Scholarly Literature

This is a database of scholarly literature that concentrates currently on natural and engineered selfish genetic elements (gene drives).  The latest are shown here.
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Meiotic drive in Lucilia cuprina and chromosomal evolution

4441
Foster, GGW, M. J.,  American Naturalist,  137:403-415. 1991-01-19 00:00:00.
In females heterozygous for pericentric inversions that alter the relative lengths of the long and short arms of a chromosome, crossing-over within the inversion can lead to unequal segregation at anaphase II, favoring the homologue with the more centrally located centromere. It is suggested that this phenomenon may have played a role in the evolution of centromere position in certain species groups.

A comparative approach to the population genetics theory of segregation distortion

4440
Feldman, MWO, Sarah P.,  American Naturalist,  137:443-456. 1991-01-18 00:00:00.
Mathematical models of four well-known naturally occurring systems of segregation distortion are compared. These include the sex-ratio chromosome of Drosophila pseudoobscura, the Segregation Distorter (SD) complex of D. melanogaster, the t locus in Mus musculus, and the sex-ratio system in Aedes aegypti. Dynamics of these models are compared with the classical one-locus multiple-allele viability system. For the SD complex and the sex-ratio model of A. aegypti, the role of recombination is reviewed. Departures from Mendelian segregation cause fascinating irregularities in the relationship between linkage and linkage disequilibrium, as well as in predictions for the evolution of recombination itself.

X-chromosome segregation distortion in Drosophila

4439
Curtsinger, JW,  American Naturalist,  137:344-348. 1991-01-17 00:00:00.
The sex-ratio trait exhibits both discrete and continuous variation in Drosophila pseudoobscura. The discrete variation is caused by X-chromosome meiotic drive. The evolutionary forces maintaining the meiotic-drive polymorphism include strong viability selection against homozygous females and virility selection in males. The relative importance of the two factors is unresolved. The evidence for a genetic component in the continuous sex-ratio variation comes from artificial-selection experiments, large-scale estimation of segregation ratios corrected for viability effects, and an examination of the rates of spermatid loss. Segregation ratio can be treated as a typical quantitative character subject to major and minor genetic modifiers.

Sex-ratio distortion caused by meiotic drive in mosquitos

4458
Wood, RJN, M. E.,  American Naturalist,  137:379-391. 1991-01-16 00:00:00.
Meiotic-drive genes have been described in two species of mosquito, Aedes aegypti and Culex quinquefasciatus. In both species, a Y (M)-linked gene causes a change in sex ratio in favor of males. More is known about the Distorter gene (D) in A. aegypti, but the gene in C. quinquefasciatus appears to be similar. D is located on the right arm of the sex chromosome, is marked with the intercalary Giemsa C-band when present, and is linked closely to the sex locus or region. D undergoes meiotic drive only when in coupling with M, the male-determining gene, which does not recombine with the centromere. Sensitivity to the MD haplotype is controlled at m, the female-determining gene. Therefore, m is considered to be the responder. The m haplotype is polymorphic for sensitivity to MD (m(r1), m(r2), m(s1)-m(s6)). Sensitivity is influenced, in some strains, by a second sex-linked gene t (tolerance to Distorter). Another sex-linked gene, A, enhances the effect of D. Meiotic drive is associated with breaks on the sex chromosomes. First seen at diplotene, mainly at four discrete positions, 90% of these breaks occur on the X (m) chromosome. They usually appear on a chiasmic arm of the bivalent, with the result that most acentric fragments remain attached to the unbroken homologue by a chiasma. Examination of developing spermatozoa in Distorter males reveals extreme sperm depletion, a high degree of abnormality (e.g., multiple axonemes), and an increased DNA content up to the 4C level. Surprisingly, however, the effective fertility of these males is hardly reduced. Evidently, spermatozoa are produced in nondistorter males in vast excess. The Distorter gene has been found in populations from Africa, America, Australia, and Sri Lanka. Resistance to it is much more widespread. The presence of natural resistance argues against the use of D for population control, but its effect has been shown to be enhanced in the presence of certain translocations and the A gene, causing it to become effective in field cage trials, even in the presence of some resistance. There is also experimental support for using D to bring about changes in populations ("population replacement").

Why is Mendelian segregation so exact

4438
Crow, JF,  Bioessays,  13:305-312. 1991-01-16 00:00:00.
The precise 1:1 segregation of Mendelian heredity is ordinarily taken for granted, yet there are numerous examples of 'cheating' genes that perpetuate themselves in the population by biasing the Mendelian process in their favor. One example is the Segregation Distortion system of Drosophila melanogaster, in which the distorting gene causes its homologous chromosome to produce a nonfunctional sperm. This system depends on three closely linked components, whose molecular basis is beginning to be understood. The system is characterized by numerous modifiers changing the degree of distortion. Mathematical theory shows that unlinked modifiers that change the degree of distortion in the direction of Mendelism always increase in the population. This provides a mechanism for removing cheaters and preserving the honesty of the Mendelian gene-shuffle.

Male sex-ratio trait in Drosophila pseudoobscura: Frequency of autosomal aneuploid sperm

4437
Cobbs, GJ, L.; Gordon, L.,  Genetics,  127:381-390. 1991-01-15 00:00:00.
Males with the SR X chromosome show the "sex-ratio" (sr) phenotype in which they produce almost entirely daughters. The few sons (about 1%) are invariably sterile X/O males and result entirely from nullo-XY sperm. The "male-sex-ratio" (msr) phenotype is a modified form of sr in which SR/Y males produce a higher frequency of sterile X/O sons. The msr trait is due to the presence of the SR X-chromosome in males which are also homozygous for one or more autosomes from the L116 strain. Here the frequency of nullo-3 and diplo-3 sperm from msr males was measured by crossing to a compound-3 strain and found to be 13.8% and 3.2%, respectively, of the total viable sperm. The sr males produced very low levels of nullo-3 sperm at a frequency not different from control X/Y males and a slightly elevated frequency of diplo-3 sperm over X/Y males. The msr males were found to have only 12% the fecundity of sr males and in matings to cause a high frequency of brown inviable eggs. These results indicate that high rates of autosomal aneuploidy are not restricted to chromosome 3 but also occur for chromosomes 2, 4 and 5. The overall frequency of autosomal aneuploid sperm is estimated to be approximately 50%. Microscopic studies of meiosis in testes from msr males indicates meiotic nondisjunction and meiotic chromosome loss are responsible for the msr phenotype. Last, microscopic studies of sperm cysts from msr males reveal high levels of spermiogenic failure.

The paternal-sex-ratio chromosome of Nasonia

4457
Werren, JH,  American Naturalist,  137:392-402. 1991-01-15 00:00:00.
Paternal sex ratio (PSR) is a supernumerary chromosome that is transmitted through sperm to fertilized eggs and then gains a transmission advantage by causing supercondensation of the paternal chromosomes (except itself). Because of haplodiploidy, this converts diploid females into haploid (PSR) males. PSR gains a transmission advantage because the unpaired chromosome has a higher frequency of transmission through male (mitotic) gametngenesis than through female (meiotic) gametogenesis. PSR increases in panmictic populations that produce more than 50% fertilized eggs. PSR frequency is typically reduced by population subdivision because of increased local competition among PSR males and reduced availability of females resulting from PSR action. Genetic and molecular studies of PSR have recently begun. PSR is highly heterochromatic and contains large tandem arrays of repetitive DNA unique to it. PSR apparently acts by "imprinting" the set of paternal chromosomes, resulting in their supercondensation during mitosis. Deletion studies are under way to characterize the genetic basis of PSR action and "protection" from its own action.

Meiotic drive in Neurospora and other fungi

Turner, BCP, D. D.,  American Naturalist,  137:416-429. 1991-01-14 00:00:00.
When a gene complex called Spore killer is heterozygous, ascospores representing two of the four products of each meiosis are killed. Only those that receive the killer complex survive. This article reviews what is known of the mode of action of the Neurospora Spore killers, their chromosomal basis, and their occurrance in nature. Similar genes or gene complexes have been found in other fungi. An example from Podospora anserina is analyzed.

Sex ratio polymorphism in Drosophila pseudoobscura

4436
Beckenbach, AT,  American Naturalist,  137:340-343. 1991-01-14 00:00:00.
I studied "sex-ratio" (SR) genotype frequencies in two populations of Drosophila pseudoobscura from southeastern Arizona: Bear Creek Canyon and Tucson. Wild-inseminated females were collected, their fecundities measured in the laboratory, and their SR genotypes inferred by cytological analysis of their progenies. A statistically significant fecundity deficiency was observed among SR/SR females from Bear Creek Canyon. The SR frequency in the Tucson population increased at a rate consistent with the operation of meiotic drive unopposed by selection.

Meiotic drive of t-haplotypes – chromosome segregation in mice with tertiary trisomy

4435
Agulnik, AIA, S. I.; Ruvinsky, A. O.,  Genetical Research,  57:51-54. 1991-01-13 00:00:00.
The properties of the t haplotypes, specific mutant states of the proximal region of chromosomes 17 in the house mouse, are of continuing interest. One such property is increased transmission of the t haplotype by heterozygous t/+ males to offspring. Using the reciprocal translocation T(16; 17)43H we have constructed males with tertiary trisomy of chromosome 17 (+ T43/ + +/Rb7 +) carrying the Robertsonian translocation Rb(16.17)7Bnr. Only the progeny of these males which had inherited either T43/ + or Rb7 from their male parent were viable. The segregation patterns in the offspring of t-bearing trisomics were analysed on days 16-18 of embryonic development. It was found that, when the t12 haplotype is in the normal acrocentric (males + + T43/ + t12 + /Rb7 + +), its presence in the gamete + t12 + / + + T43 does not produce meiotic drive. However, when t6 is in Rb7, meiotic drive was observed: 80% of offspring carried the t haplotype. It is concluded that the meiotic drive is probably inhibited by the presence of a normal homologue of chromosome 17 in the same sperm. Possible mechanisms for the t haplotype effect are discussed.

Segregation distortion in Drosophila melanogaster: Genetic and molecular analysis

4455
Temin, RGG, B.; Powers, P. A.; Lyttle, T. W.; Pimpinelli, S.; Dimitri, P.; Wu, C. I.; Hiraizumi, Y.,  American Naturalist,  137:287-331. 1991-01-13 00:00:00.
The Segregation Distorter (SD) complex in the centromeric region of chromosome 2 in Drosophila melanogaster is responsible for a naturally occurring and strong system of male meiotic drive. Earlier recombinational dissection and deletional analysis showed that the SD complex resolves into three major loci: the euchromatic Sd, or Segregation distorter gene at the base of the left arm of the chromosome (2L), and two heterochromatic genes: E(SD), the Enhancer of SD, and Rsp, the Responder, in the center of the left arm and the right arm (2R), respectively. Rsp exists in the major allelic forms, Rsp(s), for sensitive, and Rsp(i), for insensitive. Males that are heterozygous for an SD chromosome (SdE(SD)Rsp(i)) and a sensitive SD+ homologue (Sd+ E(SD)+ Rsp(s)) transmit predominantly or even exclusively the SD-bearing chromosome to the progeny. The distortion of the segregation ratio is traceable to failure in chromatin condensation and maturation of those spermatids that receive the Rsp(s) homologue during meiosis. Characterization of the properties of null alleles of Sd, E(SD), and Rsp that were generated by delection determined the precise cytological locations of the components and established the functional relationship of each to its wild-type counterpart, suggesting a model whereby a deleterious action of Sd, along with E(SD), on the Rsp(s) target sets in motion the events culminating in sperm dysfunction. Further genetic analysis of E(SD), a gene required for full expression of drive, showed that E(SD) in two doses can cause significant distortion even in the absence of Sd. This distortion is suppressible by a suppressor of SD action. Thus, E(SD) is more than a simple modifier of Sd; rather, it is an effector locus that, like Sd, can act at the Rsp(s) target. Cloning and molecular analysis of the Sd locus reveal that the alteration uniquely associated with Sd is a 5-kb tandem duplication within the polytene band 37D5, which is where Sd is known to map. The Sd-associated duplication appears to be part of a large gene about 100 kb in size. A 4.2-kb SD-specific transcript has been identified, and analyses of the cDNAs indicate a complex transcription pattern. Since Responder plays such a key role in segregation distortion, recent progress in analyzing this locus has been exciting. Studies of Rsp at the genetic, cytogenetic, and molecular levels have been mutually reinforcing and consistent in demonstrating that Rsp is an extended locus that is (1) subdivisible and (2) associated with a 120-bp repeated sequence of DNA that is rich in adenine-thymine pairs and whose copy number is correlated with the degree of sensitivity. In an exceptional situation, there are certain Sd Rsp(i)/Sd+ Rsp(s) males carrying particular modifiers in which the Rsp(i) chromosome can be transmitted at frequencies of less than 0.50 relative to the Rsp(s) chromosome, suggesting that the genetics of segregation ratios may involve even further complexities, which need to be unraveled.

Expression of meiotic drive elements Spore Killer-2 and Spore Killer-3 in asci of Neurospora tetrasperma

4454
Raju, NBP, D. D.,  Genetics,  129:25-37. 1991-01-12 00:00:00.
It was shown previously that when a chromosomal Spore killer factor is heterozygous in Neurospora species with eight-spored asci, the four sensitive ascospores in each ascus die and the four survivors are all killers. Sk-2K and Sk-3K are nonrecombining haplotypes that segregate with the centromere of linkage group III. No killing occurs when either one of these killers is homozygous, but each is sensitive to killing by the other in crosses of Sk-2K x Sk-3K. In the present study, Sk-2K and Sk-3K were transferred by recurrent backcrosses from the eight-spored species Neurospora crassa into Neurospora tetrasperma, a pseudohomothallic species which normally makes asci with four large spores, each heterokaryotic for mating type and for any other centromere-linked genes that are heterozygous in the cross. The action of Sk-2K and Sk-3K in N. tetrasperma is that predicted from their behavior in eight-spored species. A sensitive nucleus is protected from killing if it is enclosed in the same ascospore with a killer nucleus. Crosses of Sk-2K x Sk-2S, Sk-3K x Sk-3S, and Sk-2K X Sk-3K all produce four-spored asci that are wild type in appearance, with the ascospores heterokaryotic and viable. The Eight-spore gene E, which shows variable penetrance, was used to obtain N. tetrasperma asci in which two to eight spores are small and homokaryotic. When killer and sensitive alleles are segregating in the presence of E, only those ascospores that contain a killer allele survive. Half of the small ascospores are killed. In crosses of Sk-2K x Sk-3K (with E heterozygous), effectively all small ascospores are killed. The ability of N. tetrasperma to carry killer elements in cryptic condition suggests a possible role for Spore killers in the origin of pseudohomothallism, with adoption of the four-spored mode restoring ascospore viability of crosses in which killing would otherwise occur.

Meiotic drive of t haplotypes: chromosome segregation in mice with tertiary trisomy

4434
Agulnik, AIA, Sergei I.; Ruvinsky, Anatoly O.,  Genetics Research,  57:51. 1991-01-12 00:00:00.
The properties of the / haplotypes, specific mutant states of the proximal region of chromosomes17 in the house mouse, are of continuing interest. One such property is increased transmission ofthe / haplotype by heterozygous // + males to offspring. Using the reciprocal translocationT(16; 17)43H we have constructed males with tertiary trisomy of chromosome 17( + T43/+ +/Rb7 + ) carrying the Robertsonian translocation Rb(16.17)7Bnr. Only the progeny ofthese males which had inherited either T43/ + or Rb7 from their male parent were viable. Thesegregation patterns in the offspring of /-bearing trisomics were analysed on days 16-18 ofembryonic development. It was found that, when the tn haplotype is in the normal acrocentric(c?c?+ + T43/ + //2+/Rb7 + +), its presence in the gamete +/" + /+ + T43 does not producemeiotic drive. However, when t6 is in Rb7, meiotic drive was observed: 80 % of offspring carriedthe / haplotype. It is concluded that the meiotic drive is probably inhibited by the presence of anormal homologue of chromosome 17 in the same sperm. Possible mechanisms for the t haplotypeeffect are discussed

On the components of Segregation Distortion in Drosophila melanogaster 5: Molecular analysis of the SD locus

4453
Powers, PAG, B.,  Genetics,  129:133-144. 1991-01-11 00:00:00.
Segregation Distorter (SD) is a naturally occurring meiotic drive system comprising at least three distinct loci: Sd, Rsp and E(SD). Heterozygous SD/SD+ males transmit the SD chromosome in vast excess over the normal homolog. The distorted transmission involves the induced dysfunction of the spermatids that receive the SD+ chromosome. In the 220-kb region of DNA that contains the Sd gene, we identified a 5-kb tandem duplication that is uniquely associated with all SD chromosomes, absent in SD+ chromosomes, and detectably altered in Sd revertants. On northern blots, genomic probes from the tandem duplication detect an SD-specific 4-kb transcript in addition to several smaller transcripts present in both SD and SD+. Seven classes of cDNAs derived from these transcripts have been isolated. All of these cDNAs share extensive sequence identity at their 3' ends but differ at their 5' ends. Sequence analysis indicates that these cDNAs potentially encode four distinct, but related, polypeptides. Introduction of the tandem duplication into SD+ flies by germline transformation did not confer the dominant gain-of-function Sd phenotype. This result, taken together with our analysis of the Sd cDNAs, suggests that the duplication is part of a much larger gene that encodes several different polypeptides.

X-Y pairing, meiotic drive and ribosomal DNA in Drosophila melanogaster males

4452
McKee, BD,  American Naturalist,  137:332-339. 1991-01-10 00:00:00.
One of the genotypic features responsible for sex-chromosome meiotic drive and sterility in Drosophila melanogaster males has now been defined clearly. Separation of a significant fraction of X euchromatin from the X pairing site causes either meiotic drive or sterility, depending on whether the separation occurs alone or in combination with rearrangements involving the Y chromosome. The relationship between X-chromosome integrity and the late-spermatid developmental breakdowns responsible for meiotic drive and sterility is still not understood. X-Y pairing is important for some aspect of spermatogenesis in addition to its role in X-Y disjunction. Transcriptional inactivation and meiotic timing are two possibilities that are worth exploring, and there are likely to be others. With molecular probes for genes active in spermatogenesis becoming available, ideas such as the pairing dependence of transcriptional inactivation should become amenable to direct tests. It is hoped that an increased use of molecular methods will shed new light on this fascinating genetic problem.

Segregation distorters

4451
Lyttle, TW,  Annual Review of Genetics,  25:511-557. 1991-01-09 00:00:00.
Segregation distorters are genetic elements that exhibit the phenomenon of meiotic drive; that is, the mechanics of the meiotic divisions cause one member of a pair of heterozygous alleles or heteromorphic chromosomes to be transmitted to progeny in excess of the expected Mendelian proportion of 50% ( 1 34 , 1 36). In this review, we refer to these as genic or chromosomal drive, respectively. Genic meiotic drive is initially limited in its impact to the population dynamics of the drive locus itself and those loci fortuitiously in close linkage. Alleles at these latter loci may enjoy indirect drive through genetic hitchhiking, leading eventually to the establishment of drive haplotypes (64). The haplotype may be extended by incorporating chromosome rearrangements that reduce recombination and promote further linkage disequilibrium between the drive locus and more distant modifier loci ( 1 04 , 1 28, 1 64). In the extreme , the haplotype becomes coextensive with the chromosome, leading to a form of chromosomal meiotic drive. For a parent heterozygous for either type of drive system, the statistic k is used to denote the proportion of progeny (and by inference, successful gametes) that carry the allele or chromosome exhibiting segregation distortion. Thus , k can vary from 0 . 5 (Mendelian segregation segregation) to 1 .0 (complete segregation distortion with only one gamete class recovered in the progeny) .

The genetics and evolutionary biology of meiotic drive: Preface

Lyttle, TW,  American Naturalist,  137:281-282. 1991-01-08 00:00:00.
More than 30 years have passed since the concept and the term meiotic drive were introduced by Sandler and Novitski. Many years have also passed since the preceding conference, which embraced both segregation distortion in Drosophial and transmission-distortion in the mouse, and since meiotic drive in these and other organisms were reviewed comprehensively. During this perio, notable advances have been made, new exampes of meiotic drive have been reported in many organisms, including fungi and plants, and the powerful tools of molecular genetics have been applied to understanding its chromosomal basis.

The Genetic Basis of Transmission-Ratio Distortion and Male Sterility Due to the t Complex

4449
Lyon, MF,  American Naturalist,  137:349-358. 1991-01-07 00:00:00.
The abnormal transmission ratios observed in male mice heterozygous for a complete t haplotype have been shown by breeding studies to be due to three or more distorter genes acting on a responder gene. The action of the t form of the responder is relatively resistant to this harmful action. When the distorters are homozygous, their harmful action is more severe. The t form of the responder is then affected, and the males are sterile. The distorter and responder genes are distributed over a region occupying the proximal third of mouse chromosome 17. Crossover suppression between t and wild-type bapiotypes in this region is due to the presence of inversions and is thought to be selectively advantageous in locking the genetic factors together. The recessive lethals carried by many t haplotypes are also thought to be advantageous in removing the sterile males from the population. Transmission ratio is also affected by genetic background, and there is evidence of differences among t haplotypes either in the responder or in cis-acting effects of distorters.

Meiotic drive against an autosomal supernumerary segment promoted by the presence of a B-chromosome in females of the grasshopper Eyprepocnemis plorans

4448
Lopezleon, MDC, J.; Camacho, J. P. M.,  Chromosoma,  100:282-287. 1991-01-06 00:00:00.
Twenty-seven out of 50 progeny analyses performed with specimens of the grasshopper Eyprepocnemis plorans were informative about the transmission of a supernumerary heterochromatic chromosome segment. The simultaneous presence of a B chromosome in some of the parents involved in the crosses permitted us to test the relationship between both types of supernumerary heterochromatin with respect to their transmission. The results demonstrated that the supernumerary segment is partly eliminated through females possessing B chromosomes. The implications of this in relation to the occurrence of the extra segment in natural populations are discussed.

Sander,Larry – The father of meiotic drive

4447
Lindsley, DL,  American Naturalist,  137:283-286. 1991-01-05 00:00:00.
The symposium at which the following papers were presented was deprived of what surely would have been a major intellectual contribution by the sudden death of its co-organizer, Larry Sandler, in February 1987. Larry was a leading contributor to the study of segregation distortion and meiotic drive, beginning with his seminal research as a graduate student with Ed Novitski at the University of Missouri and continuing, in collaboration with Yuichiro Hiraizumi, as a post- doctoral fellow with Jim Crow and as a fledgling faculty member at the University of Wisconsin. Many of us at the conference worked with him personally and benefited from his insights and his enthusiasm for genetic analysis of meiotic problems. We all felt a great sense of loss and missed his lively contributions at the symposium.

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