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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Sperm competition and the dynamics of X chromosome drive: Stability and extinction

4326
Taylor, JEJ, J.,  Genetics,  160:1721-1731. 2002-01-04 00:00:00.
Several empirical studies of sperm competition in populations polymorphic for a driving X chromosome have revealed that Sex-ratio males (those carrying a driving X) are at a disadvantage relative to Standard males. Because the frequency of the driving X chromosome determines the population-level sex ratio and thus alters male and female mating rates, the evolutionary consequences of sperm competition for sex chromosome meiotic drive are subtle. As the SR allele increases in frequency, the ratio of females to males also increases, causing an increase in the male mating rate and a decrease in the female mating rate. While the former change may exacerbate the disadvantage of Sex-ratio males during sperm competition, the latter change decreases the incidence of sperm competition within the population. We analyze a model of the effects of sperm competition on a driving X chromosome and show that these opposing trends in male and female mating rates call result in two coexisting locally stable equlibria, one corresponding to a balanced polymorphism of the SR and ST alleles and the second to fixation of the ST allele. Stochastic fluctuations of either the Population sex ratio or the SR frequency call then drive the population away from the balanced polymorphism and into the basin of attraction for the second equilibrium, resulting in fixation of the SR allele and extinction of the population.

Sex-ratio drive in Drosophila simulans: Variation in segregation ratio of X chromosomes from a natural population

4325
Montchamp-Moreau, CC, M.,  Genetics,  162:1221-1231. 2002-01-03 00:00:00.
The sex-ratio trait that exists in a dozen Drosophila species is a case of naturally occurring X chromosome drive that causes males to produce female-biased progeny. Autosomal and Y polymorphism for suppressors are known to cause variation in drive expression, but the X chromosome polymorphism has never been thoroughly investigated. We characterized 41 X chromosomes from a natural population of Drosophila simulans that had been transferred to a suppressor-free genetic background. We found two clear-cut groups of chromosomes, sex-ratio and standard. The sex-ratio X chromosomes differed in their segregation ratio (81-96% females in the progeny), the less powerful drivers being less stable in their expression. A sib analysis, using a moderate driver, indicated that within-X variation in drive expression depended on genetic (autosomal) or epigenetic factors and that the age of the males also affected the trait. The other X chromosomes produced equal or roughly equal sex ratios, but again with significant variation. The continuous pattern of variation observed within both groups suggested that, in addition to a major sex-ratio gene, many X-linked loci of small effect modify the segregation ratio of this chromosome and are maintained in a polymorphic state. This was also supported by the frequency distribution of sex ratios produced by recombinant X chromosomes.

Segregation distortion induced by wild-type RanGAP in Drosophila

4324
Kusano, AS, C.; Ganetzky, B.,  Proceedings of the National Academy of Sciences of the United States of America,  99:6866-6870. 2002-01-02 00:00:00.
Segregation Distorter (SD) is a meiotic drive system in Drosophila that causes preferential transmission of the SD chromosome from SD/SD+ males owing to the induced dysfunction of SD+ spermatids. The key distorter locus, Sid, is a dominant neomorphic allele encoding a truncated, but enzymatically active, RanGAP (RanGTPase-activating protein) whose nuclear mislocalization underlies distortion by disrupting the Ran signaling pathway. Here, we show that even wild-type RanGAP can cause segregation distortion when it is overexpressed in the male germ line or when the gene dosage of a particular modifier locus is increased. Both manipulations result in substantial nuclear accumulation of RanGAP. Distortion can be suppressed by overexpression of Ran or Ran guanine nucleotide exchange factor (RanGEF) in the male germ line, indicating that the primary consequence of nuclear mislocalization of RanGAP is reduction of intranuclear RanGTP levels. These results prove that segregation distortion does not depend on any unique properties of the mutant RanGAP encoded by Sid and provide a unifying explanation for the occurrence of distortion in a variety of experimental situations.

Sperm development, age and sex chromosome meiotic drive in the stalk-eyed fly, Cyrtodiopsis whitei

4337
Wilkinson, GSS, M. I.,  Heredity,  87:17-24. 2001-01-15 00:00:00.
The cytological basis of X chromosome meiotic drive or sex ratio (SR) has been reported for several species of Drosophila but not for other species. Here we describe how sperm development in the stalk-eyed fly, Cyrtodiopsis whitei, influences progeny sex proportion, in order to determine if a common developmental mechanism could cause meiotic drive in these distantly related taxa. Because age has been found to affect the degree of segregation distortion in some Drosophila, we tested flies from six to 26 weeks of age. We find that spermatocyst bundles in SR males frequently contain incompletely elongated spermatid nuclei independently of male age. Older males have, however, more spermatocyst bundles in their testes than younger males. Abnormal spermatid elongation affects male fertility since SR males produce 74% as many progeny per week as ST males. The proportion of spermatocyst bundles with improperly elongated spermatid nuclei explains 71% of the variation in progeny sex proportion. After reviewing the literature on sperm development and meiotic drive, we conclude that the cytological basis of meiotic drive in diopsids closely resembles Drosophila. Across species in both groups, the production of fertile males is associated with less than half of all spermatids not elongating normally in a spermatocyst bundle. We discuss the possibility that frequency-dependent selection on male fertility could stabilize the drive polymorphism in these unusual flies.

Meiotic drive alters sperm competitive ability in stalk-eyed flies

4336
Wilkinson, GSF, C. L.,  Proceedings of the Royal Society B-Biological Sciences,  268:2559-2564. 2001-01-14 00:00:00.
Meiotic drive results when sperm carrying a driving chromosome preferentially survive development. Meiotic drive should therefore influence sperm competition because drive males produce fewer sperm than non-drive males. Whether meiotic drive also influences the competitive ability of sperm after ejaculation is unknown. Here we report the results from reciprocal crosses that are designed for estimating the sperm precedence of male stalk-eyed flies (Cyrtodiopsis whitei) with or without X-linked meiotic drive. We find that nearly half of all sex-ratio males, as compared with 14 % of non-sex-ratio males, fail to produce young in a reciprocal cross. Furthermore, the proportion of progeny sired by a sex-ratio male in a female jointly inseminated by a non-sex-ratio male was less than expected from the number of sperm transferred. These effects are not due to differential sperm storage by females because, after a single mating with a sex-ratio male, all females stored sperm and because two sex-ratio males share paternity after jointly mating with a female. In addition to demonstrating a new mechanism of sperm competition, these results provide insight into the maintenance of sex-ratio polymorphisms. Sex-ratio males have less than one-half the fertility of non-sex-ratio males, as is required in order for frequency-dependent selection on males to produce a stable sex-ratio polymorphism.

Selection and segregation distortion in a sex-differentiated population

4335
Weissing, FJvB, M.,  Theoretical Population Biology,  60:327-341. 2001-01-13 00:00:00.
We extend the classical model for selection at an autosomal locus in a sex-differentiated population to include segregation distortion. The equations remain the same, but the fitness parameters are interpreted differently and refer to alleles instead of genotypes. We derive conditions for internal and external stability of the equilibria, i.e., stability with respect to perturbations of alleles that are already present at equilibrium and stability with respect to invasion attempts by newly arising alleles. We show that, in a sex-differentiated population, external stability of an equilibrium can be judged on the basis of Shaw-Mohler criteria. Throughout, we compare the situation in populations with and without sex differentiation. Interestingly, internal stability is more difficult to achieve in a population without sex differentiation than in a population in which selection and segregation distortion are restricted to one sex. In a companion paper we show how the general results of the present paper can lead to new insights into specific systems such as the t complex of the house mouse. (C) 2001 Elsevier Science.

Competition at the Mouse t Complex: Rare Alleles Are Inherently Favored

4334
van Boven, MW, Franz J.,  Theoretical Population Biology,  60:343-358. 2001-01-12 00:00:00.
We investigate the competition between alleles at a segregation distorter locus. The focus is on the invasion prospects of rare mutant distorter alleles in a population in which a wildtype and a resident distorter allele are present. The parameters are chosen to reflect the situation at the t complex of the house mouse, one of the best-studied examples of segregation distortion. By analyzing the invasion chances of rare alleles, we provide an analytical justification of earlier simulation results. We show that a new distorter allele can successfully invade even if it is inferior both at the gamete and at the individual level. In fact, newly arising distorter alleles have an inherent rareness advantage if their negative fitness consequences are restricted to homozygous condition. Likewise, rare mutant wildtype alleles may often invade even if their viability or fertility is reduced. As a consequence, the competition between alleles at a segregation distorter locus should lead to a high degree of polymorphism. We discuss the implications of this conclusion for the t complex of the house mouse and for the evolutionary stability of “honest” Mendelian segregation.

Sex-ratio segregation distortion associated with reproductive isolation in Drosophila

4333
Tao, YH, D. L.; Laurie, C. C.,  Proceedings of the National Academy of Sciences of the United States of America,  98:13183-13188. 2001-01-11 00:00:00.
Sex-ratio distortion is the most common form of non-Mendelian segregation observed in natural populations. It may occur even more frequently than direct observations suggest, because the dysgenic population consequences of a biased sex ratio are expected to result in the rapid evolution of suppressors, resulting in suppressed or "cryptic" segregation distortion. Here we report evidence for cryptic sex-ratio distortion that was discovered by introgressing segments of the genome of Drosophila mauritiana into the genome of Drosophila simulans. The autosomal suppressor of sex-ratio distortion, which is also associated with a reduction in hybrid male fertility, has been genetically localized to a region smaller than 80-kb pairs in chromosome 3.

Sex chromosome meiotic drive

4332
Jaenike, J,  Annual Review of Ecology and Systematics,  32:25-49. 2001-01-10 00:00:00.
Sex chromosome drive refers to the unequal transmission of X and Y chromosomes from individuals of the heterogametic sex, resulting in biased sex ratios among progeny and within populations, The presence of driving sex chromosomes can reduce mean fitness within a population, bring about intragenomic conflict between the X chromosome, the Y, and the autosomes, and alter the intensity or mode of sexual selection within species. Sex chromosome drive, or its genetic equivalent, is known in plants, mammals. and flies. Many species harboring driving X chromosomes have evolved Y-linked and autosomal suppressors of drive. If a drive polymorphism is not stable, then driving chromosomes may spread to fixation and cause the extinction of a species. Certain characteristics of species, such as population density and female mating rate, may affect the probability of fixation of driving chromosomes. Thus, sex chromosome drive could be an agent of species-level selection.

The role of selfish genetic elements in eukaryotic evolution

4331
Hurst, GDDW, J. H.,  Nature Reviews Genetics,  2:597-606. 2001-01-09 00:00:00.
'Selfish genetic elements', such as transposons, homing endonucleases, meiotic drive chromosomes and heritable microorganisms, are common features of eukaryotes. However, their importance in the evolution of eukaryotic genomes is still controversial. In this review, we discuss these diverse elements and their potential importance in the evolution of genetic systems, adaptation, and the extinction and birth of species.

An unusual sex-determination system in South American field mice (genus Akodon): The role of mutation, selection, and meiotic drive in maintaining XY females

4330
Hoekstra, HEH, J. M.,  Evolution,  55:190-197. 2001-01-08 00:00:00.
The mechanism of sex determination in mammals appears highly conserved: the presence of a Y chromosome triggers the male developmental pathway, whereas the absence of a Y chromosome results in a default female phenotype. However, if the Y chromosome fails to initiate the male pathway (referred to as Y*), XY* females can result, as is the case in several species of South American field mice (genus Akodon). The breeding genetics in this system inherently select against the Y* chromosome such that the frequency of XY* females should decrease rapidly to very low frequencies. However, in natural populations of Akodon, XY* females persist at substantial frequencies; for example, 10% of females are XY* in A. azarae and 30% in A. boliviensis. We develop a mathematical model that considers the potential roles of three evolutionary forces in maintaining XY* females: Y-to-Y* chromosome transitions (mu ration), chromosome segregation distortion (meiotic drive), and differential fecundity (selection). We then test the predictions of our model using data from breeding colonies of A. azarae. We conclude that any single force is inadequate to maintain XY* females. However, a combination of segregation bias of the male and female Y chromosomes during spermatogenesis/oogenesis and increased fecundity in XY* females could account for the observed frequencies of XY* females.

Outcrossed sex allows a selfish gene to invade yeast populations

4329
Goddard, MRG, D.; Burt, A.,  Proceedings of the Royal Society B-Biological Sciences,  268:2537-2542. 2001-01-07 00:00:00.
Homing endonuclease genes (HEGs) in eukaryotes are optional genes that have no obvious effect on host phenotype except for causing chromosomes not containing a cop), of the gene to be cut, thus causing them to be inherited at a greater than Mendelian rate via gene conversion. These genes are therefore expected to increase in frequency in outcrossed populations, but not in obligately selfed populations. In order to test this idea, we compared the dynamics of the VDE HEG in six replicate outcrossed and inbred populations of yeast (Saccharomyces cerevisiae). VDE increased in frequency from 0.21 to 0.55 in four outcrossed generations, but showed no change in frequency in the inbred populations. The absence of change in the inbred populations indicates that any effect of VDE on mitotic replication rates is less than 1%. The data from the outcrossed populations best fit a model in which 82% of individuals are derived from outcrossing and VDE is inherited by 74% of the meiotic products from heterozygotes (as compared with 50% for Mendelian genes), These results empirically demonstrate how a host mating system plays a key role in determining the population dynamics of a selfish gene.

Nonrandom segregation during meiosis: the unfairness of females

4328
de Villena, FPMS, C.,  Mammalian Genome,  12:331-339. 2001-01-06 00:00:00.
Most geneticists assume that chromosome segregation during meiosis is Mendelian (i.e., each allele at each locus is represented equally in the gametes). The great majority of reports that discuss non-Mendelian transmission have focused on systems of gametic selection, such as the mouse t-haplotype and Segregation distorter in Drosophila, or on systems in which post-fertilization selection takes place, Because the segregation of chromosomes in such systems is Mendelian and unequal representation of alleles among offspring is achieved through gamete dysfunction or embryonic death, there is a common perception that true disturbances in the randomness of chromosome segregation are rare and of limited biological significance. In this review we summarize data on nonrandom segregation in a wide variety of genetic systems. Despite apparent differences between some systems, the basic requirements for nonrandom segregation can be deduced from their shared characteristics: i) asymmetrical meiotic division(s); ii) functional asymmetry of the meiotic spindle poles: and iii) functional heterozygosity at a locus that mediates attachment of a chromosome to the spindle. The frequency with which all three of these requirements al e fulfilled in natural populations is an known, but our analyses indicate that nonrandom segregation occurs with sufficient frequency during female meiosis, and in exceptional cases of male meiosis, that it has important biological, clinical, and evolutionary consequences.

Transmission ratio distortion due to the bl gene in table beet

4327
Austin, DG, I. L.,  Journal of the American Society for Horticultural Science,  126:340-343. 2001-01-05 00:00:00.
The bl gene conditions a blotchy phenotype (irregular sectors of red and white root color) in table beet (Beta vulgaris ssp, vulgaris). Segregation of the bl gene was found to be consistent with a single recessive gene, however, some evidence for a departure from a single gene model was observed when blbl plants were used as females. Tn this report, segregation of the bl gene was examined in greater detail in 10 F-2 populations derived from crosses of red blotchy-rooted females (genotype blbl, denoted blotchy) with red-rooted males (BlBl, denoted red,), and 10 Fz populations derived from the reciprocal cross. Tn blbl x BlBl crosses, the proportion of red-rooted progeny was greater than 0.75 in seven of the crosses, and was significantly greater (P = 0.005) in three crosses. A test for heterogeneity was significant, indicating that the proportion of red-rooted progeny differed significantly in these 10 crosses. In BlBl x blbl crosses, the proportion of red-rooted progeny was <0.75 in seven of the crosses and there were no significant departures from the expected 3:1 ratio in any of the individual crosses. However, a pooled estimate of the segregation ratio showed a significant (P < 0.01) departure from the 3:1 ratio (pooled estimate = 0.71.), These data demonstrate transmission ratio distortion at the bl locus when blbl plants are used as both females and males in matings with wild type plants, but the degree of distortion is greater when blbl plants are used as females. Ratio distortion in such crosses may be due to a variety of factors, including increased transmission of the bl gene through female or male gametes depending on the direction of the cross, reduced fitness of maternally derived blbl progeny, epigenetic phenomena, increased fitness of paternally derived blbl progeny, or linkage of the bl gene to viability genes.

Success in Zanzibar: Eradication of tsetse

27123
A. R. Msangi, N. Kiwia, I. I. Malele, F. Mramba, K. M. Saleh, W. A. Mussa, K. G. Juma, V. A. Dyck, M. J. B. Vreysen, A. G. Parker, U. Feldmann, Z. R. Zhu and H. Pan,  Area-Wide Control of Fruit Flies and Other Insect Pests,  2000-06-06 13:17:29.
There are about 22 species of tsetse flies found nowhere else in the world except in 36 countries of sub-Saharan Africa Tsetse flies transmit a debilitating and often fatal disease, trypanosomosis, which causes tremendous losses of livestock, and severely limits agricultural production (it reduces output of milk and meat, causes mortality, infertility and abortion in livestock, deprives the rural population of draught power and manure to improve and increase crop production) Tsetse flies also transmit human trypanosomosis, commonly known as 'sleeping sickness' It is estimated that over 55 million people living in rural sub-Saharan Africa are at risk from this fatal disease Tanzania's Zanzibar Island is situated 35 km off the eastern coast and comprises two main islands, Unguja and Pemba Previous surveys revealed that out of the seven tsetse species found on mainland Tanzania, only Glossina austeni Newstead infested Unguja Island No tsetse fly was found on the island of Pemba The fly is responsible for the cyclical transmission of trypanosomosis in livestock, the causative agents being mainly Trypanosoma congolense and, to a lesser extent, T vivax It is estimated that in Zanzibar, the disease causes annual losses of US$2 million Since fly suppression by conventional techniques has often resulted in short-term success, Tanzania has always appreciated that the long-term solution to the trypanosomosis problem is the eradication of tsetse flies in the country In 1994, the International Atomic Energy Agency (IAEA) and the United Republic of Tanzania embarked on a project with the objective of eradicating tsetse flies from Zanzibar Island by applying the sterile insect technique (SIT) (Dyck et al 1995, in press) Previous tsetse eradication efforts in Tanzania using SIT, enabled the establishment of a modest capacity on tsetse mass rearing in Tanga (Williamson et al 1983) The Zanzibar tsetse project was successfully completed in 1997 The estimated cost was US$7,941,000 but only US$5,788,097 was actually spent Financial assistance came from international donors such as the governments of Belgium, Canada, China, Sweden, the UK and the USA The results and achievements of the Zanzibar tsetse fly eradication project are presented in this paper

Glossina austeni (Diptera: Glossinidae) Eradicated on the Island of Unguja, Zanzibar, Using the Sterile Insect Technique

27121
M. J. B. Vreysen, K. M. Saleh, M. Y. Ali, A. M. Abdulla, Z.-R. Zhu, K. G. Juma, V. A. Dyck, A. R. Msangi, P. A. Mkonyi and H. U. Feldmann,  Journal of Economic Entomology,  123-135. 2000-02-01 12:59:17.
An area-wide integrated tsetse eradication project was initiated in Zanzibar in 1994 by the International Atomic Energy Agency and the governments of Tanzania and Zanzibar, to eradicate Glossina austeni Newstead from Unguja Island (Zanzibar) using the sterile insect technique. Suppression of the tsetse population on Unguja was initiated in 1988 by applying residual pyrethroids as a pour-on formulation to livestock and by the deployment of insecticide impregnated screens in some of the forested areas. This was followed by sequential releases of gamma-sterilized male flies by light aircraft. The flies, packaged in carton release containers, were dispersed twice a week along specific flight lines separated by a distance of 1–2 km. More than 8.5 million sterile male flies were released by air from August 1994 to December 1997. A sterile to indigenous male ratio of >50:1 was obtained in mid-1995 and it increased to >100:1 by the end of 1995. As a consequence the proportion of sampled young females (1–2 ovulations), with an egg in utero in embryonic arrest or an uterus empty as a result of expulsion of a dead embryo, increased from <25% in the 1st quarter to >70% in the last quarter of 1995. In addition, the age structure of the female population became significantly distorted in favor of old flies (≥4 ovulations) by the end of 1995. The apparent density of the indigenous fly population declined rapidly in the last quarter of 1995, followed by a population crash in the beginning of 1996. The last trapped indigenous male and female flies were found in weeks 32 and 36, 1996, respectively. Time for 6 fly generations elapsed between the last catch of an indigenous fly and the end of the sterile male releases in December 1997.

Co-existence of hosts and sex ratio distorters in structured populations

4343
Hatcher, MJD, A. M.; Tofts, C.,  Evolutionary Ecology Research,  2:185-205. 2000-01-21 00:00:00.
Vertically transmitted parasites occur in several invertebrate species, and alter host reproduction by a variety of mechanisms, including sex ratio distortion via feminization. Efficient feminizers are predicted to drive homogenous host populations extinct due to the absence of males. However, group (interdemic) selection may enable host-parasite co-existence through extinction-colonization turnover of local subpopulations. Here we analyse the effects of feminizers on host metapopulations, in relation to the underlying mechanism of host sex determination. We examine host metapopulations with (a) fixed probabilistic sex ratio control, (b) female heterogamety (WZ/ZZ) and (c) male heterogamety (XX/XY) with and without YY viability. Under some circumstances, host and parasite can co-exist in metapopulations despite deterministic instability of local populations, in which case the parasite persists at lower frequency than predicted for homogenous populations. However, co-existence is sensitive to host sex determining mechanism. Long-term co-existence is unlikely in chromosomal systems, where sex ratio selection and novel mating type combinations result in the loss of female-determining alleles from infected host subpopulations. The consequent loss of uninfected females precludes stochastic parasite exclusion and thus prevents local population recovery. Hence, host-feminizer co-existence via interdemic selection requires intrinsic patch recovery in addition to recolonization from neighbouring subpopulations. We conclude that metapopulation structure can only buffer host populations against parasite-mediated extinction if female-determining alleles are retained in the host population.

Persistence of selfish genetic elements: population structure and conflict

4342
Hatcher, MJ,  Trends in Ecology & Evolution,  15:271-277. 2000-01-20 00:00:00.
Selfish genetic elements are vertically transmitted factors that spread by obtaining a transmission advantage relative to the rest of the genome of their host organism, often with a cost to overall host fitness. In many cases, conventional population genetics theory predicts them spreading through populations, reaching fixation and becoming undetectable or sometimes driving the population extinct. However, in several well studied systems, these genetic elements are known to persist at relatively low, stable frequencies. Recent research suggests that several processes might explain these observations, including population structure, intragenomic conflict and coevolution.

Non-Mendelian segregation of sex chromosomes in heterospecific Drosophila males

4341
Dermitzakis, ETM, J. P.; Waldrip, H. M.; Clark, A. G.,  Genetics,  154:687-694. 2000-01-19 00:00:00.
Interspecific hybrids and backcrossed organisms generally suffer from reduced viability and/or fertility. To identify and genetically map these defects, we introgressed regions of the Drosophila sechellia genome into the D. simulans genome. A female-biased sex ratio was observed in 24 of the 221 recombinant inbred lines, and subsequent tests attributed the skew to failure of Y-bearing sperm to fertilize the eggs. Apparently these introgressed lines fail to suppl ess a normally silent meiotic drive system. Using molecular markers we mapped two regions of the Drosophila genome that appear to exhibit differences between D. simulans and D. sechellia in their regulation of sex chromosome segregation distortion. The data indicate that the sex ratio phenotype results from an epistatic interaction between at least two factors. We discuss whether this observation is relevant to the meiotic drive theory of hybrid male sterility.

A genetic test to determine the origin of maternal transmission ratio distortion: Meiotic drive at the mouse Om locus

4340
de Villena, FPMdlC-E, E.; Briscoe, T. L.; Sapienza, C.,  Genetics,  154:333-342. 2000-01-18 00:00:00.
We have shown previously that the progeny of crosses between heterozygous females and C57BL/G males show transmission ratio distortion at the Om locus on mouse chromosome 11. This result has been replicated in several independent experiments. Here we show that the distortion maps to a single locus on chromosome 11, closely linked to Om, and that gene conversion is not implicated in the origin of this phenomenon. To further investigate the origin of the transmission ratio distortion we generated a test using the well-known effect of recombination on maternal meiotic drive. The genetic test presented here discriminates between unequal segregation of alleles during meiosis and lethality, based on the analysis of genotype at both the distorted locus and the centromere of the same chromosome. We used this test to determine the cause of the transmission ratio distortion observed at the Om locus. Our results indicate that transmission ratio distortion at Om is due to unequal segregation of alleles to the polar body at the second meiotic division. Because die presence of segregation distortion at Om also depends on rile genotype of the sire, our results confirm that the sperm can influence segregation of maternal chromosomes to the second polar body.

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