7. In the fruit fly Drosophila, the SdRsp system is a classic example of segrega

Question

7. In the fruit fly Drosophila, the SdRsp system is a classic example of segregation distortion. As described in class, one model to explain the segregation distortion is that the Sd allele produces a "toxin" that disrupts spermatogenesis for gametes carrying the Rsp allele at a nearby locus on the same chromosome but not those with the Rsp allele. It has been observed that the Sd and Rsp loci exhibit a high level of linkage disequilibrium. Briefly explain two likely mechanisms that have maintained linkage disequilibrium between these two loci even though fruit flies reproduce in largely random-mating fashion?

Explanation / Answer

Segregation Distorter (SD) is a selfish, coadapted gene complex on chromosome 2 of Drosophila melanogaster that strongly distorts Mendelian transmission. SD complex is one of the best characterized meotic-drive systems. Heterozygous SD/SD+males transmit SD chromosomes to most of the progeny, though not all. When heterozygous with a sensitive homolog in the germline of a male fly, SD usually ends up in almost all the mature sperms. The transmission distortion is carried out by sabotage of rival spermatids, probably by interefering with chromatin condensation. Full strength distortion( i.e in order to end up in >95% of mature sperm) is caused by three interacting loci clustered around the centromere of chromosome 2 (an autosome): the trans-acting Segregation distorter (Sd) locus; an upward modifier, Enhancer of SD (E(SD)) located in the centric beta-heterochromatin of 2L ; and a cis-acting distortion-insensitive allele at the target locus, Responder (Rspi). It serves as a target site for the action of Sd and appears to have positive functions in the soma as well. Many experiments have been carried out to study the mechanism of Sd-rsp gene interactions, and it has been noted that the mechanism for segragation disorder phenotype is an epistatic interaction, that invloves atleast three loci. Greater effect of Sd gene products maybe observed on spermatids that have large number of Rsp repeats. For understanding the evolution of Sd gene, there have been numerous studies carried out on meotic drive systems. A close linkage between distorting locus and its target locus is required, for a meotic complex to be established successfully. This close linkage allows for the maintenance of linkage disequilibrium, where there are large number of insensitive target alleles, involved with sensitive target alleles in repulsion to distorting allele. This non-random association is helpful for the distorting gene to exert its effect fully. The Sd-Rsp coupling haplotype can be viewed as a suicide chromosome, where it disrupts its own spermatids, as well as the rival spermatids. Once the meotic drive system has been established, linked modifiers of segragation distortion also evolve in linkage disequilibrium. If epistasis is sufficiently strong, and how strong it should be has not been calculated in a finite population, then epistatis selection can generate significant linkage disequilibrium. Once that is established, selection will favour modifiers, which have favourable epistasis with the alleles which already have a beneficial interaction. This interaction can create an even greater amount of linkage disequilibrium.

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