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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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Failure of centromere positioning (MEI-S332 protein) in heterozygous αtub67CP40 mutant oocytes. FM7/X oocytes with the indicated genotypes were immunolabeled with anticore histone, antitubulin, and anti–MEI-S332 antibodies. The first column displays the projections of MEI-S332 alone (red, whereas the second columns displays the projections for both histone [green] and MEI-S332 [red]). In the first column are the projections of the MEI-S332 data, and the second column is the merged projection of the histone and MEI-S332 data. The top two rows depict oocytes heterozygous for αtub67CP40. In the oocyte displayed in the top row, a portion of the MEI-S332 immunoreactivity is found adjacent to the main chromosome mass, whereas the remainder of the protein is detected toward the center of the chromosomal mass. In the second panel, virtually all of the MEI-S332 immunoreactivity remains at one pole. The middle two rows are oocytes heterozygous for both αtub67CP40and nod (nodb17). In each of these oocytes, the MEI-S332 immunoreactivity is seen at opposite poles of the lengthening chromosomal mass, as is observed in wild-type oocytes (bottom row). Bar, 4 μm.
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Figure 3: Failure of centromere positioning (MEI-S332 protein) in heterozygous αtub67CP40 mutant oocytes. FM7/X oocytes with the indicated genotypes were immunolabeled with anticore histone, antitubulin, and anti–MEI-S332 antibodies. The first column displays the projections of MEI-S332 alone (red, whereas the second columns displays the projections for both histone [green] and MEI-S332 [red]). In the first column are the projections of the MEI-S332 data, and the second column is the merged projection of the histone and MEI-S332 data. The top two rows depict oocytes heterozygous for αtub67CP40. In the oocyte displayed in the top row, a portion of the MEI-S332 immunoreactivity is found adjacent to the main chromosome mass, whereas the remainder of the protein is detected toward the center of the chromosomal mass. In the second panel, virtually all of the MEI-S332 immunoreactivity remains at one pole. The middle two rows are oocytes heterozygous for both αtub67CP40and nod (nodb17). In each of these oocytes, the MEI-S332 immunoreactivity is seen at opposite poles of the lengthening chromosomal mass, as is observed in wild-type oocytes (bottom row). Bar, 4 μm.

Mentions: As expected, MEI-S332 protein was found on the poleward edges of the chromatin masses in FM7/X; +/+ spindles (wild-type; see Fig. 3, bottom row). In contrast, the MEI-S332 localization pattern from oocytes derived from FM7/X; αtub67CP40/+ females indicated that the centromeres were positioned abnormally (Fig. 3, top two rows). In no case (0/15) was the MEI-S332 protein properly positioned at the distal tips of the elongating chromatin mass, as is observed in wild-type oocytes (Moore et al. 1998; Fig. 3, bottom row). Rather, MEI-S332 either failed to be completely localized at opposite poles of the main chromosome mass (Fig. 3, top row) or was found entirely on one side of the main chromatin mass (Fig. 3, second row). These cytological studies demonstrate that heterozygosity for the αtub67CP40mutation leads to a defect in both chromatin stretching and centromere positioning.


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)

Failure of centromere positioning (MEI-S332 protein) in heterozygous αtub67CP40 mutant oocytes. FM7/X oocytes with the indicated genotypes were immunolabeled with anticore histone, antitubulin, and anti–MEI-S332 antibodies. The first column displays the projections of MEI-S332 alone (red, whereas the second columns displays the projections for both histone [green] and MEI-S332 [red]). In the first column are the projections of the MEI-S332 data, and the second column is the merged projection of the histone and MEI-S332 data. The top two rows depict oocytes heterozygous for αtub67CP40. In the oocyte displayed in the top row, a portion of the MEI-S332 immunoreactivity is found adjacent to the main chromosome mass, whereas the remainder of the protein is detected toward the center of the chromosomal mass. In the second panel, virtually all of the MEI-S332 immunoreactivity remains at one pole. The middle two rows are oocytes heterozygous for both αtub67CP40and nod (nodb17). In each of these oocytes, the MEI-S332 immunoreactivity is seen at opposite poles of the lengthening chromosomal mass, as is observed in wild-type oocytes (bottom row). Bar, 4 μm.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 3: Failure of centromere positioning (MEI-S332 protein) in heterozygous αtub67CP40 mutant oocytes. FM7/X oocytes with the indicated genotypes were immunolabeled with anticore histone, antitubulin, and anti–MEI-S332 antibodies. The first column displays the projections of MEI-S332 alone (red, whereas the second columns displays the projections for both histone [green] and MEI-S332 [red]). In the first column are the projections of the MEI-S332 data, and the second column is the merged projection of the histone and MEI-S332 data. The top two rows depict oocytes heterozygous for αtub67CP40. In the oocyte displayed in the top row, a portion of the MEI-S332 immunoreactivity is found adjacent to the main chromosome mass, whereas the remainder of the protein is detected toward the center of the chromosomal mass. In the second panel, virtually all of the MEI-S332 immunoreactivity remains at one pole. The middle two rows are oocytes heterozygous for both αtub67CP40and nod (nodb17). In each of these oocytes, the MEI-S332 immunoreactivity is seen at opposite poles of the lengthening chromosomal mass, as is observed in wild-type oocytes (bottom row). Bar, 4 μm.
Mentions: As expected, MEI-S332 protein was found on the poleward edges of the chromatin masses in FM7/X; +/+ spindles (wild-type; see Fig. 3, bottom row). In contrast, the MEI-S332 localization pattern from oocytes derived from FM7/X; αtub67CP40/+ females indicated that the centromeres were positioned abnormally (Fig. 3, top two rows). In no case (0/15) was the MEI-S332 protein properly positioned at the distal tips of the elongating chromatin mass, as is observed in wild-type oocytes (Moore et al. 1998; Fig. 3, bottom row). Rather, MEI-S332 either failed to be completely localized at opposite poles of the main chromosome mass (Fig. 3, top row) or was found entirely on one side of the main chromatin mass (Fig. 3, second row). These cytological studies demonstrate that heterozygosity for the αtub67CP40mutation leads to a defect in both chromatin stretching and centromere positioning.

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