The genetics of hybrid sterility between subspecies of the complex of Glossina morsitans Westwood (Diptera: Glossinidae)

1985 ◽  
Vol 75 (4) ◽  
pp. 689-699 ◽  
Author(s):  
P. Rawlings

AbstractCrosses were made between the three subspecies of the complex of Glossina morsitans Westwood and the hybrid females backcrossed. Hybrid female fecundity was highly ‘reactive’ to foreign male genes when the mother was G. morsitans centralis Machado compared with the reciprocal crosses and backcrosses. Hybrid F1 males were unable to inseminate females successfully, and although in nearly a quarter of the dissections sperm was transferred to the uterus, it did not migrate to the spermathecae. Heterozygosity between the X- and Y-chromosomes and most of the autosomes led to high frequencies of sterile males, but homozygosity between the X- and Y-chromosomes could still yield 30–50% sterility. Successive backcrosses of hybrid females between G. m. morsitans and G. m. centralis to the latter subspecies continued to increase the frequency of fertile males. Interactions between X-chromosome and autosomal gene seemed to be responsible for hybrid male sterility, and the number of sterility genes involved appeared to be very few. Crosses involving G. morsitans submorsitans Newstead generally agreed with those between the other two subspecies, but the distortion in the sex ratio of emergent adults limited the application of the data to this subspecies. Competition experiments using sterile hybrid males and fertile males in population cages (30 cm cube) showed that suppression was possible, especially when the ratio of sterile:fertile males was 2:1. The value of stetile hybrid males in tsetse control programmes and the evolution of reproductive isolation in the complex is discussed.

Genetics ◽  
1993 ◽  
Vol 135 (2) ◽  
pp. 443-453 ◽  
Author(s):  
N A Johnson ◽  
H Hollocher ◽  
E Noonburg ◽  
C I Wu

Abstract We attempted to introgress Y chromosomes between three sibling species of Drosophila: D. simulans, D. sechellia and D. mauritiana. Four D. sechellia Y chromosomes were introgressed into D. simulans without loss of fertility whereas the four reciprocal introgressions (D. simulans Y introgressed into D sechellia) all result in sterility. Both reciprocal Y introgressions of D. simulans and D. mauritiana (four of each) also result in sterility. Compared with D. simulans males, the males with the D. sechellia Y chromosome in D. simulans background had lower productivity but only after multiple matings with virgin females. These males also were inferior compared with pure species males in sperm displacement and/or remating ability. The two different Y genotype males, however, were comparable in viability, longevity and mating success in female choice tests. We also use our results to estimate the effective number of autosomal loci interacting with X-linked genes to produce hybrid male sterility.


Genetics ◽  
1994 ◽  
Vol 137 (1) ◽  
pp. 191-199 ◽  
Author(s):  
A W Davis ◽  
E G Noonburg ◽  
C I Wu

Abstract F1 hybrid females between the sibling species Drosophila simulans, Drosophila mauritiana and Drosophila sechellia are completely fertile. However, we have found that female sterility can be observed in F2 backcross females who are homozygous for D. simulans X chromosomes and homozygous for autosomal regions from either D. mauritiana or D. sechellia. Our results indicate that neither D. mauritiana autosome (2 or 3) can cause complete female sterility in a D. simulans background. The simultaneous presence of homozygous regions from both the second and third chromosomes of D. mauritiana, however, causes nearly complete female sterility which cannot be accounted for by their individual effects. The two autosomes of D. sechellia may show a similar pattern. From the same crosses, we also obtained evidence against a role for cytoplasmic or maternal effects in causing hybrid male sterility between these species. Taken with the results presented elsewhere, these observations suggest that epistatic interactions between conspecific genes in a hybrid background may be the prevalent mode of hybrid sterility between recently diverged species.


Genetics ◽  
1996 ◽  
Vol 143 (3) ◽  
pp. 1243-1255 ◽  
Author(s):  
Hope Hollocher ◽  
Chug-I Wu

Abstract A strong effect of homozygous autosomal regions on reproductive isolation was found for crosses between the species in the Drosophila simulans clade. Second chromosome regions were introgressed from D. mauritiana and D. sechellia into D. simulans and tested for their homozygous effects on hybrid male and hybrid female sterility and inviability. Most introgressions are fertile as heterozygotes, yet produce sterile male offspring when made homozygous. The density of homozygous autosomal factors contributing to hybrid male sterility is comparable to the density of X chromosome factors for this level of resolution. Female sterility was also revealed, yet the disparity between male and female levels of sterility was great, with male sterility being up to 23 times greater than female sterility. Complete hybrid inviability was also associated with some regions of the second chromosome, yet there were no strong sex differences. In conclusion, we find no evidence to support a strong X chromosome bias in the evolution of hybrid sterility or inviability but do find a very strong sex bias in the evolution of hybrid sterility. In light of these findings, we reevaluate the current models proposed to explain the genetic pattern of reproductive isolation.


Genetics ◽  
2004 ◽  
Vol 166 (2) ◽  
pp. 789-796 ◽  
Author(s):  
Kyoichi Sawamura ◽  
John Roote ◽  
Chung-I Wu ◽  
Masa-Toshi Yamamoto

Abstract Recent genetic analyses of closely related species of Drosophila have indicated that hybrid male sterility is the consequence of highly complex synergistic effects among multiple genes, both conspecific and heterospecific. On the contrary, much evidence suggests the presence of major genes causing hybrid female sterility and inviability in the less-related species, D. melanogaster and D. simulans. Does this contrast reflect the genetic distance between species? Or, generally, is the genetic basis of hybrid male sterility more complex than that of hybrid female sterility and inviability? To clarify this point, the D. simulans introgression of the cytological region 34D-36A to the D. melanogaster genome, which causes recessive male sterility, was dissected by recombination, deficiency, and complementation mapping. The 450-kb region between two genes, Suppressor of Hairless and snail, exhibited a strong effect on the sterility. Males are (semi-)sterile if this region of the introgression is made homozygous or hemizygous. But no genes in the region singly cause the sterility; this region has at least two genes, which in combination result in male sterility. Further, the males are less fertile when heterozygous with a larger introgression, which suggests that dominant modifiers enhance the effects of recessive genes of male sterility. Such an epistatic view, even in the less-related species, suggests that the genetic complexity is special to hybrid male sterility.


2010 ◽  
Vol 365 (1544) ◽  
pp. 1265-1272 ◽  
Author(s):  
Shannon R. McDermott ◽  
Mohamed A. F. Noor

Meiotic drive causes the distortion of allelic segregation away from Mendelian expected ratios, often also reducing fecundity and favouring the evolution of drive suppressors. If different species evolve distinct drive-suppressor systems, then hybrid progeny may be sterile as a result of negative interactions of these systems' components. Although the hypothesis that meiotic drive may contribute to hybrid sterility, and thus species formation, fell out of favour early in the 1990s, recent results showing an association between drive and sterility have resurrected this previously controversial idea. Here, we review the different forms of meiotic drive and their possible roles in speciation. We discuss the recent empirical evidence for a link between drive and hybrid male sterility, also suggesting a possible mechanistic explanation for this link in the context of chromatin remodelling. Finally, we revisit the population genetics of drive that allow it to contribute to speciation.


1988 ◽  
Vol 120 (11) ◽  
pp. 997-1001 ◽  
Author(s):  
R.H. Gooding

AbstractGlossina palpalis palpalis (Robineau-Desvoidy) and Glossina palpalis gambiensis Vanderplank hybridized readily in the laboratory but hybridized females produced fewer offspring than did females that mated with their own kind. Most hybrid females were fertile when backcrossed to either G. p. palpalis or G. p. gambiensis but almost all hybrid males were sterile. About half of the backcross males were able to fertilize G. p. palpalis and G. p. gambiensis. By using an X chromosome marker gene, tan, evidence was obtained that the X chromosome is involved in hybrid male sterility, either through interaction with the Y chromosome or the autosomes of the other subspecies. There was no evidence for maternally inherited sterility factors of a type that confer unidirectional sterility on hybrid or backcross males.


2021 ◽  
Vol 12 ◽  
Author(s):  
Daven C. Presgraves ◽  
Colin D. Meiklejohn

The three fruitfly species of the Drosophila simulans clade— D. simulans, D. mauritiana, and D. sechellia— have served as important models in speciation genetics for over 40 years. These species are reproductively isolated by geography, ecology, sexual signals, postmating-prezygotic interactions, and postzygotic genetic incompatibilities. All pairwise crosses between these species conform to Haldane’s rule, producing fertile F1 hybrid females and sterile F1 hybrid males. The close phylogenetic proximity of the D. simulans clade species to the model organism, D. melanogaster, has empowered genetic analyses of their species differences, including reproductive incompatibilities. But perhaps no phenotype has been subject to more continuous and intensive genetic scrutiny than hybrid male sterility. Here we review the history, progress, and current state of our understanding of hybrid male sterility among the D. simulans clade species. Our aim is to integrate the available information from experimental and population genetics analyses bearing on the causes and consequences of hybrid male sterility. We highlight numerous conclusions that have emerged as well as issues that remain unresolved. We focus on the special role of sex chromosomes, the fine-scale genetic architecture of hybrid male sterility, and the history of gene flow between species. The biggest surprises to emerge from this work are that (i) genetic conflicts may be an important general force in the evolution of hybrid incompatibility, (ii) hybrid male sterility is polygenic with contributions of complex epistasis, and (iii) speciation, even among these geographically allopatric taxa, has involved the interplay of gene flow, negative selection, and positive selection. These three conclusions are marked departures from the classical views of speciation that emerged from the modern evolutionary synthesis.


Parasitology ◽  
1982 ◽  
Vol 84 (2) ◽  
pp. 289-296 ◽  
Author(s):  
S. K. Moloo

SUMMARYInvestigations were conducted on the infection rates and transmission charecteristics of sterile male Glossina morsitans morsitans for Trypanosoma vivax, T. congolense and T. brucei. Pupae were irradiated after the first flush of female emergences with 7, 10 or 13 krad. in a 137caesium radiation source under ambient conditions. The emergent males were fed on a T. viuax-infected goat at peak parasitaemia. They were subsequently mated at 8 days old with 3-day-old normal, virgin females. A batch of sexually fertile males which had been infected as tenerals on the goat at the same time were similarly mated to serve as controls. All the tsetse were maintained on rabbits' ears; the survival and reproductive performance were monitored for seven age-group periods of 9 days each. The sterility rates of the males were 73, 91 and 98% for the 7, 10 and 13 krad. doses of radiation; the percentage of T. vivax infection rates were 78·3, 82·3 and 74·4, respectively. For the control males, the fecundity of the mated females was 90% and the infection rate was 75·7%. In all other experiments, the 10 krad. dose was selected since both the survival and the sterility of the irradiated males were good. The T. vivax-challenged cows and goats died with symptoms of anaemia. There was no difference in the transmission characteristics between sterile and fertile vectors. There was also no significant difference between the sterile and normal males in the infection rates and the transmission frequency of T. congolense and T. brucei to cattle, goats and mice. These results indicate that release of sterile male tsetse in tsetse control programmes will potentially increase the trypanosomiasis risk in the affected area. Consideration must therefore be given to integrating adequate surveillance and chemotherapeutic measures for protection of man and his domestic livestock in the region during the period of such tsetse control campaigns.


2019 ◽  
Author(s):  
Diana Lustyk ◽  
Slavomír Kinský ◽  
Kristian Karsten Ullrich ◽  
Michelle Yancoskie ◽  
Lenka Kašíková ◽  
...  

ABSTRACTF1 hybrids between mouse inbred strains PWD and C57BL/6 represent the most thoroughly genetically defined model of hybrid sterility in vertebrates. Hybrid male sterility can be fully reconstituted from three components of this model, namely the Prdm9 hybrid sterility gene, intersubspecific homeology of Mus musculus musculus and Mus musculus domesticus autosomes, and the X-linked Hstx2 locus. Hstx2 modulates the extent of Prdm9-dependent meiotic arrest and harbors two additional genetic factors responsible for intersubspecific introgression-induced oligospermia (Hstx1) and reduced global meiotic recombination rate (Meir1). To facilitate positional cloning and to overcome the recombination suppression within the 4.3 Mb genomicDob interval encompassing the Hstx2 locus we designed Hstx2-CRISPR and SPO11/Cas9 transgenes aimed to induce DNA double-strand breaks specifically within the Hstx2 locus. The resulting recombinant reduced the Hstx2 locus to 2.70 Mb (Chr X:66.51-69.21 Mb). The newly defined Hstx2 still operates as the major X-linked factor of the F1 hybrid sterility, controls meiotic chromosome synapsis, and modifies meiotic recombination rate. Despite extensive further crosses, the 2.70 Mb Hstx2 interval behaved as a recombination cold spot with reduced PRDM9-mediated H3K4 hotspots and absence of DMC1-defined DNA DSB hotspots. To search for structural anomalies as a possible cause of recombination suppression we used optical mapping of the Hstx2 interval and observed high incidence of subspecies-specific structural variants along the X chromosome, with a striking copy number polymorphism of the microRNA Mir465 cluster. Finally, we analyzed the role of one of the Hstx2 candidate genes, the Fmr1 neighbor (Fmr1nb) gene in male fertility.Article summaryEarly meiotic arrest of mouse intersubspecific hybrids depends on the interaction between the Prdm9 gene and Hybrid sterility X2 (Hstx2) locus on chromosome X. Lustyk et al. conducted high-resolution genetic and physical mapping of the Hstx2 locus, reduced it to 2.7 Mb interval within a constitutive recombination cold spot and found that the newly defined Hstx2 still operates as the X-linked hybrid sterility factor, controls meiotic chromosome synapsis, and modifies recombination rate. Optical mapping of the Hstx2 genomic region excluded inversion as a cause of recombination suppression and revealed a striking copy number polymorphism of the microRNA Mir465 cluster.


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