Loading...
All Paired Up with No Place to Go: Pairing, Synapsis, and DSB Formation in a Balancer Heterozygote
Gong, Wei J. ; McKim, Kim S. ; Hawley, R. Scott
Gong, Wei J.
McKim, Kim S.
Hawley, R. Scott
Citations
Altmetric:
Abstract
The multiply inverted X chromosome balancer FM7 strongly suppresses, or eliminates, the occurrence of crossing over when heterozygous with a normal sequence homolog. We have utilized the LacI-GFP: lacO system to visualize the effects of FM7 on meiotic pairing, synapsis, and double-strand break formation in Drosophila oocytes. Surprisingly, the analysis of meiotic pairing and synapsis for three lacO reporter couplets in FM7/X heterozygotes revealed they are paired and synapsed during zygotene/pachytene in 70%–80% of oocytes. Moreover, the regions defined by these lacO couplets undergo double-strand break formation at normal frequency. Thus, even complex aberration heterozygotes usually allow high frequencies of meiotic pairing, synapsis, and double-strand break formation in Drosophila oocytes. However, the frequencies of failed pairing and synapsis were still 1.5- to 2-fold higher than were observed for corresponding regions in oocytes with two normal sequence X chromosomes, and this effect was greatest near a breakpoint. We propose that heterozygosity for breakpoints creates a local alteration in synaptonemal complex structure that is propagated across long regions of the bivalent in a fashion analogous to chiasma interference, which also acts to suppress crossing over.
Description
Date
2005-11-18
Journal Title
Journal ISSN
Volume Title
Publisher
Public Library of Science
Collections
Files
Loading...
Gong.pdf
Adobe PDF, 423.71 KB
Research Projects
Organizational Units
Journal Issue
Keywords
Choromosome pairs, Chromosome structure and function, Chromosomes, Drosophila melanogaster, Heterozygosity, Oocytes, Synapsis, Xchromosomes
Citation
Gong, W. J., McKim, K. S., & Hawley, R. S. (2005). All Paired Up with No Place to Go: Pairing, Synapsis, and DSB Formation in a Balancer Heterozygote. PLoS Genet, 1(5). http://dx.doi.org/10.1371/journal.pgen.0010067
