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Mutations in the alpha-tubulin 67C gene specifically impair achiasmate segregation in Drosophila melanogaster.

Matthies HJ, Messina LG, Namba R, Greer KJ, Walker MY, Hawley RS - J. Cell Biol. (1999)

Bottom Line: Genetic studies demonstrate that these mutations also strongly and specifically decrease the fidelity of achiasmate chromosome segregation.Proper centromere orientation, chromatin elongation, and faithful segregation can all be restored by a decrease in the amount of the Nod chromokinesin.These results suggest that the accurate segregation of achiasmate chromosomes requires the proper balancing of forces acting on the chromosomes during prometaphase.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Section of Molecular and Cellular Biology, University of California at Davis, Davis, California 95616, USA.

ABSTRACT
Drosophila melanogaster oocytes heterozygous for mutations in the alpha-tubulin 67C gene (alphatub67C) display defects in centromere positioning during prometaphase of meiosis I. The centromeres do not migrate to the poleward edges of the chromatin mass, and the chromatin fails to stretch during spindle lengthening. These results suggest that the poleward forces acting at the kinetochore are compromised in the alphatub67C mutants. Genetic studies demonstrate that these mutations also strongly and specifically decrease the fidelity of achiasmate chromosome segregation. Proper centromere orientation, chromatin elongation, and faithful segregation can all be restored by a decrease in the amount of the Nod chromokinesin. These results suggest that the accurate segregation of achiasmate chromosomes requires the proper balancing of forces acting on the chromosomes during prometaphase.

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The αtub67CP40mutation leads to elevated levels of achiasmate chromosome missegregation. The frequencies of X (dark bars) and 4th (light bars) chromosome missegregation (nondisjunction) are displayed for various genotypes. The genotype at the αtub67C locus is represented as: +/+, two wild-type copies of the αtub67C gene; +/P40, heterozygous for the αtub67CP40 mutation; and +/P40Δ, heterozygous for the αtub67CP40 mutation. These experiments were done in both X/X and X/FM7 females, allowing us to examine segregation in oocytes with (+) or without (−) exchange on the X chromosome, respectively. N is the adjusted total of progeny scored (Hawley et al. 1993). Chromosome segregation was monitored by methods outlined in Hawley et al. 1993 and Sekelsky et al. 1999. Although females homozygous for αtub67CP40are sterile, αtub67CP40Δ/+ females are fully fertile and viable.
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Figure 4: The αtub67CP40mutation leads to elevated levels of achiasmate chromosome missegregation. The frequencies of X (dark bars) and 4th (light bars) chromosome missegregation (nondisjunction) are displayed for various genotypes. The genotype at the αtub67C locus is represented as: +/+, two wild-type copies of the αtub67C gene; +/P40, heterozygous for the αtub67CP40 mutation; and +/P40Δ, heterozygous for the αtub67CP40 mutation. These experiments were done in both X/X and X/FM7 females, allowing us to examine segregation in oocytes with (+) or without (−) exchange on the X chromosome, respectively. N is the adjusted total of progeny scored (Hawley et al. 1993). Chromosome segregation was monitored by methods outlined in Hawley et al. 1993 and Sekelsky et al. 1999. Although females homozygous for αtub67CP40are sterile, αtub67CP40Δ/+ females are fully fertile and viable.

Mentions: As shown in Fig. 4, FM7/X; αtub67CP40/+ females display 20-fold higher levels of X chromosome nondisjunction than do FM7/X; +/+ control females, suggesting that most, if not all, of these cases of X chromosome nondisjunction are due to a failure of achiasmate segregation. Indeed, even those few nondisjunction events that were observed in X/X; αtub67CP40/+ females occurred in the 5–8% of the oocytes in which the two X chromosomes failed to undergo exchange (data not shown). An additional mutant allele, derived from αtub67CP40and denoted αtub67CP40Δ, displayed an enhancement of meiotic chromosome missegregation relative to the original P element allele (Fig. 4). The αtub67CP40Δ allele differs from the original P element insertion only in that a substantial internal portion of the P element has been removed. Heterozygosity for αtub67C P40Δ, as assayed in FM7/X females, leads to high levels of achiasmate nondisjunction; however, the αtub67CP40Δ mutant has little or no effect on the segregation of chiasmate X chromosomes (in X/X females). For both of these alleles, the observed chromosome missegregation must primarily be due to nondisjunction rather than loss, as the frequency of diplo-X exceptions always equals or slightly exceeds that of o-X exceptions (data not shown).


Mutations in the alpha-tubulin 67C gene specifically impair achiasmate segregation in Drosophila melanogaster.

Matthies HJ, Messina LG, Namba R, Greer KJ, Walker MY, Hawley RS - J. Cell Biol. (1999)

The αtub67CP40mutation leads to elevated levels of achiasmate chromosome missegregation. The frequencies of X (dark bars) and 4th (light bars) chromosome missegregation (nondisjunction) are displayed for various genotypes. The genotype at the αtub67C locus is represented as: +/+, two wild-type copies of the αtub67C gene; +/P40, heterozygous for the αtub67CP40 mutation; and +/P40Δ, heterozygous for the αtub67CP40 mutation. These experiments were done in both X/X and X/FM7 females, allowing us to examine segregation in oocytes with (+) or without (−) exchange on the X chromosome, respectively. N is the adjusted total of progeny scored (Hawley et al. 1993). Chromosome segregation was monitored by methods outlined in Hawley et al. 1993 and Sekelsky et al. 1999. Although females homozygous for αtub67CP40are sterile, αtub67CP40Δ/+ females are fully fertile and viable.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2168102&req=5

Figure 4: The αtub67CP40mutation leads to elevated levels of achiasmate chromosome missegregation. The frequencies of X (dark bars) and 4th (light bars) chromosome missegregation (nondisjunction) are displayed for various genotypes. The genotype at the αtub67C locus is represented as: +/+, two wild-type copies of the αtub67C gene; +/P40, heterozygous for the αtub67CP40 mutation; and +/P40Δ, heterozygous for the αtub67CP40 mutation. These experiments were done in both X/X and X/FM7 females, allowing us to examine segregation in oocytes with (+) or without (−) exchange on the X chromosome, respectively. N is the adjusted total of progeny scored (Hawley et al. 1993). Chromosome segregation was monitored by methods outlined in Hawley et al. 1993 and Sekelsky et al. 1999. Although females homozygous for αtub67CP40are sterile, αtub67CP40Δ/+ females are fully fertile and viable.
Mentions: As shown in Fig. 4, FM7/X; αtub67CP40/+ females display 20-fold higher levels of X chromosome nondisjunction than do FM7/X; +/+ control females, suggesting that most, if not all, of these cases of X chromosome nondisjunction are due to a failure of achiasmate segregation. Indeed, even those few nondisjunction events that were observed in X/X; αtub67CP40/+ females occurred in the 5–8% of the oocytes in which the two X chromosomes failed to undergo exchange (data not shown). An additional mutant allele, derived from αtub67CP40and denoted αtub67CP40Δ, displayed an enhancement of meiotic chromosome missegregation relative to the original P element allele (Fig. 4). The αtub67CP40Δ allele differs from the original P element insertion only in that a substantial internal portion of the P element has been removed. Heterozygosity for αtub67C P40Δ, as assayed in FM7/X females, leads to high levels of achiasmate nondisjunction; however, the αtub67CP40Δ mutant has little or no effect on the segregation of chiasmate X chromosomes (in X/X females). For both of these alleles, the observed chromosome missegregation must primarily be due to nondisjunction rather than loss, as the frequency of diplo-X exceptions always equals or slightly exceeds that of o-X exceptions (data not shown).

Bottom Line: Genetic studies demonstrate that these mutations also strongly and specifically decrease the fidelity of achiasmate chromosome segregation.Proper centromere orientation, chromatin elongation, and faithful segregation can all be restored by a decrease in the amount of the Nod chromokinesin.These results suggest that the accurate segregation of achiasmate chromosomes requires the proper balancing of forces acting on the chromosomes during prometaphase.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Section of Molecular and Cellular Biology, University of California at Davis, Davis, California 95616, USA.

ABSTRACT
Drosophila melanogaster oocytes heterozygous for mutations in the alpha-tubulin 67C gene (alphatub67C) display defects in centromere positioning during prometaphase of meiosis I. The centromeres do not migrate to the poleward edges of the chromatin mass, and the chromatin fails to stretch during spindle lengthening. These results suggest that the poleward forces acting at the kinetochore are compromised in the alphatub67C mutants. Genetic studies demonstrate that these mutations also strongly and specifically decrease the fidelity of achiasmate chromosome segregation. Proper centromere orientation, chromatin elongation, and faithful segregation can all be restored by a decrease in the amount of the Nod chromokinesin. These results suggest that the accurate segregation of achiasmate chromosomes requires the proper balancing of forces acting on the chromosomes during prometaphase.

Show MeSH
Related in: MedlinePlus