JURNAL DROSOPHILA MELANOGASTER PDF

PLOS Genetics 11 10 : e Sex chromosomes have a large effect on reproductive isolation and play an important role in hybrid inviability. In Drosophila hybrids, X -linked genes have pronounced deleterious effects on fitness in male hybrids, which have only one X chromosome. Several studies have succeeded at locating and identifying recessive X -linked alleles involved in hybrid inviability.

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PLOS Genetics 11 10 : e Sex chromosomes have a large effect on reproductive isolation and play an important role in hybrid inviability. In Drosophila hybrids, X -linked genes have pronounced deleterious effects on fitness in male hybrids, which have only one X chromosome.

Several studies have succeeded at locating and identifying recessive X -linked alleles involved in hybrid inviability. Nonetheless, the density of dominant X -linked alleles involved in interspecific hybrid viability remains largely unknown.

In this report, we study the effects of a panel of small fragments of the D. We find that the X -chromosome from D. We then compare these effects on hybrid viability with two D. Unlike the interspecific crosses, we found no X -linked alleles that cause lethality in intraspecific crosses.

Our results reveal the existence of dominant alleles on the X -chromosome of D. These alleles only cause inviability in hybrid males, yet have little effect in hybrid females. This suggests that X -linked elements that cause hybrid inviability in males might not do so in hybrid females due to differing sex chromosome interactions.

The inviability or sterility of interspecific hybrids is one of the mechanisms of reproductive isolation that keep species apart. In this report, we use the genetic tools of Drosophila melanogaster to assess the cytological locations and relative frequency of dominant X -linked alleles involved in hybrid inviability in three different interspecific crosses. We map the genomic regions of the D. For each hybrid inviability allele we identified, we characterized the developmental defects that occur in the inviable hybrids.

Our results show that the effect of these X -linked lethal regions is lineage-specific, as is the total number of alleles that cause hybrid inviability. These results can be expanded and will allow for the exact identification of X -linked D. PLoS Genet 10 4 : e Editor: David J.

This is an open-access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist. One of the most intensely studied forms of reproductive isolation is intrinsic postzygotic isolation: the inviability or sterility of interspecific hybrids that arises during development.

The genetic mechanisms underlying this type of reproductive isolation are thought to be irreversible in evolutionary time [1] , [2]. The study of postzygotic isolating mechanisms can reveal the molecular changes that have arisen between species [3] , [4].

There is both theoretical and empirical evidence for the role of postzygotic isolation in completing the process of speciation through the action of natural selection [5] — [7] , as enhanced prezygotic isolation might evolve as a byproduct of maladaptive hybridization, thus furthering the speciation process [6] , [8].

In the Dobzhansky-Muller model DM model of the evolution of reproductive isolation, the genetic basis of hybrid breakdown involves at minimum two loci with an ancestral genotype of A 1 A 1 B 1 B 1.

The ancestral species splits into two descendant species that eventually acquire genotypes A 1 A 1 B 2 B 2 and A 2 A 2 B 1 B 1 through natural selection, meiotic drive or, less likely, genetic drift. This model posits that postzygotic isolation arises in allopatry as a collateral effect of the evolutionary divergence between these two isolated populations.

In this case, although species having genotypes A 1 A 1 B 2 B 2 and A 2 A 2 B 1 B 1 at two loci are fit, the hybrid progeny will have a genotype A 1 A 2 B 1 B 2 and therefore might be unfit: either sterile or inviable because the A 2 and B 2 alleles do not interact properly [1] , [3] , [9] , [10].

The DM model presents a general mechanism for the evolution of postzygotic isolation, and explains a substantial proportion of the cases in which we know the genetic basis of hybrid breakdown [for exceptions see 11] , [12] , [ reviewed in 13]. Concerted mapping efforts have localized a number of hybrid incompatibility genes those involved in Dobzhansky-Muller incompatibilities, or DMI to small chromosomal regions [reviewed in 4] , [13] , [14] and have yielded some general patterns about the biology of genes involved in reproductive isolation.

The first general pattern of hybrid inviability, Haldane's rule, pre-dates genetic mapping. In a wide variety of organisms, if hybrids of only one of the sexes are inviable or sterile, it will be the heterogametic sex [1] , [15] , [16].

Second, many but not all of the genes that cause hybrid breakdown have evolved under the influence of natural selection or meiotic drive, suggesting that rapid evolution within species leads to the evolution of DMI in hybrids [17] — [19]. Third, the X -chromosome, when compared with the autosomes, plays a disproportionately large role in postzygotic isolation [1] , [20]. Fourth, mapping results have shown that the predictions from the DM model hold at the genomic level, and that the number of genes involved in hybrid inviability evolves faster than the accumulation of neutral genetic differences between species [21] — [23].

Finally, hybrid incompatibilities are asymmetric i. These asymmetries often result from DMIs involving uniparentally inherited genetic factors such as cytoplasmic—nuclear interactions [24] — [29]. Of these five patterns, two—Haldane's rule and the large effect of the X -chromosome on hybrid inviability—can be explained by the hemizygosity of the sex chromosome and the dominance theory [30] — [33] ; see [34] for alternative explanations of Haldane's rule in animals lacking a heterogametic sex.

In Drosophila , X -linked genes can have a disproportional effect on hybrid fitness because the heterogametic hybrid males suffer from both the dominant and recessive deleterious X -linked alleles [35] — [37].

In the homogametic females, however, the deleterious effects of recessive alleles are masked by the presence of a second X -chromosome. In Drosophila hybrids, several studies have suggested the presence of recessive alleles in one of the X -chromosomes that can cause hybrid inviability in females when uncovered with a genetic lesion [38].

Surprisingly, in some of these crosses, hybrid males are viable despite all the recessive factors from one X -chromosome being fully exposed [31] , [39]. One hypothesis for why males, but not females, can survive in these cases is that epistatic interactions between the two X -chromosomes lead to inviability in females. This idea, first formalized by Orr [30] , states that since female hybrids carry two X -chromosomes, they suffer twice as many interactions involving the sex chromosomes but as the alleles involved in hybrid breakdown are on average recessive, the heterogametic sex is still much more prone to suffer hybrid breakdown.

The hypothesis that the homogametic sex females in Drosophila suffers from negative epistatic interactions between X -chromosomes remains largely untested but see [40] , [41]. One of the prerequisites of such interactions is the existence of dominant partners on one of the X -chromosomes that could potentially cause hybrid inviability in females but not in males.

The aim of this study is to determine if this sex-specific epistasis is present in interspecific hybrids and reveal dominant partners in the interactions. Drosophila melanogaster is particularly useful for the study of the genetic architecture of hybrid inviability because of its armamentarium of genetic tools that can be used to establish the identity and density of alleles involved in DMIs. To date, two studies have used deficiencies in D.

Coyne et al. Matute et al. In parallel, Matute et al. The results from that study indicated at least 13 recessive alleles residing on the D. However, these deficiency-mapping efforts focused on identifying a single hybrid inviability allele from what certainly could be complex epistatic interactions involving three or more loci; [3] , [19] , [42] — [45]. These studies both localized recessive alleles in the genome of the paternal species either D.

QTL-mapping and introgression-based approaches share the same drawback: even though they reveal a portrait of the genes involved in hybrid breakdown e. Three studies have aimed not only to identify single alleles that contribute to hybrid inviability but also to determine the interacting partners of such alleles.

Presgraves [48] pursued a genome-wide identification of D. In this case, if the D. Sawamura and Yamamoto [40] used a D. Fine functional analyses, also aided by the use of Dp 1;Y translocations have revealed that zhr is a repetitive bp DNA satellite, derived in D. Finally, Cattani and Presgraves [41] expanded the results from Coyne et al.

Their results point to the existence of one dominant factor that interacts with at least one recessive factor in the heterochromatic region of the D.

These two mapping efforts have uncovered most of the known X -linked dominant DMI partners in Drosophila. Here, we explore the possibility of negative epistatic interactions between X -chromosomes in several interspecific hybrids by taking advantage of a comprehensive tiling set of duplications of the D. In this report, we show the possibility of producing D. Second, we examine inviable hybrid males from several crosses D.

The cross of wild-type D. The reciprocal cross does not produce any progeny as premating isolation seems to be complete in that direction [53].

Figure S1 shows two morphological traits of these previously undescribed hybrid males, number of teeth in the sex combs and abdominal pigmentation. Crosses between D. The Y mel -chromosome has no effect on hybrid male viability, see text. These females can be crossed to D. Results for this screening are shown in Figure 3. Because we can produce hybrid males with and without Y mel , we asked first whether this chromosome had any affect on hybrid male viability, or longevity. Males of these two genotypes showed no differences in viability at any developmental stage Figure S2.

The two types of hybrid males were both sterile and showed similar longevity Figure S2 ; Tables S1 and S2. Despite the morphological defects of these hybrid males, particularly in abdominal segments, they survive almost as long as virgin males from both parental species Figure S2. More specifically, the number of teeth in their sex-combs is not significantly different between left and right Paired Wilcoxon signed rank test with continuity correction on sex comb teeth, left vs.

All hybrid males were sterile and had atrophied testes lacking motile sperm. These results indicate that these hybrids are true males are not gynandromorphs or otherwise sexually chimeric.

Hybrid female embryos carrying only the C 1 RM chromosome manifest an abdominal ablation in the posterior, very similar to that which we described for wild-type hybrid males who carry an X mel [53]. These results indicate that either one or two copies of X mel chromosome in the absence of another X -chromosome can induce hybrid inviability regardless of the sex of the hybrid in the three interspecific crosses. In crosses of wild-type D.

Those that fail to hatch from embryogenesis manifest cuticular defects typified by A. In crosses between D. Those that fail to hatch are typified by D. To determine which factors residing on X mel are involved in hybrid inviability we then undertook a duplication mapping screen to identify the regions of X mel that cause lethality in males carrying a D.

Our goal was to identify the dominant regions on X mel that can cause hybrid lethality in the presence of the X -chromosome from another species. All fly stocks are listed in Tables S3 and S4. As the duplication mapping approach [40] , [41] has no balancer sibling or other internal controls, this study is limited to the identification of alleles that cause complete rather than partial lethality.

We used two different criteria to describe dominant lethals. This approach is limited because the cut-off is arbitrary, but our data were resilient to more quantitative analyses see Methods.

This approach therefore does not detect putative semi-lethal alleles or those that can cause significant, but incomplete, reductions in viability. To exclude pre-mating isolation from our observations, we only included data from matings in which we observed inseminated females.

Twenty females from each of three replicates were dissected for each cross and their reproductive tracts were inspected for the presence of sperm, either motile or dead.

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Genetic Analysis of the Claret Locus of Drosophila Melanogaster

Key scientific discoveries have resulted from genetic studies of Drosophila melanogaster , using a multitude of transgenic fly strains, the majority of which are constructed in a genetic background containing mutations in the white gene. Here we report that white mutant flies from w strain undergo retinal degeneration. We observed also that w mutants have progressive loss of climbing ability, shortened life span, as well as impaired resistance to various forms of stress. We conclude that beyond the classical eye-color phenotype, mutations in Drosophila white gene could impair several biological functions affecting parameters like mobility, life span and stress tolerance. Consequently, we suggest caution and attentiveness during the interpretation of old experiments employing white mutant flies and when planning new ones, especially within the research field of neurodegeneration and neuroprotection.

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