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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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Quantitation of the failure of chromatin stretching due to the αtub67CP40 mutation. Shown are plots of chromatin length distributions in the indicated genotypes (A, B, and C), spindle versus chromatin length (D, E, and F), and finally, spindle length versus axial ratio of the chromatin (chromatin length/chromatin width) (G, H, and I).
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Figure 2: Quantitation of the failure of chromatin stretching due to the αtub67CP40 mutation. Shown are plots of chromatin length distributions in the indicated genotypes (A, B, and C), spindle versus chromatin length (D, E, and F), and finally, spindle length versus axial ratio of the chromatin (chromatin length/chromatin width) (G, H, and I).

Mentions: Chromatin masses in wild-type spindles appear almost spherical as spindle assembly initiates, but elongate as spindle assembly progresses. However, in αtub67CP40/+ oocytes, the chromatin remains almost spherical, even on fully elongated spindles. A plot of the chromatin mass length from oocytes with two wild-type copies of the αtub67C gene reveals a wide distribution of chromatin lengths (Fig. 2 A). In contrast, a plot of the chromatin mass length from oocytes heterozygous for αtub67CP40 exhibits a very narrow distribution (Fig. 2 B) that is centered at a much shorter length (Fig. 2 B). The chromatin mass ranged in length from 3.1–18 μm in control oocytes, whereas in FM7/X; αtub67CP40/+ oocytes, chromatin length was observed to vary from 2.4–5.8 μm. Thus, in oocytes heterozygous for the αtub67CP40mutation, the chromatin mass fails to elongate properly.


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)

Quantitation of the failure of chromatin stretching due to the αtub67CP40 mutation. Shown are plots of chromatin length distributions in the indicated genotypes (A, B, and C), spindle versus chromatin length (D, E, and F), and finally, spindle length versus axial ratio of the chromatin (chromatin length/chromatin width) (G, H, and I).
© Copyright Policy
Related In: Results  -  Collection

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

Figure 2: Quantitation of the failure of chromatin stretching due to the αtub67CP40 mutation. Shown are plots of chromatin length distributions in the indicated genotypes (A, B, and C), spindle versus chromatin length (D, E, and F), and finally, spindle length versus axial ratio of the chromatin (chromatin length/chromatin width) (G, H, and I).
Mentions: Chromatin masses in wild-type spindles appear almost spherical as spindle assembly initiates, but elongate as spindle assembly progresses. However, in αtub67CP40/+ oocytes, the chromatin remains almost spherical, even on fully elongated spindles. A plot of the chromatin mass length from oocytes with two wild-type copies of the αtub67C gene reveals a wide distribution of chromatin lengths (Fig. 2 A). In contrast, a plot of the chromatin mass length from oocytes heterozygous for αtub67CP40 exhibits a very narrow distribution (Fig. 2 B) that is centered at a much shorter length (Fig. 2 B). The chromatin mass ranged in length from 3.1–18 μm in control oocytes, whereas in FM7/X; αtub67CP40/+ oocytes, chromatin length was observed to vary from 2.4–5.8 μm. Thus, in oocytes heterozygous for the αtub67CP40mutation, the chromatin mass fails to elongate properly.

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