Heritable variation of sex ratio in a polychaete worm

Ophryotrocha labronica is a gonochoristic polychaete worm whose sex determining mechanism and sex ratio control are supposed to be polygenic. From a lab population, whose sex ratio (i.e., proportion of males) was 0.5, the estimate of sex ratio heritability by offspring-father regression was 0.54 ± 0.15 and by offspring-mother regression was not significantly different from 0. Estimate of sex ratio repeatability between successive broods of a pair was 0.64 ± 0.33. Since female parents do not contribute in any way to the variability of sex ratio, sex ratio variation seems to be largely a paternal character. On the basis of these estimates we advance the hypothesis that in this species sex is determined by a multilocus genetic system, allowing the combined effects of a female major sex gene (which could give rise to a form of female heterogamety) and masculinizing modifiers. The hypothesis that the male sex has the least canalised sexual differentiation is supported by the observation that some old males developed oocytes.     

Conflict between Feminizing Sex Ratio Distorters and an Autosomal Masculinizing Gene in the Terrestrial Isopod Armadillidium Vulgare Latr

Female sex determination in the pill bug Armadillidium vulgare is frequently under the control of feminizing parasitic sex factors (PSF). One of these PSF is an intracytoplasmic Wolbachia-like bacterium (F), while the other (f) is suspected of being an F-bacterial DNA sequence unstably integrated into the host genome. In most wild populations harboring PSF, all individuals are genetic males (ZZ), and female phenotypes occur only due to the presence of PSF which overrides the male determinant carried by the Z chromosome (females are thus ZZ +F or ZZ +f neo-females). Here we report the effects of the conflict between these PSF and a dominant autosomal masculinizing gene (M) on phenotypes. The M gene is able to override the feminizing effect of the f sex factor and, consequently, male sex may be restored. However, M is unable to restore male sex when competing with the F bacteria. It seems that the main effect of M is to delay the expression of F bacteria slightly, inducing intersex phenotypes. Most of these intersexes are functional females, able to transmit the masculinizing gene. The frequency of M and its effects on the sex ratio in wild populations are discussed.     

Antiandrogen blocks estrogen-induced masculinization of the song system in female zebra finches

Song behavior and the neural song system that serves it are sexually dimorphic in zebra finches. In this species, males sing and females normally do not. The sex differences in the song system include sex differences in the proportion of neurons that express androgen receptors, which is higher in specific brain regions of males. Estradiol (E2) administered in early development profoundly masculinizes the song system of females, including the proportion of neurons expressing androgen receptors. We examined whether or not the expression of these androgen receptors was causally related to the E2-induced masculinization of this system by co-administering Flutamide, which blocks androgen action at the receptor, along with E2 at hatching. E2 alone had its usual masculinizing effect on the female song system, measured in adulthood: increasing the size of song nuclei, the size of neurons in HVC, RA, and 1MAN, and the number of neurons in HVC. E2's masculinizing action, however, was significantly diminished on all measures by co-administering Flutamide. Indeed, females receiving both E2 and Flutamide were never significantly more masculine than controls on any measure. Flutamide alone had no effect. Our results strongly suggest that the activation of androgen receptors is necessary for the E2-induced masculinization of the song system in females.     

Rainbow trout gonadal masculinization induced by inhibition of estrogen synthesis is more physiological than masculinization induced by androgen supplementation

The present study was designed to obtain new insights into fish gonadal sex differentiation by comparing the effects of two different masculinizing treatments on some candidate gene expression profiles. Masculinization was induced in rainbow trout, Oncorhynchus mykiss, genetic all-female populations using either an active fish androgen (11betaAnd, 11beta-hydroxyandrostenedione) or an aromatase inhibitor (ATD, 1,4,6-androstatriene-3,17-dione). The expression profiles of 100 candidate genes were obtained by real-time RT-PCR, and 46 profiles displayed a significant differential expression between control populations (males and females) and ATD/11betaAnd-treated populations. These expression profiles were grouped in four temporally correlated expression clusters. Among the common responses shared by the two masculinizing treatments, the inhibition of some early female differentiating genes (cyp19a1, foxl2a, fst, and fshb) appears to be crucial for effective masculinization, suggesting that these genes act together via a short regulation loop to maintain high sex-specific ovarian expression of cyp19a1. This simultaneous down-regulation of female-specific genes could be triggered by some testicular genes, such as dmrt1, nr0b1 (also known as dax1), and pdgfra, which are quickly up-regulated by the two masculinizing treatments. In contrast to 11betaAnd, ATD quickly restored the expression levels of steroidogenesis related genes (cyp11b2.1, cyp11b2.2, hsd3b1, cyp17a, star, and nr5a1) and some Sertoli cell markers (sox9a2 and amh) to the expression levels observed during control testicular differentiation. This demonstrates that these genes are probably not needed for active masculinization and that the inhibition of endogenous estrogen synthesis produces a much more complete and specific testicular pattern of gene expression than that observed following androgen-induced masculinization.     

Role of peanut-lectin-affinity molecules (PLAM) on primordial germ cells in the initial determination of sex in anura

Peanut lectin (PNA) or N-acetylgalactosamine (galNA, a part of the disaccharide unit which is recognized by PNA) was injected into the coelomic cavity of anuran larvae at the developmental stages during which the genital ridges were growing, and the effect of these compounds on the initial determination of gonadal sex was examined. The treatment with PNA tended to inhibit (or perturb) the expression of feminizing gene(s) in Rana japonica, and of both feminizing and masculinizing genes in R. nigromaculata. In contrast, treatment with galNA suppressed the expression of masculinizing gene(s) considerably. In terms of the initial determination of gonadal sex during normal development, these results suggest that the PNA-affinity molecule (PLAM) of primordial germ cells acts as a trigger for the expression of genes that control sexual differentiation of somatic cells. Furthermore, the somatic cells (perhaps mesenchymal and/or epithelial cells), which respond to the stimulus via the PLAM of primordial germ cells, may differ in terms of the threshold for such a response between genetic males and females. This result suggests the mesenchymal and/or epithelial cells are not sexually predetermined, but rather that sexual determination follows the response to some signal(s) mediated by the PLAM.     

Estrogens counteract the masculinizing effect of tributyltin in zebrafish

Recently, it has been demonstrated that the biocide tributyltin (TBT) can interfere with fish sex differentiation, leading to a bias of sex toward males. On the contrary, it is well known that estrogenic compounds can induce fish feminization. Yet, the combined effects of mixtures of androgenic and estrogenic compounds on fish sex differentiation have never been investigated before, even though in the environment animals are frequently exposed to both groups of xenobiotics. Therefore, in order to investigate whether exposure to estrogenic compounds can block the masculinizing effect of TBT, 5 days post-fertilization zebrafish (Danio rerio) larvae were exposed for a four month period to TBT and to the synthetic estrogen-ethinylestradiol (EE2). The fish were fed a diet containing TBT at nominal concentrations of 25 and 100 ng TBT/g, and two groups of animals were also dosed with TBT plus EE2 at nominal water concentration of 3.5 ng/L, using a flow-through design. As expected, fish exposed to TBT showed a bias of sex toward males (62.5% males in control tanks and 86% and 82% in TBT 25 and TBT 100 ng TBT/g, respectively). Co-exposure to EE2 completely blocked the masculinizing effect of TBT, with 7% males in the TBT 25 ng/g + EE2 treatment and 0% in the EE2 alone and in the TBT 100 ng/ + EE2 exposed groups. These results clearly indicate that EE2, at environmentally relevant concentrations, can block the TBT masculinizing effects in zebrafish, which suggests that in the aquatic environment the presence of estrogens may neutralize the fish masculinizing effect of TBT. Our findings highlight the need of testing the combined effects of contaminants, as single exposure studies may not be sufficient to predict the effects of mixtures of xenobiotics with antagonistic properties.     

西农莎能山羊间性遗传机制研究

本文从解剖学、组织学、细胞遗传学及遗传学方面对西农药莎能山羊的间性个性进行了研究。发现从雌性假间性到性逆转雄性的一系列类型的间性,全部是遗传雌性（６０,ＸＸ）,核型正常。这些间性个体完全受基因作用,使雌性转化,引起性别异常,因而间性基因是雄性化基因,位于常染色体,属隐性遗传。     

Number of preoptic GnRH-immunoreactive cells correlates with sexual phase in a protandrously hermaphroditic fish, the dusky anemonefish (Amphiprionmelanopus)

The populations of gonadotropin-releasing hormone (GnRH)-producing cells within the preoptic area (POA) and terminal nerve (TN) of the brain have been suggested as the neuronal systems mediating social control of sex and gonadogenesis in sequentially hermaphroditic teleosts. In the present study, the number and soma size of GnRH-immunoreactive (GnRH-ir) cells in the POA and TN were studied in male, female and juvenile individuals of the dusky anemonefish (Amphiprionmelanopus), a species which displays both male to female sex change and socially controlled sexual maturation. The results showed that the number of POA (but not TN) GnRH-ir cells differ significantly between sexual phases, with males displaying higher cell numbers than both females and juveniles. Soma sizes of POA and TN GnRH-ir cells were larger in females than in males and juveniles. However, this relationship was fully explained by differences in body size. The results indicate that high POA GnRH cell numbers are part of a masculinizing mechanism and support the hypothesis that the POA GnRH cell population plays a central role in initiating or mediating the process of socially induced gonadal and/or behavioural transformations in sequential hermaphrodites. Accepted: 9 June 1997     

A direct comparison of the masculinizing effects of testosterone,androstenedione, estrogen,and progesterone on the development of the zebra finch song system

To assess which hormones are capable of masculinizing the neural song system of zebra finch hatchlings, we implanted female hatchlings with estrogen (estradiol [E2], 75 μg, n = 9), testosterone (T, 75–88 μg, n = 13), androstenedione (AE, 75 μg, n = 7), progesterone (P, 117 μg, n = 10), or nothing (Blanks, n = 10) and compared these to unimplanted males (n = 7). Implants, consisting of a hormone and Silastic mixture encased in polyethylene tubing, were placed under the skin of the breast on the day of hatching. Birds were killed when they were subadult (58 to 68 days old). We measured volumes of area X, the higher vocal center (HVC), and the robust nucleus of the archistriatum (RA); measured soma sizes in the lateral magnocellular nucleus of the neostriatum (IMAN), HVC, and RA: and counted RA neurons. E2 masculinized all measures in the song system and nearly sex-reversed the size of RA neurons. T masculinized volumes of nuclei and soma sizes but not the number or spacing of RA neurons. E2 was always at least as effective as T in masculinizing measures of the song system and was usually more effective. AE and P did not significantly masculinize any measure. These data suggest that E2 is more potent than aromatizable androgens or P in masculinizing the female song system in development and that the action of E2 alone may be sufficient to masculinize the volume of song control nuclei and the size and number of neurons. © 1995 John Wiley & Sons, Inc.     

Neonatal Androgen Affects Copulatory Behavior in the Female Musk Shrew

The role of neonatal testosterone in the development of copulatory behavior was examined in an insectivore, the musk shrew (Suncus murinus). Female musk shrews were treated with testosterone propionate (TP) for the first 5 days of life and then tested in adulthood for either female or male-like copulatory behavior. Early TP had a masculinizing effect; neonatally treated animals mounted a stimulus female more frequently, and with shorter latencies, in response to adult testosterone treatment than did control females. Neonatally androgenized females also showed deficits in female sexual behavior; few received ejaculations from stud males. This difference was likely caused by increased aggression exhibited by the neonatally TP-treated females toward males. In turn, female aggression decreased efficiency of male partners' intromission attempts. Early TP treatments also caused structural abnormalities in the ovaries, but did not effect their capacity to ovulate in response to either gonadotropin-releasing hormone or human chorionic gonadotropin injection. In sum, exposure to TP during development augmented display of male-like behavior in females and had subtle deleterious effects on expression of feminine behavior.     

Further evidence for masculinization of female rats by males located caudally in utero

The morphology and behavior of female rodents is partially masculinized as a result of residence near males in the same uterine horn (Clemens effect). Two hypothetical mechanisms have been proposed to account for this effect. In the first hypothesis (“contiguity”) androgens secreted by males in utero are proposed to diffuse across the amniotic membrane, reaching adjacent fetuses. In the second hypothesis (“caudal male”) androgens are transported via the cervical-to-ovarian blood flow and may diffuse directly between closely apposed uterine veins and arteries. This study was designed to test directly which of these mechanisms appears more influential in masculinizing the morphology of female rats. Pregnant Sprague-Dawley rats were decapitated early on Day 22 of gestation and pups were Caesarean delivered. Their anogenital distance and body weight were recorded, location in utero coded by means of footpad tatooing, and each litter fostered to a maternal female. Measurements were taken again when the animals were weaned. Statistical analysis revealed that the presence of one or more males caudal to a female in the uterine horn has a more critical influence on that female's morphology than contiguity per se. Such a mechanism may result in partial masculinization of dimorphic behaviors later in life.     

XY gonadal dysgenesis with female phenotype (author's transpl)]

In this paper, we are dealing with the study of a case of multiple somatic malformations, with external female genitals and 46 XY caryotype. The anatomical and histological study of the genital organs, allows us to verify the existence of internal genital organs; consisting essentially in tubes, bicornous uterus, a gonadal ligament in a normotopical position, Wolffian remains and the absence of a vagina. The external female genitals are completely normal. When we interpreted these findings, we paid special attention to the relation existing between the abnormal presence of the Wolffian remains, male genotype, and typical female genital structures. Taking account of the latest scientific advances concerning genital development, we considered the possibility of the existence of secretions of a "masculinizing" substance from the gonad, before its morphological differentiation, which was interrupted by an etiological undetermined noxa. When this evolution was arrested, together with the secretions of the masculinizing substance, the genital development continued normally for a female. The terminal teratogenic period for this malformation is situated from the 5th to the 6th week of gestation (human embryos from 11 to 14 mm., Streeter Horizon XVII).     

The logic of Ménage à Trois.

Recent studies of socially monogamous species have shown that in many cases females do not copulate exclusively with their pair mates, but are also receptive to other males. The explanation usually given for unfaithful female behavior is that most females are unable to bond with a male they would prefer as genetic father to their offspring. To secure male assistance the female therefore pairs with an available male but also copulates with males of supposedly higher genetic quality. Here we offer an alternative evolutionary explanation for female infidelity, which does not rely upon this ''Good Genes hypothesis of female choice. We show with a simple model that in an evolutionary game between three players, a male, a female and a male lover, solutions exist in which the female can secure more assistance from her mate by being receptive to other males. We conclude that female sexuality can have a decisive role in regulating social behaviour, in which the fertile female is the driving force.     

Genetic variation in male effects on female reproduction and the genetic covariance between the sexes

Abstract.— Males of many insect species increase the fecundity and/or egg size of their mates through the amount or composition of their nuptial gifts or ejaculate. The genetic bases of such male effects on fecundity or egg size are generally unknown, and thus their ability to evolve remains speculative. Likewise, the genetic relationship between male and female investment into reproduction in dioecious species, which is expected to be positive if effects on fecundity are controlled by at least some of the same genes in males and females, is also unknown. Males of the seed beetle Stator limbatus contribute large ejaculates to females during mating, and the amount of donated ejaculate is positively correlated with male body mass. Females mated to large males lay more eggs in their lifetime than females mated to small males. We describe an experiment in which we quantify genetic variation in the number of eggs sired by males (mated to a single female) and found that a significant proportion of the phenotypic variance in the number of eggs sired by males was explained by their genotype. Additionally, the number of eggs sired by a male was highly positively genetically correlated with his body mass. The between-sex genetic correlation, that is, the genetic correlation between the number of eggs sired by males and the number of eggs laid by females, was highly positive when eggs were laid on Acacia greggii seeds. This indicates that males that sire many eggs have sisters that lay many eggs. Thus, some of the genes that control male ejaculate size (or some other fecundity-enhancing factor) when expressed in males appear to control fecundity when expressed in females. We found no significant interaction between male and female genotype on fecundity.     

Influence of fetal position on neonatal androgen-induced sterility and sexual behavior in female rats

Two aspects of reproductive function were examined in relation to female fetus' contiguity to intrauterine male littermates. Following injection of 3.5 μg testosterone propionate (TP) on Day 3, females that had been positioned in utero between two males became sterile earlier in life than those located in utero between two females. Anogenital distances on Days 1 and 3 prior to neonatal treatment with TP were greater in females located in utero between two males than in females residing between two females in utero, suggesting that females developing between two males may have been exposed prenatally to a masculinizing substance, presumably an androgen. No reliable contribution of litter composition was apparent with respect to differentiation of female sexual behavior. Results indicate that littermate hormonal influence is present or effective and can be detected in a neonatally androgenized preparation.     

Inheritance of gynandromorphism in the parasitic wasp Nasonia vitripennis

The parasitic wasp Nasonia vitripennis has haplo-diploid sex determination. Males develop from unfertilized eggs and are haploid, whereas females develop from fertilized eggs and are diploid. Females and males can be easily distinguished by their morphology. A strain that produces individuals with both male and female features (gynandromorphs) is studied. We provide data on female/male patterning within and between individuals, on environmental effects influencing the occurrence of gynandromorphism, and on its pattern of inheritance. A clear anterior/posterior pattern of feminization is evident in gynandromorphic individuals that developed from unfertilized haploid eggs. The proportion of gynandromorphic individuals can be increased by exposing the mothers to high temperature and also by exposing embryos at early stages of development. Selection for increased gynandromorph frequency was successful. Backcross and introgression experiments showed that a combination of a nuclear and a heritable cytoplasmic component causes gynandromorphism. Analyses of reciprocal F(2) and F(3) progeny indicate a maternal effect locus (gyn1) that maps to chromosome IV. Coupled with previous studies, our results are consistent with a N. vitripennis sex determination involving a maternal/zygotic balance system and/or maternal imprinting. Genetics and temperature effects suggest a temperature-sensitive mutation of a maternally produced masculinizing product that acts during a critical period in early embryogenesis.     

A re-examination of the lordosis response in female rats given high doses of testosterone propionate or estradiol benzoate in the neonatal period

High lordosis quotients (LQ) were observed when female Wistar rats injected with 1.25 mgm of testosterone propionate (TP) on Day 4 of postnatal life were tested as intact adults. The high LQ was not due to testing during the lights-on period, the age at which the females were tested, the use of a strain that was insensitive to the masculinizing action of TP or estradiol benzoate (EB), the age at which the females were injected with TP or EB, or an abnormal response to estrogen. High LQ values were found in similar tests on adult female rats of two other strains injected with 1.25 mgm TP on Day 4 of life. A marked reduction of the facilitatory action of progesterone on receptivity in estrogen-primed animals was demonstrated in the females of all three strains treated with TP or EB during the neonatal period and for males after castration as adults.Analysis of the experimental records of the mating tests showed that females anovulatory following TP or EB administration during the neonatal period and tested either intact and under the influence of endogenous hormones or under the influence of exogenous estrogen showed a rapid and highly significant increase in receptivity during the course of prolonged (20 min) tests with two or three active stimulus males. This effect was very much reduced if the treated females were under the influence of exogenous estrogen plus progesterone. The effect was not seen in males castrated as adults and treated with estrogen, or in females not treated with steroids in the neonatal period and tested intact at proestrus alone or under the influence of exogenous steroids after ovariectomy. A significant increase in LQ during the test period was observed in females of the Wistar strain which were anovulatory as a result of exposure to constant light and were tested intact without any exogenous hormone being administered.It is suggested that although tests involving a limited number of mounts or attempts to mount at low rates over a short period of time may be adequate to determine the degree of receptivity of normal female rats they are not adequate to establish the capacity of female rats treated with steroid hormones during the neonatal period to display the lordosis response.