Why is mendelian segregation so exact?

Crow, James F.

doi:10.1002/bies.950130609

Cited by 122 publications

(160 citation statements)

References 36 publications

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“…Genetic enhancers and suppressors of segregation distortion have different linkage requirements: enhancers will evolve in cis with the distorter, whereas suppressors can evolve anywhere in the genome in trans with the distorter (Thomson and Feldman 1974;Hartl 1975b;Crow 1991). The regions of the genome under strongest pressure to evolve suppressors are those directly targeted by the distorter (e.g., the target locus should evolve from a sensitive to an insensitive state).…”

Section: Other Modifiers Of the Sd Systemmentioning

confidence: 99%

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The SelfishSegregation DistorterGene Complex ofDrosophila melanogaster

2012

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Segregation Distorter (SD) is an autosomal meiotic drive gene complex found worldwide in natural populations of Drosophila melanogaster. During spermatogenesis, SD induces dysfunction of SD + spermatids so that SD/SD + males sire almost exclusively SD-bearing progeny rather than the expected 1:1 Mendelian ratio. SD is thus evolutionarily "selfish," enhancing its own transmission at the expense of its bearers. Here we review the molecular and evolutionary genetics of SD. Genetic analyses show that the SD is a multilocus gene complex involving two key loci-the driver, Segregation distorter (Sd), and the target of drive, Responder (Rsp)-and at least three upward modifiers of distortion. Molecular analyses show that Sd encodes a truncated duplication of the gene RanGAP, whereas Rsp is a large pericentromeric block of satellite DNA. The Sd-RanGAP protein is enzymatically wild type but mislocalized within cells and, for reasons that remain unclear, appears to disrupt the histone-to-protamine transition in drive-sensitive spermatids bearing many Rsp satellite repeats but not drive-insensitive spermatids bearing few or no Rsp satellite repeats. Evolutionary analyses show that the Sd-RanGAP duplication arose recently within the D. melanogaster lineage, exploiting the preexisting and considerably older Rsp satellite locus. Once established, the SD haplotype collected enhancers of distortion and suppressors of recombination. Further dissection of the molecular genetic and cellular basis of SD-mediated distortion seems likely to provide insights into several important areas currently understudied, including the genetic control of spermatogenesis, the maintenance and evolution of satellite DNAs, the possible roles of small interfering RNAs in the germline, and the molecular population genetics of the interaction of genetic linkage and natural selection.Mendelian inheritance is a marvelous device for making evolution by natural selection an efficient process.... The Mendelian system works with maximum efficiency only if it is scrupulously fair to all genes. It is in constant danger, however, of being upset by genes that subvert the meiotic process to their own advantage. James F. Crow (1979) S EGREGATION Distorter (SD) is a selfish, coadapted gene complex on chromosome 2 (an autosome) found at low frequency in nearly all natural populations of the fruit fly, Drosophila melanogaster. In heterozygous males carrying SD and a typical wild-type second chromosome (SD/SD + ), most SD + -bearing spermatid nuclei fail to complete the histoneto-protamine transition during spermiogenesis, so that primarily SD-bearing spermatids develop properly and go on to fertilize eggs. SD/SD + males thus sire almost exclusively SD-inheriting progeny. This distortion of classic Mendelian ratios has intrigued geneticists and evolutionary biologists for more than 50 years-and for good reason. As we describe below, SD is a newly evolved system that subverts one of the fundamental laws of inheritance by exploiting an ancient molecular pathway. I...

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Section: Other Modifiers Of the Sd Systemmentioning

confidence: 99%

“…With Hiraizumi, Sandler had a chance to tackle the basis of a naturally occurring meiotic drive system in a well-studied genetic model species. In the few years that followed, the two would publish eight articles on SD together (reviewed in Crow 1991;Ganetzky 1999).…”

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confidence: 99%

The SelfishSegregation DistorterGene Complex ofDrosophila melanogaster

2012

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“…Since gametes from mothers with higher recombination rates have fewer D alleles than expected, drive in their daughters is less efficient. Ultimately, the granddaughters of females with higher recombination rates suffer less from the deleterious fitness effects of drive systems (e.g., Crow 1991).…”

Section: Two-locus Drive Systemsmentioning

confidence: 99%

Scrambling Eggs: Meiotic Drive and the Evolution of Female Recombination Rates

2012

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Theories to explain the prevalence of sex and recombination have long been a central theme of evolutionary biology. Yet despite decades of attention dedicated to the evolution of sex and recombination, the widespread pattern of sex differences in the recombination rate is not well understood and has received relatively little theoretical attention. Here, we argue that female meiotic drivers-alleles that increase in frequency by exploiting the asymmetric cell division of oogenesis-present a potent selective pressure favoring the modification of the female recombination rate. Because recombination plays a central role in shaping patterns of variation within and among dyads, modifiers of the female recombination rate can function as potent suppressors or enhancers of female meiotic drive. We show that when female recombination modifiers are unlinked to female drivers, recombination modifiers that suppress harmful female drive can spread. By contrast, a recombination modifier tightly linked to a driver can increase in frequency by enhancing female drive. Our results predict that rapidly evolving female recombination rates, particularly around centromeres, should be a common outcome of meiotic drive. We discuss how selection to modify the efficacy of meiotic drive may contribute to commonly observed patterns of sex differences in recombination.

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“…Although segregation distorters are found in a broad variety of taxa, they seem to be unusual and occur at a low frequency in any particular population (Crow, 1991;Hall, 2004). For decades, there has been considerable interest in explaining why these genes are rare given their obvious advantages, as long as they can gain fitness simply by increasing their transmission (for example, Prout et al, 1973;Liberman, 1976;Eshel, 1985;Haig and Grafen, 1991;Weissing and van Boven, 2001;Ú beda andHaig, 2004, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…However, although they are difficult to detect, segregation distorters could be more frequent than currently believed (Taylor and Ingvarsson, 2003). In fact, most cases of meiotic drive found so far occur in the best circumstances to be detected, for example when there is a strong bias in segregation (normally the transmission rate, k40.9; for example, McMeniman and Barker, 2006); when meiotic drive causes a sex ratio distortion, so that the sex acts as a natural marker (Crow, 1991;Jiggins et al, 1999;Hurst and Werren, 2001;Jaenike, 2008); or when distorters cause deleterious effects on fitness by themselves or by the action of other linked genes (for example, Buckler et al, 1999). By contrast, in less ideal situations, their detection from the whole genome of an organism can be quite difficult even when distorter genes are common.…”

Section: Introductionmentioning

confidence: 99%

Evidence of subtle departures from Mendelian segregation in a wild lesser kestrel (Falco naumanni) population

2009

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Some alleles are inherited more frequently than expected from Mendel's rule. This phenomenon, known as transmission ratio distortion (TRD), is found in a broad variety of taxa, but it is thought to be unusual and occurs at a low frequency in any particular population. Here, we used seven microsatellite markers to search for possible TRD in a wild lesser kestrel (Falco naumanni) population. Among the nine alleles analysed with at least 200 known meioses for each sex, we found that two of them (156-AG5 in males and 362-FN1.11 in females) presented subtle (k ¼ 0.6) but significant departures from Mendelian segregation. Moreover, in a sample of 53 alleles with at least 15 known meioses, we found a positive correlation between their transmission rates and their frequencies in the population. To estimate the transmission scores for the loci and individuals, we developed a method that allowed us to discover that another locus, FP-46, showed significant TRD, despite the lack of a significant deviation from parity for the alleles considered individually. Finally, we found a consistent transmission bias both within loci and within individuals across loci. Inter-individual differences in TRD support the idea that distorters act over several loci that are evenly distributed across the whole genome, particularly in individuals bearing the distorter alleles. Overall, these findings suggest that TRD might be a more widespread phenomenon than previously revealed by analyses at the allele level.

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Why is mendelian segregation so exact?

Cited by 122 publications

References 36 publications

The SelfishSegregation DistorterGene Complex ofDrosophila melanogaster

The SelfishSegregation DistorterGene Complex ofDrosophila melanogaster

Scrambling Eggs: Meiotic Drive and the Evolution of Female Recombination Rates

Evidence of subtle departures from Mendelian segregation in a wild lesser kestrel (Falco naumanni) population

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