Meiotic segregation of chromosomes in Drosophila melanogaster oocytes

Chromosoma ◽  
1977 ◽  
Vol 63 (3) ◽  
pp. 273-286 ◽  
Author(s):  
J. Puro ◽  
S. Nokkala
Development ◽  
1990 ◽  
Vol 108 (2) ◽  
pp. 251-260
Author(s):  
J. Casal ◽  
C. Gonzalez ◽  
F. Wandosell ◽  
J. Avila ◽  
P. Ripoll

Since spermatogenesis in Drosophila is a series of interconnected and interdependent steps and most of the spermatogenic events take place in the absence of transcription, failures in a given stage can give rise to a cascade of defects later on. The asp locus of Drosophila melanogaster codes for a non-tubulin component implicated in proper spindle structure and/or function (Ripoll et al. 1985). Homozygous asp males exhibit abnormal meiotic spindles giving rise to altered segregation of chromosomes and mitochondria and failures in cytokinesis. Postmeiotic spermatogenic stages of asp males show a series of alterations that we interpret as due to the previously occurring defective meiosis because meiotic spindles are the only microtubular structure altered in mutant testes. The most conspicuous alterations are: (i) variable size of nuclei and nebenkerns of early spermatids, which are also multinucleate instead of having single and uniformly sized nuclei; (ii) elongating spermatids in which abnormal-sized mitochondrial derivatives elongate alongside more than one axoneme; (iii) failures in the individualization process, where abnormal spermatids remain syncytial, and seem to be eliminated during the coiling stage.


2019 ◽  
Author(s):  
Michaelyn Hartmann ◽  
James Umbanhowar ◽  
Jeff Sekelsky

AbstractCrossovers are essential in meiosis of most organisms to ensure the proper segregation of chromosomes. The lack or improper placement of crossovers can result in nondisjunction and aneuploidy in progeny. Crossovers near the centromere can cause nondisjunction; centromere-proximal crossovers are suppressed by what is termed the centromere effect, but the mechanism is unknown. Here, we investigate contributions to centromere-proximal crossover suppression in Drosophila melanogaster. We mapped a large number of centromere-proximal crossovers and find that crossovers are essentially absent from the highly-repetitive (HR)-heterochromatin surrounding the centromere but occur at a low frequency within the less-repetitive (LR)-heterochromatic region and adjacent euchromatin. Previous research suggested that flies that lack the Bloom syndrome helicase (Blm) lose meiotic of crossover patterning, including the centromere effect. Mapping of centromere-proximal crossovers in Blm mutants reveals that the suppression within the HR-heterochromatin is intact, but the centromere effect is lost. We conclude that centromere-proximal crossovers are suppressed by two separable mechanisms: the HR-heterochromatin effect, which completely suppresses crossovers in the HR-heterochromatin, and the centromere effect, which suppresses crossovers with a dissipating effect with distance from the centromere.


1982 ◽  
Vol 39 (2) ◽  
pp. 157-168 ◽  
Author(s):  
Arthur J. Hilliker ◽  
David G. Holm ◽  
R. Appels

SummaryIn this report we examine the meiotic segregation of compound second autosomes sharing varying extents of heterochromatic and euchromatic homology. The second chromosome heterochromatin does not appear to influence the random meiotic segregation of compound second autosomes during spermatogenesis; however, the proximal euchromatin is implicated in male meiotic pairing. We conclude that male autosomal meiotic pairing sites are specific euchromatic chromosomal regions.


Andrologia ◽  
2010 ◽  
Vol 42 (1) ◽  
pp. 27-34 ◽  
Author(s):  
A. Perrin ◽  
F. Morel ◽  
N. Douet-Guilbert ◽  
M.-J. Le Bris ◽  
J. Amice ◽  
...  

1983 ◽  
Vol 41 (1) ◽  
pp. 103-103

Genet. Res., Camb. (1982), 39, pp. 157–168The relationship between heterochromatic homology and meiotic segregation of compound second autosomes during spermatogenesis in Drosophila melanogasterBy Arthur J. Hilliker, David G. Holm and R. AppelsSeveral errors occurred in the headings of Table 4, on p. 162: the table should read as follows:


Genetics ◽  
1993 ◽  
Vol 134 (3) ◽  
pp. 825-835 ◽  
Author(s):  
W L Whyte ◽  
H Irick ◽  
T Arbel ◽  
G Yasuda ◽  
R L French ◽  
...  

Abstract The regular segregation of achiasmate chromosomes in Drosophila melanogaster females is ensured by two distinct segregational systems. The segregation of achiasmate homologs is assured by the maintenance of heterochromatic pairing; while the segregation of heterologous chromosomes is ensured by a separate mechanism that may not require physical association. AxsD (Aberrant X segregation) is a dominant mutation that specifically impairs the segregation of achiasmate homologs; heterologous achiasmate segregations are not affected. As a result, achiasmate homologs frequently participate in heterologous segregations at meiosis I. We report the isolation of two intragenic revertants of the AxsD mutation (Axsr2 and Axsr3) that exhibit a recessive meiotic phenotype identical to that observed in AxsD/AxsD females. A third revertant (Axsr1) exhibits no meiotic phenotype as a homozygote, but a meiotic defect is observed in Axsr1/Axsr2 females. Therefore mutations at the AxsD locus define a gene necessary and specific for homologous achiasmate segregation during meiosis. We also characterize the interactions of mutations at the Axs locus with two other meiotic mutations (ald and ncd). Finally, we propose a model in which Axs+ is required for the normal separation of paired achiasmate homologs. In the absence of Axs+ function, the homologs are often unable to separate from each other and behave as a single segregational unit that is free to segregate from heterologous chromosomes.


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