Reduced Fertility of Drosophila melanogaster Hybrid male rescue (Hmr) Mutant Females Is Partially Complemented by Hmr Orthologs From Sibling Species

Aruna, S.; Flores, Heather A.; Barbash, Daniel A.

doi:10.1534/genetics.108.100057

Cited by 36 publications

(60 citation statements)

References 43 publications

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“…Subsequently, females carrying the si I or ma I mtDNAs were crossed to D. melanogaster In(1)AB,w males. The In(1)AB chromosome carries a mutation that rescues F1 hybrid female viability and fertility (Hutter et al 1990; Aruna et al 2009). D. simulans simw 501 (mitochondrial haplotype si II) females were crossed directly to In(1)AB,w males, as F1 female viability and fertility are also rescued in this cross.…”

Section: Methodsmentioning

confidence: 99%

Mitochondrial-Nuclear Epistasis Affects Fitness Within Species but Does Not Contribute to Fixed Incompatibilities Between Species of Drosophila

et al. 2010

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Efficient mitochondrial function requires physical interactions between the proteins encoded by the mitochondrial and nuclear genomes. Co-evolution between these genomes may result in the accumulation of incompatibilities between divergent lineages. We test whether mitochondrialnuclear incompatibilities have accumulated within the Drosophila melanogaster species subgroup by combining divergent mitochondrial and nuclear lineages and quantifying the effects on relative fitness. Precise placement of nine mtDNAs from D. melanogaster, D. simulans and D. mauritiana into two D. melanogaster nuclear genetic backgrounds reveals significant mitochondrial-nuclear epistasis affecting fitness in females. Combining the mitochondrial genomes with three different D. melanogaster X chromosomes reveals significant epistasis for male fitness between X-linked and mitochondrial variation. However, we find no evidence that the more than 500 fixed differences between the mitochondrial genomes of D. melanogaster and the D. simulans species complex are incompatible with the D. melanogaster nuclear genome. Rather, the interactions of largest effect occur between mitochondrial and nuclear polymorphisms that segregate within species of the D. melanogaster species subgroup. We propose that a low mitochondrial substitution rate, resulting from a low mutation rate and/or efficient purifying selection, precludes the accumulation of mitochondrial-nuclear incompatibilities among these Drosophila species.

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Section: Methodsmentioning

confidence: 99%

Mitochondrial-Nuclear Epistasis Affects Fitness Within Species but Does Not Contribute to Fixed Incompatibilities Between Species of Drosophila

et al. 2010

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“…For example, increased dosage of the wild-type D. melanogaster Hmr gene reduces hybrid female viability, and under some conditions Hmr can cause dominant sterility and lethality (8). In contrast, within D. melanogaster, Hmr has the opposite genetic properties: Its absence reduces viability and fertility, and these effects are purely recessive (13). I propose that the results of Matute et al reveal that hybrids are more sensitive to haploinsufficiency than pure species.…”

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Comment on “A Test of the Snowball Theory for the Rate of Evolution of Hybrid Incompatibilities”

Barbash

2011

Science

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Matute et al. (Reports, 17 September 2010, p. 1518 tested the theory that the number of genes involved in hybrid incompatibility increases faster than linearly. However, the method they used is inappropriate because it detects genes that are haploinsufficient in a hybrid background but that would not contribute to lethality in wild-type hybrids, thus overestimating the frequency of hybrid inviability.M atute et al.(1) tested the prediction that the number of genes involved in hybrid incompatibility increases faster than linearly with the divergence time between species. They used Drosophila melanogaster strains heterozygous for multigene deletions to screen for chromosomal regions that reduce viability in female F1 hybrids. They found many more regions that reduce viability in D. santomea hybrids (71) compared with D. simulans hybrids (10) and concluded that their data support the theory that Dobzhansky-Muller (DM) hybrid incompatibility (HI) genes accumulate exponentially (or snowball) with respect to the time of divergence. However, one confounding factor in their study is that the sample sizes were much larger in crosses with D. santomea compared with D. simulans [from table S1 in (1): n = 453 crosses with D. santomea, mean number of balancer females = 87.4, SD = 70.6; from table S2 in (1): n = 226 crosses with D. simulans, mean number of balancer females = 53.5, SD = 51.8; P = 4.04 × 10 −12 by 2-tailed t test]. There was thus substantially more power to detect deviations from a 1:1 ratio of progeny with D. santomea than with D. simulans.More fundamentally, Matute et al.'s method of screening will potentially detect regions that reduce hybrid viability due to haploinsufficiency rather than because they contain DM HI genes. The authors searched for regions that, when hemizygous for either D. simulans or D. santomea genes, reduce viability of F1 female hybrids compared with normal (fully diploid) hybrid females. Because wild-type female hybrids are never hemizygous for chromosomal regions, it is essential to consider how the putative DM HI regions identified in their screen would function in normal hybrids. If the reported viability effects only occur in hemizygous deletion hybrids, then they would never contribute to incompatibility in normal hybrids and thus do not contain DM HI genes. Matute et al. described their screen as having "uncovered" or "exposed" recessive hybrid lethality genes from either D. simulans or D. santomea. If so, then these putative recessive HI genes must also cause HI when homozygous in normal hybrids but not when heterozygous in hybrids (since F1 female hybrids would then be lethal). For a gene to cause HI when both homozygous and hemizygous, but not when heterozygous, strongly implies that the HI gene is behaving like a loss-of-function mutation in a hybrid background. It is clear, however, that many HI genes do not behave as loss-of-function mutations, because it is not how four of the best-characterized Drosophila HI loci function. These loci have the opposite property whereby the ...

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“…Viability of rescued hybrid males is highly sensitive to temperature (Hutter and Ashburner 1987;Aruna et al 2009). In several crosses, such as with mle 1 , mle 9 , and msl-3 1 , a significant enhancement was observed at ,25°, but few or no hybrid males were produced at 25°.…”

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confidence: 99%

Genetic Testing of the Hypothesis That Hybrid Male Lethality Results From a Failure in Dosage Compensation

Barbash

2010

Genetics

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Several recent studies have suggested that F 1 hybrid male lethality in crosses between Drosophila melanogaster and D. simulans is due to a failure in dosage compensation, caused by incompatibilities between D. simulans dosage compensation proteins and the D. melanogaster X chromosome. Contrary to the predictions of this hypothesis, mutations in four essential D. melanogaster dosage compensation genes are shown here to moderately increase rather than decrease hybrid male viability.

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Reduced Fertility of Drosophila melanogaster Hybrid male rescue (Hmr) Mutant Females Is Partially Complemented by Hmr Orthologs From Sibling Species

Cited by 36 publications

References 43 publications

Mitochondrial-Nuclear Epistasis Affects Fitness Within Species but Does Not Contribute to Fixed Incompatibilities Between Species of Drosophila

Mitochondrial-Nuclear Epistasis Affects Fitness Within Species but Does Not Contribute to Fixed Incompatibilities Between Species of Drosophila

Comment on “A Test of the Snowball Theory for the Rate of Evolution of Hybrid Incompatibilities”

Genetic Testing of the Hypothesis That Hybrid Male Lethality Results From a Failure in Dosage Compensation

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