All paired up with no place to go: pairing, synapsis, and DSB formation in a balancer heterozygote.
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.
Gong
Wei J
WJ
Stowers Institute for Medical Research, Kansas City, Missouri, United States of America.
McKim
Kim S
KS
Hawley
R Scott
RS
D000818:Animals; D023902:Chromosome Pairing; D003434:Crossing Over, Genetic; D004330:Drosophila; D017930:Genes, Reporter; D005821:Genetic Techniques; D006579:Heterozygote; D008540:Meiosis; D008957:Models, Genetic; D009154:Mutation; D009865:Oocytes / Q000378:metabolism; D051135:Rad51 Recombinase / Q000378:metabolism; D014960:X Chromosome
D051135:Rad51 Recombinase