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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Autosomal suppressors of sex-ratio in Drosophila mediopunctata

4422
Decarvalho, ABK, L. B.,  Heredity,  71:546-551. 1993-01-20 00:00:00.
The sex-ratio trait has been described as the production of progenies with excess of females due to X-linked meiotic drive in the parental males. This trait has a variable expression in Drosophila mediopunctata. We describe here the existence and chromosomal localization of autosomal suppressors of sex-ratio in this species. There are at least four such genes (one on each major autosome) and the strongest effect.is localized on chromosome IV. These genes possibly result from the operation of 'Fisher's Principle'; a mechanism of Natural Selection leading to a 1:1 sex ratio.

Didymium iridis reproductive systems: Additions and meiotic drive

4421
Clark, JL, J. C.,  Mycologia,  85:764-768. 1993-01-19 00:00:00.
Three heterothallic Mexican isolates (Mex 1, Mex 2, and Mex 3) of Didymium iridis belong to the reproductively isolated A5 mating series of this morphospecies. This was unexpected in that the sole previous A5 isolate was from Georgia and the Mexican isolates were collected in southern Mexico adjacent to the Central American Al series region. The Mexican isolates were also unusual in that mating alleles did not generally segregate in a normal 1:1 ratio. The A5(3) or A5(4) mating types, when present in a plasmodium, caused the partial or total elimination of the other mating allele during growth or sporulation. Isolates from Guatemala (Gua 2) and Panama (Pan 8) were found to belong to the Central American Al mating series. Each of these isolates was collected as a haploid selfed plasmodium which contained a single mating type respectively designated A1(13) and A1(14). Four nonheterothallic isolates from California (Ca 8), Guatemala (Gua 1), Japan (jap 1) and South Africa (SA 2) were also investigated.

Deletion analysis of the selfish B-chromosome, Paternal Sex-Ratio (PSR), in the parasitic wasp Nasonia vitripennis

4420
Beukeboom, LWW, J. H.,  Genetics,  133:637-648. 1993-01-18 00:00:00.
Paternal Sex Ratio (PSR) is a ''selfish'' B chromosome in the parasitoid wasp Nasonia vitripennis. It is transmitted via sperm, but causes supercondensation and destruction of the paternal chromosomes in early fertilized eggs. Because this wasp has haplodiploid sex determination, the effect of PSR is to convert diploid (female) eggs into haploid (male) eggs that carry PSR. Characterizing its genetic structure is a first step toward understanding mechanisms of PSR action. The chromosome is largely heterochromatic and contains several tandemly repeated DNA sequences that are not present on the autosomes. A deletion analysis of PSR was performed to investigate organization of repeats and location of functional domains causing paternal chromosome destruction. Deletion profiles using probes to PSR-specific repetitive DNA indicate that most repeats are organized in blocks on the chromosome. This study shows that the functional domains of PSR can be deleted, resulting in nonfunctional PSR chromosomes that are transmitted to daughters. A functional domain may be linked with the psr22 repeat, but function may also depend on abundance of PSR-specific repeats on the chromosome. It is hypothesized that the repeats act as a ''sink'' for a product required for proper paternal chromosome processing. Almost all deletion chromosomes remained either functional of nonfunctional in subsequent generations following their creation. One chromosome was exceptional in that it reverted from nonfunctionality to functionality in one lineage. Transmission rates of nonfunctional deletion chromosomes were high through haploid males, but low through diploid females.

Transmission and expression of the parasitic Paternal Sex-Ratio (PSR) chromosome

4419
Beukeboom, LWW, J. H.,  Heredity,  70:437-443. 1993-01-17 00:00:00.
B-chromosomes are often considered genomic parasites. They are extra to the normal chromosomal complement, are unnecessary for survival of an individual, and are often inherited at higher than Mendelian rates. Paternal Sex Ratio (PSR) is an extreme example of a parasitic B-chromosome in the wasp Nasonia vitripennis. It is transmitted via sperm but then destroys the other paternal chromosomes in the early fertilized egg. PSR disrupts the normal haplodiploid sex determination system of this wasp by converting diploid (female) eggs into haploid eggs that develop into PSR-bearing males. Transmission and expression of PSR was measured in single pair crosses between carrier males and standard females. Presence of the chromosome was detected by probing offspring with PSR-specific repetitive DNA. Most (equal to or more than 90 per cent) PSR males produced all-male offspring. Overall transmission rates of PSR to fertilized eggs varied beween 0.94 and 1.0. Some males (up to 10 per cent) produced daughters at varying frequencies. Of 226 daughters tested, only one carried PSR (and this may have been a laboratory error) indicating that daughters result from failure of transmission rather than loss of expression. Transmission of PSR to males in families that included female offspring varied from 0 to 94 per cent. Incomplete transmission is most likely the result of loss of PSR in some spermatogonial cell lineages and indicates some mitotic instability. Implications of the results to the aetiology and population genetics of PSR are discussed.

Meiotic drive on aberrant Chromosome-1 in the mouse is determined by a linked distorter

4418
Agulnik, SIS, I. D.; Orlova, G. V.; Ruvinsky, A. O.,  Genetical Research,  61:91-96. 1993-01-16 00:00:00.
An aberrant chromosome 1 carrying an inverted fragment with two amplified DNA regions was isolated from wild populations of Mus musculus. Meiotic drive favouring the aberrant chromosome was demonstrated for heterozygous females. Its cause was preferential passage of aberrant chromosome 1 to the oocyte. Genetic analysis allowed us to identify a two-component system conditioning deviation from equal segregation of the homologues. The system consists of a postulated distorter and responder. The distorter is located on chromosome 1 distally to the responder, between the ln and Pep-3 genes, and it acts on the responder when in trans position. Polymorphism of the distorters was manifested as variation in their effect on meiotic drive level in the laboratory strain and mice from wild populations.

The peculiar journey of a selfish chromosome: Mouse t-haplotypes and meiotic drive

4428
Silver, LM,  Trends in Genetics,  9:250-254. 1993-01-06 00:00:00.
Mouse t haplotypes are descendents of a variant form of chromosome 17 that evolved the ability to propagate itself at the expense of the wild-type homolog from heterozygous +/t males. Although once enigmatic, these widespread selfish chromosomes have revealed many of their secrets in response to a combined assault with molecular, genetic and phylogenetic techniques. This review summarizes the current understanding of t haplotypes and their raison d'etre.

Meiotic behavior of B- chromosomes in the grasshopper Omocestus burri: A case of drive in females

4427
Santos, JLD, A. L.; Fernandez, A.; Diez, M.,  Hereditas,  118:139-143. 1993-01-05 00:00:00.
The meiotic behaviour of an iso-B chromosome of the grasshopper Omocestus burri has been studied in a natural population located at Villar del Cobo (Teruel, Spain) by means of cytological observations of male and female meiosis. Whereas B chromosomes do not accumulate in the male germ line, they are included in the secondary oocyte at an increased frequency over mendelian expectations. Therefore, an accumulation mechanism of the accessory chromosome based on meiotic drive takes place in the females of this species.

Evolutionary dynamics of spore killers

4426
Nauta, MJH, R. F.,  Genetics,  135:923-930. 1993-01-04 00:00:00.
Spore killing in ascomycetes is a special form of segregation distortion. When a strain with the Killer genotype is crossed to a Sensitive type, spore killing is expressed by asci with only half the number of ascospores as usual, all surviving ascospores being of the Killer type. Using population genetic modeling, this paper explores conditions for invasion of Spore killers and for polymorphism of Killers, Sensitives and Resistants (which neither kill, nor get killed), as found in natural populations. The models show that a population with only Killers and Sensitives can never be stable. The invasion of Killers and stable polymorphism only occur if Killers have some additional advantage during the process of spore killing. This may be due to the effects of local sib competition or some kind of ''heterozygous'' advantage in the stage of ascospore formation or in the short diploid stage of the life cycle. This form of segregation distortion appears to be essentially different from other, well-investigated forms, and more field data are needed for a better understanding of spore killing.

Cheaters sometimes prosper: Distortion of Mendelian segregation by meiotic drive

4425
Lyttle, TW,  Trends in Genetics,  9:205-210. 1993-01-03 00:00:00.
Two of Mendel's three laws were quickly discarded as information on the organization and transmission of genes accumulated at the beginning of this century, but bis law of segregation has shown remarkable staying power. In fact, within most of population genetic theory for sexual diploids is buried the tacit assumption that heterozygous alleles are represented in gametes in a 1:1 ratio. Nevertheless, there is a small, but important, group of genetic systems that subvert the law of segregation, and show 'meiotic drive.'

The evolution of unusual chromosomal systems in coccoids: Extraordinary sex-ratios revisited

4424
Haig, D,  Journal of Evolutionary Biology,  6:69-77. 1993-01-02 00:00:00.
Coccoids (scale insects) exhibit a wide variety of chromosomal systems. In many species, paternal chromosomes are eliminated from the male germline such that all of a male's sperm transmit an identical set of maternal chromosomes. In such species, an offspring's sex is determined by whether or not paternal chromosomes are inactivated in the egg's cytoplasm after fertilization. This paper presents a model of the evolution of paternal genome loss in coccoids from an ancestral system of XX-XO sex determination. The model is based on Hamilton's (1967) theory that different genetic elements within the genome have different unbeatable sex ratios. In this model (1) meiotic drive by the X chromosome in XO males causes female-biased sex ratios; (2) the maternal set of autosomes in males evolves effective sex linkage to exploit X-drive; and (3) genes expressed in mothers are selected to convert some of their XX daughters into sons. A similar model may explain the evolution of haplodiploidy.

Selfish genes in mosquitos

6274
C. F. Curtis,  Nature,  357:450. 1992-06-11 16:47:56.
Hurst and coUeagues1.2 state that "within any population of [the mosquito] Culex pipiens there are two sorts of individual, those that bear/harbour Wolbachia [bacteria] and those that do not". But, according to Yen and Barr3, all wild-type C. pipiens appropriately examined before 1973 were found to carry Wolbachia, It was only when Yen and Barr produced uninfected individuals artificially by tetracycline treatment that it was found that matings of uninfected females x infected males were sterile, whereas all matings by uninfected males were fertile.

The New World Screwworm Eradication Programme. North Africa 1988-1992

25556
Food and Agriculture Organization,  FAO,  1992-06-01 08:59:36.
This book documents a programme which was unusual in several respects. The campaign to eradicate the New World screwworm from North Africa was unusually large in financial terms. At the same time it was unusually short. Era dica tion itself took about six months, although it was preceded by one year of preparation and followed by one year of continued surveillance and preventive actions. It involved an unusually large array of partners: 22 donors, eight countries at immediate risk, four UN agencies and several con­tractors from the private sector. What have been the main factors contributing to the success of the pro­gramme?

Evolution of the mouse t-haplotype – Recent and worldwide introgression to Mus musculus

4433
Morita, TK, H.; Murata, K.; Nozaki, M.; Delarbre, C.; Willison, K.; Satta, Y.; Sakaizumi, M.; Takahata, N.; Gachelin, G.; Matsushiro, A.,  Proceedings of the National Academy of Sciences of the United States of America,  89:6851-6855. 1992-01-11 00:00:00.
Mouse t haplotypes are variants of chromosome 17, consisting of four inversions. Despite the homozygous lethality and pleiotropic effect on embryonic development, sperm production, and recombination, they have widely spread in natural populations of the house mouse (10-40% in frequency) because of the meiotic drive advantage. We sequenced 14 Tcp-1 (t-complex polypeptide 1) genes from four t haplotypes, nine wild mice, and a rat as a reference. From a comparison of intron sequences of 610 base pairs, we dated the origin of t haplotypes to 2.9 +/- 0.7 million years ago, which predates the splitting of Mus musculus subspecies (almost-equal-to 1 million years ago). However, the Tcp-1 intron sequences of t haplotypes from different M. musculus subspecies from various parts of the world show no divergence, indicating the recent introgression (no earlier than 0.8 million years ago) of a single ancestral type. Nucleotide changes in coding regions are also consistent with this conclusion. Hence, polymorphisms among t haplotypes including lethality factors have accumulated during this short time period independently in each M. musculus subspecies.

Male and female segregation distortion for heterochromatic supernumerary segments on the s(8) chromosome of the grasshopper Chorthippus jacobsi

4432
Lopezleon, MDC, J.; Camacho, J. P. M.,  Chromosoma,  101:511-516. 1992-01-10 00:00:00.
The mode of inheritance of supernumerary segments located on three different chromosome pairs was investigated in controlled crosses with specimens of the grasshopper Chorthippus jacobsi. While extra segments located on chromosomes M5 and M6 showed Mendelian inheritance, that on S8 did not. Thus, the two supernumerary heterochromatic chromosome segments located distally on the S8 chromosome accumulated through non-Mendelian transmission through both sexes. The observed transmission patterns may be explained by gametic selection for spermatozoa carrying segmented S8 chromosomes, in addition to meiotic drive for segmented S8 chromosomes in heterozygous females. The significance of these findings for the maintenance of these polymorphisms in natural populations is discussed.

Population genetics of a parasitic chromosome – Experimental analysis of PSR in subdivided populaltions

4431
Beukeboom, LWW, J. H.,  Evolution,  46:1257-1268. 1992-01-09 00:00:00.
Nasonia vitripennis is a parasitoid wasp that harbors several non-Mendelian sex-ratio distorters. These include MSR (Maternal Sex Ratio), a cytoplasmic element that causes nearly all-female families, and PSR (Paternal Sex Ratio), a supernumerary chromosome that causes all-male families. As in other hymenoptera, N. vitripennis has haplodiploid sex determination. Normally, unfertilized (haploid) eggs develop into males and fertilized (diploid) eggs develop into females. The PSR chromosome violates this normal pattern; it is inherited through sperm, but then causes destruction of the paternal chromosomes (except itself, thus converting diploid fertilized eggs (normally females) into haploid eggs that develop into PSR-bearing males. PSR is an extreme example of "parasitic" or "selfish" DNA. Because N. vitripennis has a highly subdivided population structure in nature, population-level selection may be important in determining the dynamics of PSR in natural populations. A theoretical analysis shows that subdivided population structure reduces PSR frequency, whereas high fertilization proportion (such as produced by the MSR element) increases PSR frequency. Population experiments using two deme sizes (3- and 12-foundress groups) and strains producing two fertilization proportions [wild-type (LabII)-57-67% female, and MSR (MI)-90-93% female] confirm these predictions. PSR achieved frequencies over 0.90 in 12-foundress group MSR populations in contrast to 0.20-0.40 in wild-type 12-foundress populations. PSR was selected against in wild-type populations composed of three-foundress groups. In MSR populations with three-foundress groups, presence of PSR selected against the MSR cytoplasmic element, eventually leading to low frequencies of both PSR and MSR. Complicated dynamics may occur when these two sex-ratio distorters are both present in highly subdivided populations. The existence of PSR in natural populations may depend on the presence of MSR. Results indicate that population subdivision could be important in determining the frequency of sex ratio distorters in N. vitripennis.

Can transposable elements be used to drive disease refractoriness genes into vector populations?

6271
M. G. Kidwell and J. M. C. Ribeiro,  Parasitology Today,  8:325-329. 1992-01-08 16:40:55.
A number of biological procedures are currently being considered as alternatives to insecticide-based methods for the control of insect vectors of disease. Among these are the adaptation of various genetic mechanisms to drive genes of interest, such as refractoriness to malaria in mosquitoes, into natural populations, for vector control purposes. Here, Margaret Kidwell and Jose Ribeiro develop a rationale for the possible use of transposable genetic elements, one of these potential drive mechanisms, and some of the problems being faced in seeking to determine the feasibility of such a strategy are described.

Effects of deletions on mitotic stability of the Paternal Sex-Ratio (PSR) chromosome from Nasonia

4430
Beukeboom, LWR, K. M.; Werren, J. H.,  Chromosoma,  102:20-26. 1992-01-08 00:00:00.
Paternal-Sex-Ratio (PSR) is a B chromosome that causes all-male offspring in the parasitoid wasp Nasonia vitripennis. It is only transmitted via sperm of carrier males and destroys the other paternal chromosomes during the first mitotic division of the fertilized egg. Because of haplodiploidy, the effect of PSR is to convert diploid (female) eggs into haploid eggs that develop into PSR-bearing males. The PSR chromosome was previously found to contain several families of repetitive DNA, which appear to be present in local blocks. PSR chromosomes with irradiation-induced deletions have decreased rates of transmission and increased variation in transmission. This study investigates whether these differences in transmission of deletion chromosomes are due to mitotic instability. Two deletion chromosomes (E306 and F316) and the wild-type PSR chromosome were examined. A cytogenetic assay of testes revealed that wild-type PSR males contained the chromosome in 98%-100% of their spermatocytes. Similar counts from carriers of two deletion chromosomes were lower and varied between individuals from 50%-100%. One F316 male did not contain the chromosome in any of its spermatocytes although the chromosome was present in somatic tissues based on hybridization to PSR-specific repetitive DNA. A molecular analysis of males found the wild-type PSR chromosome to be present in all somatic tissues. Tissue specific differences in the presence or PSR were found in several males from the two deletion lines. The results show that deletions can result in mosaicism due to increased mitotic instability of PSR. Such individuals sometimes partially or completely fail to transmit the chromosome. Patterns of mosaicism of 13 chromosomes in other organisms are discussed.

Meiotic drive for the aberrant Chromosome-1 in mice is determined by a linked distorter

4429
Agulnik, SIS, I. D.; Orlova, G. V.; Ruvinsky, A. O.,  Genetika,  28:47-57. 1992-01-07 00:00:00.
AN aberrant chromosome 1 carrying an inverted fragment with two amplified DNA regions was isolated from natural populations of Mus musculus. A meiotic drive favouring the aberrant chromosome was previously demonstrated for heterozygous females. The cause for this was the preferential passage of the chromosome 1 to the oocyte. Genetic analysis made it possible to identify a two-component system conditioning the deviation from equal segregation of the homologues. The system consists of the postulated distorter and a responder. The distorter is located on the chromosome 1 distally to the responder, between the ln and Pep 3 genes, the former acting on the responder when in the trans position. Polymorphism of the distorters was manifested as variation in their effect on the meiotic drive level in the laboratory strain and mice from natural populations.

Genetic scrambling as a defense against meiotic drive

4443
Haig, DG, A.,  Journal of Theoretical Biology,  153:531-558. 1991-01-21 00:00:00.
Genetic recombination has important consequences, including the familiar rules of Mendelian genetics. Here we present a new argument for the evolutionary function of recombination based on the hypothesis that meiotic drive systems continually arise to threaten the fairness of meiosis. These drive systems act at the expense of the fitness of the organism as a whole for the benefit of the genes involved. We show that genes increasing crossing over are favoured, in the process of breaking up drive systems and reducing the fitness loss to organisms.

Divergence of meiotic drive-suppression systems as an explanation for sex-biased hybrid sterility and inviability

4442
Frank, SA,  Evolution,  45:262-267. 1991-01-20 00:00:00.
Two empirical generalizations about speciation remain unexplained: the tendency of the heterogametic sex to be sterile or inviable in F1 hybrids (Haldane's rule), and the tendency of the X chromosome to harbor the genetic elements that cause this sex bias in hybrid fitness. I suggest that divergence of meiotic drive systems on the sex chromosomes can explain these observations. The theory follows from two simple facts. First, sex chromosomes are particularly susceptible to the forces of meiotic drive. Second, divergence of meiotic drive systems can cause hybrid sterility and inviability. The main objection to the theory is that meiotic drive is apparently rare, whereas the observed pattern of hybrid fitness is widespread. I answer this objection by showing that divergence of meiotic drive systems can explain the two generalizations even if large departures from Mendelian segregation are rarely observed.

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