scholarly journals THE GENETICS OF ASYMMETRICAL MALE STERILITY IN DROSOPHILA MOJAVENSIS AND DROSOPHILA ARIZONENSIS HYBRIDS: INTERACTIONS BETWEEN THE Y -CHROMOSOME AND AUTOSOMES

Evolution ◽  
1986 ◽  
Vol 40 (6) ◽  
pp. 1160-1170 ◽  
Author(s):  
Gilles Vigneault ◽  
E. Zouros
Keyword(s):  
Male Sterility ◽  
Y Chromosome ◽  
Drosophila Mojavensis

scholarly journals An autosomal factor from Drosophila arizonae restores normal spermatogenesis in Drosophila mojavensis males carrying the D. arizonae Y chromosome.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 309-318
Author(s):  
A C Pantazidis ◽  
V K Galanopoulos ◽  
E Zouros
Keyword(s):  
Y Chromosome ◽  
Hybrid Sterility ◽  
Light And Electron Microscopy ◽  
Genetic Material ◽  
Drosophila Mojavensis ◽  
Fourth Chromosome ◽  
Motility Factor ◽  
Drosophila Arizonae ◽  
Male Hybrid ◽  
Necessary And Sufficient

Abstract Males of Drosophila mojavensis whose Y chromosome is replaced by the Y chromosome of the sibling species Drosophila arizonae are sterile. It is shown that genetic material from the fourth chromosome of D. arizonae is necessary and sufficient, in single dose, to restore fertility in these males. In introgression and mapping experiments this material segregates as a single Mendelian factor (sperm motility factor, SMF). Light and electron microscopy studies of spermatogenesis in D. mojavensis males whose Y chromosome is replaced by introgression with the Y chromosome of D. arizonae (these males are symbolized as mojYa) revealed postmeiotic abnormalities all of which are restored when the SMF of D. arizonae is co-introgressed (these males are symbolized as mojYaSMFa). The number of mature sperm per bundle in mojYaSMFa is slightly less than in pure D. mojavensis and is even smaller in males whose fertility is rescued by introgression of the entire fourth chromosome of D. arizonae. These observations establish an interspecific incompatibility between the Y chromosome and an autosomal factor (or more than one tightly linked factors) that can be useful for the study of the evolution of male hybrid sterility in Drosophila and the genetic control of spermatogenesis.

scholarly journals The Contribution of the Y Chromosome to Hybrid Male Sterility in House Mice

Genetics ◽  
2012 ◽  
Vol 191 (4) ◽  
pp. 1271-1281 ◽  
Author(s):  
Polly Campbell ◽  
Jeffrey M. Good ◽  
Matthew D. Dean ◽  
Priscilla K. Tucker ◽  
Michael W. Nachman
Keyword(s):  
Male Sterility ◽  
Y Chromosome ◽  
House Mice ◽  
Hybrid Male ◽  
Hybrid Male Sterility

scholarly journals The genetic basis of Haldane's rule and the nature of asymmetric hybrid male sterility among Drosophila simulans, Drosophila mauritiana and Drosophila sechellia.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 251-260 ◽  
Author(s):  
L W Zeng ◽  
R S Singh
Keyword(s):  
Male Sterility ◽  
Y Chromosome ◽  
Genetic Basis ◽  
Drosophila Simulans ◽  
Hybrid Male ◽  
Hybrid Male Sterility ◽  
Haldane’S Rule ◽  
Drosophila Sechellia ◽  
Haldane's Rule ◽  
Drosophila Mauritiana

Abstract Haldane's rule (i.e., the preferential hybrid sterility and inviability of heterogametic sex) has been known for 70 years, but its genetic basis, which is crucial to the understanding of the process of species formation, remains unclear. In the present study, we have investigated the genetic basis of hybrid male sterility using Drosophila simulans, Drosophila mauritiana and Drosophila sechellia. An introgression of D. sechellia Y chromosome into a fairly homogenous background of D. simulans did not show any effect of the introgressed Y on male sterility. The substitution of D. simulans Y chromosome into D. sechellia, and both reciprocal Y chromosome substitutions between D. simulans and D. mauritiana were unsuccessful. Introgressions of cytoplasm between D. simulans and D. mauritiana (or D. sechellia) also did not have any effect on hybrid male sterility. These results rule out the X-Y interaction hypothesis as a general explanation of Haldane's rule in this species group and indicate an involvement of an X-autosome interaction. Models of symmetrical and asymmetrical X-autosome interaction have been developed which explain the Y chromosome substitution results and suggest that evolution of interactions between different genetic elements in the early stages of speciation is more likely to be of an asymmetrical nature. The model of asymmetrical X-autosome interaction also predicts that different sets of interacting genes may be involved in different pairs of related species and can account for the observation that hybrid male sterility in many partially isolated species is often nonreciprocal or unidirectional.

scholarly journals Genetic Analysis of a Y-Chromosome Region That Induces Triplosterile Phenotypes and Is Essential for Spermatid Individualization in Drosophila melanogaster

Genetics ◽  
2000 ◽  
Vol 155 (1) ◽  
pp. 179-189
Author(s):  
Benjamin Timakov ◽  
Ping Zhang
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Male Sterility ◽  
Y Chromosome ◽  
Fluorescent Probes ◽  
Male Fertility ◽  
Chromosome Region ◽  
The Other ◽  
Axonemal Dynein ◽  
Dynein Arms

Abstract The heterochromatic Y chromosome of Drosophila melanogaster contains ~40 Mb of DNA but has only six loci mutable to male sterility. Region h1-h9 on YL, which carries the kl-3 and kl-5 loci, induces male sterility when present in three copies. We show that three separate segments within the region are responsible for the triplosterility and have an additive effect on male fertility. The triplosterile males displayed pleiotropic defects, beginning at early postmeiotic stages. However, the triplosterility was unaffected by kl-3 or kl-5 alleles. These data suggest that region h1-h9 is complex and may contain novel functions in addition to those of the previously identified kl-3 and kl-5 loci. The kl-3 and kl-5 mutations as well as deficiencies within region h1-h9 result in loss of the spermatid axonemal outer dynein arms. Examination using fluorescent probes showed that males deficient for h1-h3 or h4-h9 displayed a postmeiotic lesion with disrupted individualization complexes scattered along the spermatid bundle. In contrast, the kl-3 and kl-5 mutations had no effect on spermatid individualization despite the defect in the axonemes. These results demonstrate that region h1-h9 carries genetically separable functions: one required for spermatid individualization and the other essential for assembling the axonemal dynein arms.

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