Sexual Dimorphism In Mammals Research Articles

The Contribution of Y Chromosome Genes to Spontaneous Differentiation of Human Embryonic Stem Cells into Embryoid Bodies In Vitro.

Objective Sexual dimorphism in mammals can be described as subsequent transcriptional differences from their distinct sex chromosome complements. Following X inactivation in females, the Y chromosome is the major genetic difference between sexes. In this study, we used a male embryonic stem cell line (Royan H6) to identify the potential role of the male-specific region of the Y chromosome (MSY) during spontaneous differentiation into embryoid bodies (EBs) as a model of early embryonic development. Materials and Methods In this experimental study, RH6 cells were cultured on inactivated feeder layers and Matrigel. In a dynamic suspension system, aggregates were generated in the same size and were spontaneously differentiated into EBs. During differentiation, expression patterns of specific markers for three germ layers were compared with MSY genes. Results Spontaneous differentiation was determined by downregulation of pluripotent markers and upregulation of fourteen differentiation markers. Upregulation of the ectoderm markers was observed on days 4 and 16, whereas mesoderm markers were upregulated on the 8th day and endodermic markers on days 12-16. Mesoderm markers correlated with 8 MSY genes namely DDX3Y, RPS4Y1, KDM5D, TBL1Y, BCORP1, PRY, DAZ, and AMELY, which were classified as a mesoderm cluster. Endoderm markers were co-expressed with 7 MSY genes, i.e. ZFY, TSPY, PRORY, VCY, EIF1AY, USP9Y, and RPKY, which were grouped as an endoderm cluster. Finally, the ectoderm markers correlated with TXLNGY, NLGN4Y, PCDH11Y, TMSB4Y, UTY, RBMY1, and HSFY genes of the MSY, which were categorized as an ectoderm cluster. In contrast, 2 MSY genes, SRY and TGIF2LY, were more highly expressed in RH6 cells compared to EBs. ConclusionWe found a significant correlation between spontaneous differentiation and upregulation of specific MSY genes. The expression alterations of MSY genes implied the potential responsibility of their gene co-expression clusters for EB differentiation. We suggest that these genes may play important roles in early embryonic development.

Sex Chromosomes and Sex Phenotype Contribute to Biased DNA Methylation in Mouse Liver.

Sex biases in the genome-wide distribution of DNA methylation and gene expression levels are some of the manifestations of sexual dimorphism in mammals. To advance our understanding of the mechanisms that contribute to sex biases in DNA methylation and gene expression, we conducted whole genome bisulfite sequencing (WGBS) as well as RNA-seq on liver samples from mice with different combinations of sex phenotype and sex-chromosome complement. We compared groups of animals with different sex phenotypes, but the same genetic sexes, and vice versa, same sex phenotypes, but different sex-chromosome complements. We also compared sex-biased DNA methylation in mouse and human livers. Our data show that sex phenotype, X-chromosome dosage, and the presence of Y chromosome shape the differences in DNA methylation between males and females. We also demonstrate that sex bias in autosomal methylation is associated with sex bias in gene expression, whereas X-chromosome dosage-dependent methylation differences are not, as expected for a dosage-compensation mechanism. Furthermore, we find partial conservation between the repertoires of mouse and human genes that are associated with sex-biased methylation, an indication that gene function is likely to be an important factor in this phenomenon.

Sexual size dimorphism and sexual selection in primates

Abstract In most animals, females are larger than males. Paradoxically, sexual size dimorphism is biased towards males in most mammalian species. An accepted explanation is that sexual dimorphism in mammals evolved by intramale sexual selection. I tested this hypothesis in primates, by relating sexual size dimorphism to seven proxies of sexual selection intensity: operational sex ratio, mating system, intermale competition, group sex ratio, group size, maximum mating percentage (percentage of observed copulations involving the most successful male), and total paternity (a genetic estimate of the percentage of young sired by the most successful male). I fitted phylogenetic generalised least squares models using sexual size dimorphism as the dependent variable and each of the seven measures of intensity of sexual selection as independent variables. I conducted this comparative analysis with data from 50 extant species of primates, including Homo sapiens, Pan troglodytes, and Gorilla spp. Sexual dimorphism was positively related to the four measures of female monopolisation (operational sex ratio, mating system, intermale competition, and group sex ratio) and in some cases to group size, but was not associated with maximum mating percentage or total paternity. Additional regression analyses indicated that maximum mating percentage and total paternity were negatively associated with group size. These results are predicted by reproductive skew theory: in large groups, males can lose control of the sexual behaviour of the other members of the group or can concede reproductive opportunities to others. The results are also consistent with the evolution of sexual size dimorphism before polygyny, due to the effects of natural, rather than sexual, selection. In birds, the study of molecular paternity showed that variance in male reproductive success is much higher than expected by behaviour. In mammals, recent studies have begun to show the opposite trend, i.e. that intensity of sexual selection is lower than expected by polygyny. Results of this comparative analysis of sexual size dimorphism and sexual selection intensity in primates suggest that the use of intramale sexual selection theory to explain the evolution of polygyny and sexual dimorphism in mammals should be reviewed, and that natural selection should be considered alongside sexual selection as an evolutionary driver of sexual size dimorphism and polygyny in mammals.

FGF-21 ameliorates essential hypertension of SHR via baroreflex afferent function

Hypertension is a common complication of metabolic abnormalities associated with cardiovascular system and characterized by sexual dimorphism in mammals. Fibroblast growth factor-21 (FGF-21) plays a critical role in metabolic-disorder related hypertension through the afferent loop of baroreflex. However, the gender difference in FGF-21-mediated blood pressure (BP) regulation via sexual dimorphic expression of FGFRs in the nodose (NG) and nucleus tractus solitarius (NTS) were not elucidated in physiological and genomic form of hypertension. The gene and protein expression of FGFRs were tested by qRT-PCR, immunoblotting and immunostaining; the serum level of FGF21 was tested using ELISA; The BP was monitored while FGF21 was nodose microinjected. The results showed that more potent BP reduction was confirmed in female vs. male rats by nodose microinjection of rhFGF-21 along with higher expression of FGFR2 and FGFR4 in the nodose compared with age-match male and ovariectomized (OVX) rats, rather than other receptor subtypes, which is consistent well with immunohistochemical analysis. Additionally, serum FGF-21 was significantly higher in female-WKY, and this level of FGF-21 was dramatically declined in spontaneous hypertensive rats (SHR) with significant down-regulation of FGFR1/R4 for male-SHR and FGFR2/FGFR4 for female-SHR, respectively. Apparently, high BP of SHR of either sex could be reduced by rhFGF-21 nodose microinjection. These data extends our current understanding that sexual-specific distribution/expression of FGF-21/FGFRs is likely to contribute at least partially to sexual dimorphism of baroreflex afferent function on BP regulation in rats. FGF-21-mdiated BP reduction sheds new light on clinical management of primary/genomic form of hypertension.

The role of sex steroids in white adipose tissue adipocyte function.

With the increasing knowledge that gender influences normal physiology, much biomedical research has begun to focus on the differential effects of sex on tissue function. Sexual dimorphism in mammals is due to the combined effects of both genetic and hormonal factors. Hormonal factors are mutable particularly in females in whom the estrous cycle dominates the hormonal milieu. Given the severity of the obesity epidemic and the fact that there are differences in the obesity rates in men and women, the role of sex in white adipose tissue function is being recognized as increasingly important. Although sex differences in white adipose tissue distribution are well established, the mechanisms affecting differential function of adipocytes within white adipose tissue in males and females remain largely understudied and poorly understood. One of the largest differences in the endocrine environment in males and females is the concentration of circulating androgens and estrogens. This review examines the effects of androgens and estrogens on lipolysis/lipogenesis, adipocyte differentiation, insulin sensitivity and adipokine production in adipocytes from white adipose tissue with a specific emphasis on the sexual dimorphism of adipocyte function in white adipose tissue during both health and disease.

The Human Placental Sexome Differs between Trophoblast Epithelium and Villous Vessel Endothelium

Molecular mechanisms underlying sexual dimorphism in mammals, fetal sex influences on intrauterine development, and the sex-biased susceptibility for selected diseases in adulthood are novel areas of current research. As importantly, two decades of multifaceted research has established that susceptibility to many adult disorders originates in utero, commonly secondary to the effects of placental dysfunction. We hypothesized that fetal sex influences gene expression and produces functional differences in human placentas. We thus extended previous studies on sexual dimorphism in mammals, which used RNA isolated from whole tissues, to investigate the effects of sex on four cell-phenotypes within a single key tissue, human placental villi. The cells studied included cytotrophoblasts, syncytiotrophoblast, arterial and venous endothelial cells. The cells were isolated from placentas of male or female fetuses and subjected to microarray analysis. We found that fetal sex differentially affected gene expression in a cell-phenotype dependent manner among all four cell-phenotypes. The markedly enriched pathways in males were identified to be signaling pathways for graft-versus-host disease as well as the immune and inflammatory systems that parallel the reported poorer outcome of male fetuses. Our study is the first to compare global gene expression by microarray analysis in purified, characterized, somatic cells from a single human tissue, i.e. placental villi. Importantly, our findings demonstrate that there are cell-phenotype specific, and tissue-specific, sex-biased responses in the human placenta, suggesting fetal sex should be considered as an independent variable in gene expression analysis of human placental villi.

Sexual dimorphism and ontogenetic allometry of soft tissues in Rattus norvegicus.

Most studies of sexual dimorphism in mammals focus on overall body size. However, relatively little is known about the differences in growth trajectories that produce dimorphism in organ and muscle size. We weighed six organs and four muscles in Rattus norvegicus to determine what heterochronic and allometric scaling differences exist between the sexes. This cross-sectional growth study included 113 males and 109 females with ages ranging from birth to 200 days of age. All muscle and organ weights were ultimately greater in males than in females, because males grew for a longer period of time, had a greater maximum rate of growth, and spent more time near the maximum rate. No ontogenetic scaling differences existed between the sexes in organ weight except for lungs and gonads. During growth, organ weights were negatively allometric to body weight. No scaling differences relative to body weight existed between the sexes for muscles; however, there was variation in the allometric relations among muscles relative to body weight. Sexual dimorphism in muscles and organs appears to be a size difference resulting from differences in the duration and rates of growth.

Sexual dimorphism and ontogenetic allometry of soft tissues in Rattus norvegicus

Most studies of sexual dimorphism in mammals focus on overall body size. However, relatively little is known about the differences in growth trajectories that produce dimorphism in organ and muscle size. We weighed six organs and four muscles in Rattus norvegicus to determine what heterochronic and allometric scaling differences exist between the sexes. This cross-sectional growth study included 113 males and 109 females with ages ranging from birth to 200 days of age. All muscle and organ weights were ultimately greater in males than in females, because males grew for a longer period of time, had a greater maximum rate of growth, and spent more time near the maximum rate. No ontogenetic scaling differences existed between the sexes in organ weight except for lungs and gonads. During growth, organ weights were negatively allometric to body weight. No scaling differences relative to body weight existed between the sexes for muscles; however, there was variation in the allometric relations among muscles relative to body weight. Sexual dimorphism in muscles and organs appears to be a size difference resulting from differences in the duration and rates of growth. J. Morphol. 242:57–66, 1999. © 1999 Wiley-Liss, Inc.

Regulation of sexual dimorphism in mammals.

Sexual dimorphism in humans has been the subject of wonder for centuries. In 355 BC, Aristotle postulated that sexual dimorphism arose from differences in the heat of semen at the time of copulation. In his scheme, hot semen generated males, whereas cold semen made females (Jacquart, D., and C. Thomasset. Sexuality and Medicine in the Middle Ages, 1988). In medieval times, there was great controversy about the existence of a female pope, who may have in fact had an intersex phenotype (New, M. I., and E. S. Kitzinger. J. Clin. Endocrinol. Metab. 76: 3-13, 1993.). Recent years have seen a resurgence of interest in mechanisms controlling sexual differentiation in mammals. Sex differentiation relies on establishment of chromosomal sex at fertilization, followed by the differentiation of gonads, and ultimately the establishment of phenotypic sex in its final form at puberty. Each event in sex determination depends on the preceding event, and normally, chromosomal, gonadal, and somatic sex all agree. There are, however, instances where chromosomal, gonadal, or somatic sex do not agree, and sexual differentiation is ambiguous, with male and female characteristics combined in a single individual. In humans, well-characterized patients are 46, XY women who have the syndrome of pure gonadal dysgenesis, and a subset of true hermaphrodites are phenotypic men with a 46, XX karyotype. Analysis of such individuals has permitted identification of some of the molecules involved in sex determination, including SRY (sex-determining region Y gene), which is a Y chromosomal gene fulfilling the genetic and conceptual requirements of a testis-determining factor. The purpose of this review is to summarize the molecular basis for syndromes of sexual ambiguity seen in human patients and to identify areas where further research is needed. Understanding how sex-specific gene activity is orchestrated may provide insight into the molecular basis of other cell fate decisions during development which, in turn, may lead to an understanding of aberrant cell fate decisions made in patients with birth defects and during neoplastic change.

SEX CHROMOSOMES AND THE EVOLUTION OF SEXUAL DIMORPHISM.

The evolutionary significance of sex chromosomes has generally been associated with their effect on sex determination (see Mittwoch, 1967; Ohno 1967, 1979 for review). Here I will evaluate the idea that sex chromosomes also play an important role in the evolution of sexually dimorphic traits. As a premise I will assume that sexual dimorphism results from natural selection that favors different phenotypic characteristics in the two sexes. For example, in bighorn sheep (Ovis canadensis) horn size and shape are sexually dimorphic. The massive recurved horns of males are presumably an adaptive compromise between the need to blunt head-to-head collisions between fighting males and to act as weapons against predators. The smaller dagger-like horns of females are favored in this' sex since their sole function is defense against predators (Geist, 1971). Many less obvious characteristics are also likely to differ in their selective value between the sexes. In an extensive review of sexual dimorphism in mammals, Glucksmann (1981) suggested that traits such as growth rate, thermoregulation, metabolic rate, biorhythms, sensory modality, and a wide variety of other traits differ between the sexes in their optimal value. Characteristics that are selectively favored in one sex but selected against in the other will be referred to as traits. Consider the evolution of a sexually dimorphic trait from a monomorphic state. For example, Geist (1971) used paleontological evidence and taxonomy to argue that the sexually dimorphic horns of bighorn sheep evolved from a sexually monomorphic ancestor. Because an exact record of this evolutionary change is unavailable, I will arbitrarily assume for the purpose of illustration that the size of female horns remained unchanged while the size of male horns increased. The evolution of sexual dimorphism in horn size could have proceeded in at least two ways: 1) The increase in frequency of genes that enhanced horn size in males but not in females, and 2) The increase in frequency of genes that enhanced horn size in both sexes followed by the evolution of modifier genes that restricted the expression of increased horn size to males. The first way will be referred to as the pleiotropy-mechanism. It requires genetic variability that simultaneously produces the sexually-antagonistic trait (increased horn size) and is sex-limited in its expression. The second way will be referred to as the modifermechanism. It requires genetic variability for both the sexually-antagonistic trait (increased horn size) and sex-limited expression of this trait. A similar classification was previously proposed by Turner (1978) for the evolution of sexlimited traits in butterflies. Most mutations that have been studied carefully in the laboratory have not been found to be completely sex-limited in their expression. Thus it seems reasonable to assume that most of the genetic variability available for the evolution of sexual dimorphism would be initially expressed in both sexes. This assumption may be unreasonable when considering the enhancement of an established sexually dimorphic trait since developmental canalization (Waddington, 1962) may facilitate sex-limited gene expression. However, during the initial evolution of sexual dimorphism from a monomorphic state, a feasible sequence of events would be the modifier-mechanism described above. In the following model I will suggest how the sex chromosomes can facilitate

Sexual dimorphism in two subspecies of Ethiopian Baboons (Papio Hamadryas) and their hybrids.

Sexual dimorphism in mammals has been related to such variables as absolute body size, ecology, and various aspects of social behavior. Attempts to relate dimorphism to any of these variables have necessarily used small heterogeneous samples to represent the relevant species. We are concerned by the inevitable exclusion of any measure of variability in dimorphism and the consequent impossibility of assessing the significance of observed interspecific differences. In this paper we describe aspects of sexual dimorphism in anubis, hamadryas, and hybrid baboons from Ethiopia. Samples are large enough to permit a measure of intrapopulational variability. Hamadryas baboons are more dimorphic than anubis in epigamic features, but not in postcanine dentition, nor, contrary to previous reports, in body weight or canine tooth size. Hybrid males are more hamadryas-like and hybrid females more anubis-like, as would be predicted by the proposed mechanism for the establishment of the hybrid zone, namely the capture of anubis females by hamadryas males.

Book Reviews

Book reviewed in this article: ECOLOGY AND MANAGEMENT OF EUROPEAN HARE POPULATIONS Edited by Zygmund Pielowski & Zdzislaw Pucek. Polish Hunting Association, Warsaw, 1976. THE BIOLOGY OF MARSUPIALS Edited by Bernard Stonehouse & Desmond Gilmore AFRICAN UNGULATES: a comparative review of their ethology and behavioural ecology By Walter Leuthold. ECOLOGY OF RED DEER By Brian Mitchell, Brian W. Staines & David Welch. Institute of Terrestrial Ecology THE NATURAL HISTORY OF THE WHALE by L. Harrison Matthews. THE MAMMALS OF THE PALEARCTIC REGION: a taxonomic review by G. B. Corbet. British Museum DEVELOPMENT IN MAMMALS Volume 3. Edited by Martin H. Johnson. RECENT ADVANCES IN PRIMATOLOGY edited by D. J. Chivers and others Volume 1 ‐Behaviour; edited by D. J. Chivers & J. Herbert: Pp 980, 19.20. Volume 2 ‐Conservation; edited by D. J. Chivers Volume 3 ‐ Evolution; edited by D. J. Olivers & K. A. Joysey SEX DETERMINATION AND SEXUAL DIMORPHISM IN MAMMALS by Alfred Glucksmann HANDBUCH DER SAUGETIERE EUROPAS. Band 1: Nagetiere 1. Edited by Jochen Niethammer and Franz Krapp. MAMMALS ‐ THEIR LATIN NAMES EXPLAINED by A. F. Gotch. EVOLUTIONARY PRINCIPLES OF THE MAMMALIAN MIDDLE EAR By Gerald Fleischer. Springer‐Verlag

Sexual Dimorphism in Mammals: Avian Models and Unanswered Questions

Current models for the evolution of polygyny and sexual dimorphism are largely derived from data on passerine birds. These models are less appropriate for taxa such as mammals, in which males emphasize mating strategies, than for those such as passerines, in which males emphasize progeny rearing strategies. The Orians-Verner model is inadequate as a general explanation of the evolution of polygyny in mammals because many species do not meet one or more of its assumptions: that the need for male parental care is the main factor opposing the evolution of polygyny; that females choose to mate with particular males; and that the female raises her young on the resources contained in the territory of the male with which she mates. A two-factor model incorporating the concept of sexual bimaturism, developed by Wiley for grouse, is more appropriate for many mammals but still too simple. In mammals, large male parental investment is a good predictor of both monogamy and reduced sexual dimorphism, but small male in...