.