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All paired up with no place to go: pairing, synapsis, and DSB formation in a balancer heterozygote.

Gong WJ, McKim KS, Hawley RS - PLoS Genet. (2005)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Stowers Institute for Medical Research, Kansas City, Missouri, United States of America.

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.

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Related in: MedlinePlus

The Multiply Inverted Balancer Chromosome FM7(A) Schematic diagram of the generation of chromosomal inversions from X to FM7. Color represents the regions that are involved in inversions, and arrows are used to indicate the orientation of each region with respect to the centromere. Circles represent the centromeres. The numbers below each structure represent positions of the standard polytene map.(B) A hypothetical structure displaying the pairing relations of the two homologs in an FM7/X heterozygote.(C) A picture of DAPI-stained chromosome at meiotic metaphase I in FM7/X oocytes (courtesy of W. Gilliland). The two X and 4th chromosomes are positioned between the two autosomal bivalents and the poles, with the dot-like 4th chromosomes located closer to the poles. The FM7 chromosome (denoted by the brighter DAPI staining at its tip) is located between the autosomes and the upper pole, while the normal sequence X chromosome lies in the lower half of the spindle. Note that the X and FM7 chromosomes are not connected by chiasmata.
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pgen-0010067-g001: The Multiply Inverted Balancer Chromosome FM7(A) Schematic diagram of the generation of chromosomal inversions from X to FM7. Color represents the regions that are involved in inversions, and arrows are used to indicate the orientation of each region with respect to the centromere. Circles represent the centromeres. The numbers below each structure represent positions of the standard polytene map.(B) A hypothetical structure displaying the pairing relations of the two homologs in an FM7/X heterozygote.(C) A picture of DAPI-stained chromosome at meiotic metaphase I in FM7/X oocytes (courtesy of W. Gilliland). The two X and 4th chromosomes are positioned between the two autosomal bivalents and the poles, with the dot-like 4th chromosomes located closer to the poles. The FM7 chromosome (denoted by the brighter DAPI staining at its tip) is located between the autosomes and the upper pole, while the normal sequence X chromosome lies in the lower half of the spindle. Note that the X and FM7 chromosomes are not connected by chiasmata.

Mentions: Specifically, we set out to examine the effects of an X chromosome balancer known as FM7 [12]. As shown in Figure 1A, the FM7 chromosome differs from a normal sequence homolog by three separate but overlapping paracentric inversions: a large inversion, (In(1)sc8), that spans the length of the X chromosome, and two smaller inversions, (In(1)dl-49 and In(1)15DE-20AE), that both lie within In(1)sc8. Thus, FM7 differs in sequence from a normal sequence X chromosome by six breakpoints distributed along the length of the X chromosome, four of which (1B, 4D, 11F, and 15DE) disrupt the euchromatin. The remaining two breaks (20A and 20E) disrupt the centric heterochromatin. The complex juxtaposition of homologs that would be required to fully pair both X chromosomes in FM7/X heterozygotes is displayed in Figure 1B.


All paired up with no place to go: pairing, synapsis, and DSB formation in a balancer heterozygote.

Gong WJ, McKim KS, Hawley RS - PLoS Genet. (2005)

The Multiply Inverted Balancer Chromosome FM7(A) Schematic diagram of the generation of chromosomal inversions from X to FM7. Color represents the regions that are involved in inversions, and arrows are used to indicate the orientation of each region with respect to the centromere. Circles represent the centromeres. The numbers below each structure represent positions of the standard polytene map.(B) A hypothetical structure displaying the pairing relations of the two homologs in an FM7/X heterozygote.(C) A picture of DAPI-stained chromosome at meiotic metaphase I in FM7/X oocytes (courtesy of W. Gilliland). The two X and 4th chromosomes are positioned between the two autosomal bivalents and the poles, with the dot-like 4th chromosomes located closer to the poles. The FM7 chromosome (denoted by the brighter DAPI staining at its tip) is located between the autosomes and the upper pole, while the normal sequence X chromosome lies in the lower half of the spindle. Note that the X and FM7 chromosomes are not connected by chiasmata.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1285065&req=5

pgen-0010067-g001: The Multiply Inverted Balancer Chromosome FM7(A) Schematic diagram of the generation of chromosomal inversions from X to FM7. Color represents the regions that are involved in inversions, and arrows are used to indicate the orientation of each region with respect to the centromere. Circles represent the centromeres. The numbers below each structure represent positions of the standard polytene map.(B) A hypothetical structure displaying the pairing relations of the two homologs in an FM7/X heterozygote.(C) A picture of DAPI-stained chromosome at meiotic metaphase I in FM7/X oocytes (courtesy of W. Gilliland). The two X and 4th chromosomes are positioned between the two autosomal bivalents and the poles, with the dot-like 4th chromosomes located closer to the poles. The FM7 chromosome (denoted by the brighter DAPI staining at its tip) is located between the autosomes and the upper pole, while the normal sequence X chromosome lies in the lower half of the spindle. Note that the X and FM7 chromosomes are not connected by chiasmata.
Mentions: Specifically, we set out to examine the effects of an X chromosome balancer known as FM7 [12]. As shown in Figure 1A, the FM7 chromosome differs from a normal sequence homolog by three separate but overlapping paracentric inversions: a large inversion, (In(1)sc8), that spans the length of the X chromosome, and two smaller inversions, (In(1)dl-49 and In(1)15DE-20AE), that both lie within In(1)sc8. Thus, FM7 differs in sequence from a normal sequence X chromosome by six breakpoints distributed along the length of the X chromosome, four of which (1B, 4D, 11F, and 15DE) disrupt the euchromatin. The remaining two breaks (20A and 20E) disrupt the centric heterochromatin. The complex juxtaposition of homologs that would be required to fully pair both X chromosomes in FM7/X heterozygotes is displayed in Figure 1B.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Stowers Institute for Medical Research, Kansas City, Missouri, United States of America.

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.

Show MeSH
Related in: MedlinePlus