A bidirectional kinesin motor in live Drosophila embryos.

Spindle assembly and elongation involve poleward and away-from-the-pole forces produced by microtubule dynamics and spindle-associated motors. Here, we show that a bidirectional Drosophila Kinesin-14 motor that moves either to the microtubule plus or minus end in vitro unexpectedly causes only minor spindle defects in vivo. However, spindles of mutant embryos are longer than wild type, consistent with increased plus-end motor activity.

Assembly pathway of the anastral Drosophila oocyte meiosis I spindle.

Oocyte meiotic spindles of many species are anastral and lack centrosomes to nucleate microtubules. Assembly of anastral spindles occurs by a pathway that differs from that of most mitotic spindles. Here we analyze assembly of the Drosophila oocyte meiosis I spindle and the role of the Nonclaret disjunctional (Ncd) motor in spindle assembly using wild-type and mutant Ncd fused to GFP.

Nonlinear dynamics of a Bose-Einstein condensate in a magnetic waveguide.

We have studied the internal and external dynamics of a Bose-Einstein condensate in an anharmonic magnetic waveguide. An oscillating condensate experiences a strong coupling between the center of mass motion and the internal collective modes. Because of the anharmonicity of the magnetic potential, not only the center of mass motion shows harmonic frequency generation, but also the internal dynamics exhibit nonlinear frequency mixing.

Assembly and dynamics of an anastral:astral spindle: the meiosis II spindle of Drosophila oocytes.

The meiosis II spindle of Drosophila oocytes is distinctive in structure, consisting of two tandem spindles with anastral distal poles and an aster-associated spindle pole body between the central poles. Assembly of the anastral:astral meiosis II spindle occurs by reorganization of the meiosis I spindle, without breakdown of the meiosis I spindle. The unusual disk- or ring-shaped central spindle pole body forms de novo in the center of the elongated meiosis I spindle, followed by formation of the central spindle poles.

Spindle dynamics during meiosis in Drosophila oocytes.

Mature oocytes of Drosophila are arrested in metaphase of meiosis I. Upon activation by ovulation or fertilization, oocytes undergo a series of rapid changes that have not been directly visualized previously. We report here the use of the Nonclaret disjunctional (Ncd) microtubule motor protein fused to the green fluorescent protein (GFP) to monitor changes in the meiotic spindle of live oocytes after activation in vitro.

Enhancement of the ncdD microtubule motor mutant by mutants of alpha Tub67C.

Ncd is a kinesin-related microtubule motor protein required for chromosome segregation in Drosophila oocytes and early embryos. In tests for interactions with other proteins, we find that mutants of alpha Tub67C, which affect an oocyte- and early embryo-specific alpha-tubulin, enhance meiotic nondisjunction and zygotic loss of ncdD, a partial loss-of-function mutant of ncd. The enhancement is dominant and allele-specific with respect to alpha Tub67C, and depends on the recessive effects of ncdD.

Centrosome and spindle function of the Drosophila Ncd microtubule motor visualized in live embryos using Ncd-GFP fusion proteins.

The Ncd microtubule motor protein is required for meiotic and early mitotic chromosome distribution in Drosophila. Null mutant females expressing the Ncd motor fused to the Aequorea victoria green fluorescent protein (GFP), regulated by the wild-type ncd promoter, are rescued for chromosome segregation and embryo viability. Analysis of mitosis in live embryos shows cell cycle-dependent localization of Ncd-GFP to centrosomes and spindles.

Haploidy and androgenesis in Drosophila.

Adrogenesis, development from paternal but not maternal chromosomes, can be induced to occur in some organisms, including vertebrates, but has only been reported to occur naturally in interspecific hybrids of the Sicilian stick insect. Androgenesis has not been described previously in Drosophila. We now report the recovery of androgenetic offspring from Drosophila melanogaster females mutant for a gene that affects an oocyte- and embryo-specific alpha-tubulin.

Mutants of the Drosophila ncd microtubule motor protein cause centrosomal and spindle pole defects in mitosis.

Nonclaret disjunctional (ncd) is a kinesin-related microtubule motor protein required for meiotic and early mitotic chromosome distribution in Drosophila. ncd translocates on microtubules with the opposite polarity to kinesin, toward microtubule minus ends, and is associated with spindles in chromosome/spindle preparations. Here we report a new mutant of ncd caused by partial deletion of the predicted coiled-coil central stalk.

Magnification in Drosophila: evidence for an inducible rDNA-specific recombination system.

An experiment is described that provides evidence for an exchange mechanism to explain the increase in ribosomal gene number that occurs during bobbed magnification. We show that bobbed and bobbed-lethal alleles do not magnify in closed X chromosomes, but that a spontaneous ring opening restores normal magnification. The results provide strong evidence that the elementary magnifying event is unequal sister chromatid exchange, and can be interpreted in the framework of an inducible rDNA-specific recombination system as the basis of ribosomal gene magnification.

Constitutive magnification by the Ybb- chromosome of Drosophila melanogaster.

Ybb- is an rDNA-deficient chromosome of Drosophila that has often been used in magnification experiments to induce high-frequency reversion of bobbed (bb) chromosomes. We observed previously that Ybb- causes ring chromosome loss even when the rings are bb+, suggesting that Ybb- induces magnifying sister chromatid exchanges in bb+ rings. Here we show that the Ybb- chromosome causes low levels of bb magnification in bb+ flies.

Separation of meiotic and mitotic effects of claret non-disjunctional on chromosome segregation in Drosophila.

The claret (ca) locus in Drosophila encodes a kinesin-related motor molecule that is required for proper distribution of chromosomes in meiosis in females and in the early mitotic divisions of the embryo. Here we demonstrate that a mutant allele of claret non-disjunctional (ca(nd)), non-claret disjunctional Dominant (ncdD), causes abnormalities in meiotic chromosome segregation, but is near wild-type with respect to early mitotic chromosome segregation. DNA sequence analysis of this mutant allele reveals two missense mutations compared with the predicted wild-type protein.

The claret locus in Drosophila encodes products required for eyecolor and for meiotic chromosome segregation.

The claret (ca) locus in Drosophila encodes products that are needed both for wild-type eyecolor and for correct meiotic chromosome segregation. Mutants described previously provide evidence that two mutationally independent coding regions are present at ca. We have recovered six new P element-induced and one spontaneous ca mutant.

Mutant alleles of the meiotic locus, mei-9, differ in degree of effects on rod chromosome magnification and ring chromosome transmission in Drosophila.

Two mutant alleles of the meiotic locus, mei-9, have been examined for their effect on magnification of a rod Xbb chromosome and transmission of a ring Xbb chromosome under magnifying conditions. Our results indicate that the effects of these two mutations are allele-specific: mei-9a strongly inhibits both rod chromosome magnification and ring chromosome loss under magnifying conditions, while mei-9b has a smaller inhibitory effect on rod chromosome magnification and on the transmission of ring chromosomes under magnifying conditions. These observations can be explained by a difference in leakiness between the two alleles.

Incomplete Y chromosomes promote magnification in male and female Drosophila.

We have recently shown that magnification, an increase in the number of ribosomal RNA genes (rDNA) in gametes produced by rDNA-deficient flies, can occur in female Drosophila if they have a Y chromosome. We now have tested several X-Y translocation and recombinant chromosomes to determine which parts of the Y chromosome are necessary for magnification to occur in females. Our data indicate that the required region is the distal part of the long arm of the Y chromosome, YL.

Magnification of the ribosomal genes in female Drosophila melanogaster.

The genetically induced increase in the number of 18S + 28S ribosomal genes known as magnification has been reported to occur in male Drosophila but has not previously been observed in females. We now report that bobbed magnified (bbm) is recovered in progeny of female Drosophila carrying three different X bobbed (Xbb) chromosomes and the helper XYbb chromosome, which is a derivative of the Ybb- chromosome. Using different combinations of bb or bb+ X and Y chromosomes, we show that magnification in females requires both a deficiency in ribosomal genes and the presence of a Y chromosome: X/X females that are rDNA-deficient but do not carry a Y chromosome do not produce bbm; similarly, X/X/Y females that carry a Y chromosome but are not rDNA-deficient do not produce bbm.

One-step and stepwise magnification of a bobbed lethal chromosome in Drosophila melanogaster.

Bobbed lethal (bbl) chromosomes carry too few ribosomal genes for homozygous flies to be viable. Reversion of bbl chromosomes to bb or nearly bb+ occurs under magnifying conditions at a low frequency in a single generation. These reversions occur too rapidly to be accounted for by single unequal sister chromatid exchanges and seem unlikely to be due to multiple sister strand exchanges within a given cell lineage.

Ring chromosomes and rDNA magnification in Drosophila.

Tartof showed that ribosomal gene magnification in Drosophila was inhibited in a ring X chromosome. The present studies extend this observation by showing that ring X chromosomes are lost meiotically in male Drosophila undergoing ribosomal gene magnification as evidenced by the recovery of a lower number of ring-bearing progeny under magnifying conditions compared with nonmagnifying conditions. Associated with ring chromosome loss is a highly significant increase in the number of double-sized dicentric ring chromosomes in meiotic cells from magnifying males.