scholarly journals Masculinised Behaviour of XY Females in a Mammal with Naturally Occurring Sex Reversal

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Paul A. Saunders ◽  
Thomas Franco ◽  
Camille Sottas ◽  
Tangui Maurice ◽  
Guila Ganem ◽  
...  

Abstract Most sex differences in phenotype are controlled by gonadal hormones, but recent work on laboratory strain mice that present discordant chromosomal and gonadal sex showed that sex chromosome complement can have a direct influence on the establishment of sex-specific behaviours, independently from gonads. In this study, we analyse the behaviour of a rodent with naturally occurring sex reversal: the African pygmy mouse Mus minutoides, in which all males are XY, while females are of three types: XX, XX* or X*Y (the asterisk represents an unknown X-linked mutation preventing masculinisation of X*Y embryos). X*Y females show typical female anatomy and, interestingly, have greater breeding performances. We investigate the link between sex chromosome complement, behaviour and reproductive success in females by analysing several behavioural features that could potentially influence their fitness: female attractiveness, aggressiveness and anxiety. Despite sex chromosome complement was not found to impact male mate preferences, it does influence some aspects of both aggressiveness and anxiety: X*Y females are more aggressive than the XX and XX*, and show lower anxiogenic response to novelty, like males. We discuss how these behavioural differences might impact the breeding performances of females, and how the sex chromosome complement could shape the differences observed.

Endocrinology ◽  
2013 ◽  
Vol 154 (3) ◽  
pp. 1092-1104 ◽  
Author(s):  
Xuqi Chen ◽  
Rebecca McClusky ◽  
Yuichiro Itoh ◽  
Karen Reue ◽  
Arthur P. Arnold

Abstract Three different models of MF1 strain mice were studied to measure the effects of gonadal secretions and sex chromosome type and number on body weight and composition, and on related metabolic variables such as glucose homeostasis, feeding, and activity. The 3 genetic models varied sex chromosome complement in different ways, as follows: 1) “four core genotypes” mice, comprising XX and XY gonadal males, and XX and XY gonadal females; 2) the XY* model comprising groups similar to XO, XX, XY, and XXY; and 3) a novel model comprising 6 groups having XO, XX, and XY chromosomes with either testes or ovaries. In gonadally intact mice, gonadal males were heavier than gonadal females, but sex chromosome complement also influenced weight. The male/female difference was abolished by adult gonadectomy, after which mice with 2 sex chromosomes (XX or XY) had greater body weight and percentage of body fat than mice with 1 X chromosome. A second sex chromosome of either type, X or Y, had similar effects, indicating that the 2 sex chromosomes each possess factors that influence body weight and composition in the MF1 genetic background. Sex chromosome complement also influenced metabolic variables such as food intake and glucose tolerance. The results reveal a role for the Y chromosome in metabolism independent of testes and gonadal hormones and point to a small number of X–Y gene pairs with similar coding sequences as candidates for causing these effects.


2014 ◽  
Vol 35 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Bharti Manwani ◽  
Kathryn Bentivegna ◽  
Sharon E Benashski ◽  
Venugopal Reddy Venna ◽  
Yan Xu ◽  
...  

Epidemiologic studies have shown sex differences in ischemic stroke. The four core genotype (FCG) mouse model, in which the testes determining gene, Sry, has been moved from Y chromosome to an autosome, was used to dissociate the effects of sex hormones from sex chromosome in ischemic stroke outcome. Middle cerebral artery occlusion (MCAO) in gonad intact FCG mice revealed that gonadal males (XXM and XYM) had significantly higher infarct volumes as compared with gonadal females (XXF and XYF). Serum testosterone levels were equivalent in adult XXM and XYM, as was serum estrogen in XXF and XYF mice. To remove the effects of gonadal hormones, gonadectomized FCG mice were subjected to MCAO. Gonadectomy significantly increased infarct volumes in females, while no change was seen in gonadectomized males, indicating that estrogen loss increases ischemic sensitivity. Estradiol supplementation in gonadectomized FCG mice rescued this phenotype. Interestingly, FCG male mice were less sensitive to effects of hormones. This may be due to enhanced expression of the transgene Sry in brains of FCG male mice. Sex differences in ischemic stroke sensitivity appear to be shaped by organizational and activational effects of sex hormones, rather than sex chromosomal complement.


2021 ◽  
Author(s):  
Elizabeth A. Sneddon ◽  
Lindsay N. Rasizer ◽  
Natalie G. Cavalco ◽  
Asa H. Jaymes ◽  
Noah J. Ostlie ◽  
...  

AbstractAlcohol use and high-risk alcohol drinking behaviors among women are rapidly rising. In rodent models, females typically consume more ethanol (EtOH) than males. Here, we used the Four Core Genotypes (FCG) mouse model to investigate the influence of gonadal hormones and sex chromosome complement to EtOH drinking behaviors. FCG mice were given access to escalating concentrations of EtOH in a two-bottle, 24-h continuous access drinking paradigm to assess consumption and preference. Relapse-like behavior was measured by assessing escalated intake following repeated cycles of deprivation and re-exposure. Twenty-four hour EtOH consumption was greater in mice with ovaries (Sry−), relative to those with testes, and in mice with the XX chromosome complement, relative to those with XY sex chromosomes. EtOH preference was higher in XX vs. XY mice but not influenced by gonad type. Escalated intake following repeated cycles of deprivation and re-exposure emerged only in XX mice (vs. XY). These results demonstrate that aspects of EtOH drinking behavior may be independently regulated by sex hormones and chromosomes and inform our understanding of the neurobiological mechanisms which contribute to EtOH dependence in male and female mice. Future investigation of the contribution of sex chromosomes to EtOH drinking behaviors is warranted.


2017 ◽  
Vol 31 (4) ◽  
pp. 300-306 ◽  
Author(s):  
Maria Julia Cambiasso ◽  
Carla Daniela Cisternas ◽  
Isabel Ruiz-Palmero ◽  
Maria Julia Scerbo ◽  
Maria Angeles Arevalo ◽  
...  

Author(s):  
Ana Gil-Fernández ◽  
Paul A. Saunders ◽  
Marta Martín-Ruiz ◽  
Marta Ribagorda ◽  
Pablo López-Jiménez ◽  
...  

ABSTRACTSex chromosomes of eutherian mammals are highly different in size and gene content, and share only a small region of homology (pseudoautosomal region, PAR). They are thought to have evolved through an addition-attrition cycle involving the addition of autosomal segments to sex chromosomes and their subsequent differentiation. The events that drive this process are difficult to investigate because sex chromosomes in most mammals are at a very advanced stage of differentiation. Here, we have taken advantage of a recent translocation of an autosome to both sex chromosomes in the African pygmy mouse Mus minutoides, which has restored a large segment of homology (neo-PAR). By studying meiotic sex chromosome behavior and identifying fully sex-linked genetic markers in the neo-PAR, we demonstrate that this region shows unequivocal signs of early sex-differentiation. First, synapsis and resolution of DNA damage intermediates are delayed in the neo-PAR during meiosis. Second, recombination is suppressed in a large portion of the neo-PAR. However, the inactivation process that characterizes sex chromosomes during meiosis does not extend to this region. Finally, the sex chromosomes show a dual mechanism of association at metaphase-I that involves the formation of a chiasma in the neo-PAR and the preservation of an ancestral achiasmate mode of association in the non-homologous segments. We show that the study of meiosis is crucial to apprehend the onset of sex chromosome differentiation, as it introduces structural and functional constrains to sex chromosome evolution. Synapsis and DNA repair dynamics are the first processes affected in the incipient differentiation of X and Y chromosomes, and they may be involved in accelerating their evolution. This provides one of the very first reports of early steps in neo-sex chromosome differentiation in mammals, and for the first time a cellular framework for the addition-attrition model of sex chromosome evolution.AUTHOR SUMMARYThe early steps in the evolution of sex chromosomes are particularly difficult to study. Cessation of recombination around the sex-determining locus is thought to initiate the differentiation of sex chromosomes. Several studies have investigated this process from a genetic point of view. However, the cellular context in which recombination arrest occurs has not been considered as an important factor. In this report, we show that meiosis, the cellular division in which pairing and recombination between chromosomes takes place, can affect the incipient differentiation of X and Y chromosomes. Combining cytogenetic and genomic approaches, we found that in the African pygmy mouse Mus minutoides, which has recently undergone a sex chromosome-autosome fusion, synapsis and DNA repair dynamics are altered along the newly added region of the sex chromosomes, likely interfering with recombination and thus contributing to the genetic isolation of a large segment of the Y chromosome. Therefore, the cellular events that occur during meiosis are crucial to understand the very early stages of sex chromosome differentiation. This can help to explain why sex chromosomes evolve very fast in some organisms while in others they have barely changed for million years.


Endocrinology ◽  
2020 ◽  
Vol 161 (9) ◽  
Author(s):  
Samuel J Harp ◽  
Mariangela Martini ◽  
Wendy J Lynch ◽  
Emilie F Rissman

Abstract The organizational/activational hypothesis suggests that gonadal steroid hormones like testosterone (T) and estradiol (E2) are important at 2 different times during the lifespan when they perform 2 different functions. First steroids “organize” brain structures early in life and during puberty, and in adults these same hormones “activate” sexually dimorphic behaviors. This hypothesis has been tested and proven valid for a large number of behaviors (learning, memory, social, and sexual behaviors). Sex differences in drug addiction are well established both for humans and animal models. Previous research in this field has focused primarily on cocaine self-administration by rats. Traditionally, observed sex differences have been explained by the sex-specific concentrations of gonadal hormones present at the time of the drug-related behavior. Studies with gonadectomized rodents establishes an activational role for E2 that facilitates vulnerability in females, and when E2 is combined with progesterone, addiction is attenuated. Literature on organizational actions of steroids is sparse but predicts that T, after it is aromatized to E2, changes aspects of the neural reward system. Here we summarize these data and propose that sex chromosome complement also plays a role in determining sex-specific drug-taking behavior. Future research is needed to disentangle the effects of hormones and sex chromosome complement, and we propose the four core genotype mouse model as an effective tool for answering these questions.


2009 ◽  
Vol 277 (1684) ◽  
pp. 1049-1056 ◽  
Author(s):  
Frederic Veyrunes ◽  
Pascale Chevret ◽  
Josette Catalan ◽  
Riccardo Castiglia ◽  
Johan Watson ◽  
...  

Therian mammals have an extremely conserved XX/XY sex determination system. A limited number of mammal species have, however, evolved to escape convention and present aberrant sex chromosome complements. In this study, we identified a new case of atypical sex determination in the African pygmy mouse Mus minutoides , a close evolutionary relative of the house mouse. The pygmy mouse is characterized by a very high proportion of XY females (74%, n = 27) from geographically widespread Southern and Eastern African populations. Sequencing of the high mobility group domain of the mammalian sex determining gene Sry , and karyological analyses using fluorescence in situ hybridization and G-banding data, suggest that the sex reversal is most probably not owing to a mutation of Sry , but rather to a chromosomal rearrangement on the X chromosome. In effect, two morphologically different X chromosomes were identified, one of which, designated X*, is invariably associated with sex-reversed females. The asterisk designates the still unknown mutation converting X*Y individuals into females. Although relatively still unexplored, such an atypical sex chromosome system offers a unique opportunity to unravel new genetic interactions involved in the initiation of sex determination in mammals.


Sign in / Sign up

Export Citation Format

Share Document