Mutations in the α-Tubulin 67C Gene Specifically Impair Achiasmate Segregation in Drosophila melanogaster

Abstract

Drosophila melanogaster oocytes heterozygous for mutations in the α-tubulin 67C gene (αtub67C) 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 αtub67C 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.

Somatic pairing, endomitosis and chromosome aberrations in snakes (Viperidae and Colubridae)

“…Further, it was demonstrated that the Nod kinesin-like protein is specifically required for achiasmate chromosome segregation in Drosophila melanogaster (Zhang et al 1990). Also it was shown that α-tubulin 67C gene impair achiasmate chromosome segregation in this species (Matthies et al 1999). According to our assumption, the cells with somatic pairing and premeiotic endoreduplication would enter directly to second meiosis division (m II).…”

Chromokinesin Kid and kinetochore kinesin CENP-E differentially support chromosome congression without end-on attachment to microtubules

“…On meiotic chromosomes in Drosophila melanogaster, NOD, a non-motile kinesin-10, is suggested to push the chromosome arms towards the spindle equator by binding to polymerizing microtubule plus-ends [38][39][40] . End-on attachment contributes not only to chromosome motion towards the spindle equator, but also to maintaining chromosome oscillation around the spindle equator, which is dependent on Kif18A 8 .…”

Orphan Kinesin NOD Lacks Motile Properties But Does Possess a Microtubule-stimulated ATPase Activity

“…Chromatin stretching has been observed during Drosophila female meiosis (Theurkauf and Hawley, 1992;Page and Orr-Weaver, 1997;Matthies et al, 1999). At the onset of Drosophila female meiosis, chromatin exists as a compact sphere of 4 -5 m, which is capable of elongating into a structure of up to 20 m in length (Page and Orr-Weaver, 1997;Matthies et al, 1999) in a microtubule-dependent manner (Page and Orr-Weaver, 1997).…”

“…At the onset of Drosophila female meiosis, chromatin exists as a compact sphere of 4 -5 m, which is capable of elongating into a structure of up to 20 m in length (Page and Orr-Weaver, 1997;Matthies et al, 1999) in a microtubule-dependent manner (Page and Orr-Weaver, 1997). This stretching of chromatin may be due in part to the action of microtubule-based motors.…”

“…Genetic and molecular studies of the dominant nod mutation nod DTW and its partial revertants have demonstrated that the motor domain of NOD is critical for its function (Rasooly et al, 1991(Rasooly et al, , 1994. The genetic and cytological characterizations of NOD strongly suggest that it exerts a plateward (or antipolar) force (Rasooly et al, 1991(Rasooly et al, , 1994Theurkauf and Hawley, 1992;Afshar et al, 1995a;Karpen et al, 1996;Matthies et al, 1999) and NOD is found along the surface of meiotic chromosomes (Afshar et al, 1995a). Assuming that the polarity of MTs in the oocyte meiosis I spindle is canonical, NOD must act as either a plus-end-directed motor or as a brake.…”