دوز کروموزوم X رفتار جنسی مرد را تحت تاثیر قرار می دهد
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|35904||2012||8 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Hormones and Behavior, Volume 61, Issue 4, April 2012, Pages 565–572
Sex differences in the brain and behavior are primarily attributed to dichotomous androgen exposure between males and females during neonatal development, as well as adult responses to gonadal hormones. Here we tested an alternative hypothesis and asked if sex chromosome complement influences male copulatory behavior, a standard behavior for studies of sexual differentiation. We used two mouse models with non-canonical associations between chromosomal and gonadal sex. In both models, we found evidence for sex chromosome complement as an important factor regulating sex differences in the expression of masculine sexual behavior. Counter intuitively, males with two X-chromosomes were faster to ejaculate and display more ejaculations than males with a single X. Moreover, mice of both sexes with two X-chromosomes displayed increased frequencies of mounts and thrusts. We speculate that expression levels of a yet to be discovered gene(s) on the X-chromosome may affect sexual behavior in mice and perhaps in other mammals.
The original studies on mammalian sexual differentiation of behavior identified androgen, produced in the developing testes, as the critical factor responsible for differences between adult male and female behavior (Phoenix et al., 1959). Testosterone, acting both directly, and after aromatization to estradiol, binds to its receptors in the brain and modifies neural circuits. In adults, these modifications lead to increased expression of behaviors more typical of males, and decreased display of behaviors more often shown by females. However, in addition to androgen differences, there are genetic differences between males and females caused by unequal dosage of sex chromosome genes. In mammals, and many other species, sex is determined by genetic inheritance of sex chromosomes. Normal female mammals (XX) have two X-chromosomes while males (XY) have a single X- and a Y-chromosome. The X-chromosome encodes hundreds of genes with no direct paralogs on Y, whereas the Y-chromosome encodes many fewer genes, including the testis-determining factor Sry ( Ellegren, 2011 and Koopman et al., 1991). In addition to Sry, genetic differences between XX and XY individuals are now recognized as a source of variation that shapes sex differences in brain and behaviors ( Arnold, 2009). Over the last decade, several mutant mice with atypical sex chromosome arrangements have been developed and used to test the effects of sex chromosome complement on sexual differentiation (Arnold, 2009). Here we employ the Four Core Genotypes (FCG) and Y* models, which are described in Table 1. In FCG mice, males and females can have either XX or XY sex chromosomes (De Vries et al., 2002). Sry (testis determining gene) is deleted on the FCG Y-chromosome and a transgenic copy of Sry is located on an autosome, thereby unlinking differentiation of the gonads from the sex chromosomes. Autosomal inheritance of the Sry transgene causes testes development in both XX and XY mice (gonadal males), and ovaries develop in mice without the autosomal transgene (gonadal females). Since same gonadal sex FCG mice differ by XX and XY genotypes, sex chromosome effects revealed by the FCG can be attributed to one of three major mechanisms: genes on Y, genes that escape X-inactivation, and paternally imprinted X-genes. Table 1. Genotype and sex chromosome complement of FCG and Y* mice. The gonadal sex and dose of sex chromosomes are shown among genotypes of the Four Core Genotypes (FCG) and Y* models. In the genotypes column, the first X represents the maternally inherited sex chromosome, and the second sex chromosome is paternally inherited. Y−, Sry deleted Y-chromosome. Sry, sex-determining region of Y (FCG Sry is a transgene within an autosome). Copies of X, dose of X-chromosome specific genes. Copies of Y, dose of Y-chromosome specific genes. Composition of sex chromosome regions Genotype Gonads Sry Copies of Y Copies of X FCG XYM XY−Sry Testes 1 1 1 XXM XXSry Testes 1 0 2 XYF XY− Ovaries 0 1 1 XXF XX Ovaries 0 0 2 Y* 1XM XY* Testes 1 1 1 2XM XXY⁎ Testes 1 1 2 1XF XY⁎x Ovaries 0 0 1 2XF XX Ovaries 0 0 2 Table options The Y* model is used to determine whether sex chromosome effects present in the FCG are due to dose of X- or Y-chromosome genes. The Y*-chromosome was generated by a spontaneous translocation and inverted duplication of the pseudoautosomal region (PAR) of Y (Eicher et al., 1991). During meiosis, the altered PAR of Y* recombines aberrantly with the X-chromosome and generates male gametes with four sex chromosomes: non-recombined X and Y*, and recombined Y*X (PAR without unique X and Y genes) and XY⁎ (an X attached to Y chromosome). Gonadal male and female Y* mice can have one or two copies of the X-chromosome, whereas only males have a Y-chromosome. Therefore, while FCG XX and XY genotypes differ in both dose of X and presence of Y, Y* mice of the same gonadal sex only differ in dose of X (Table 1). If dosage of X-chromosome genes is important for the observed differences in FCG, we expect to see the same, or perhaps more pronounced, sex chromosome effects in Y* mice. Using these mouse models, herein we examined the sex chromosome hypothesis by studying two highly sexually dimorphic behaviors: masculine sexual behavior and aggression (Bonthuis et al., 2010). We found a strong effect of X-chromosome number on several aspects of masculine sexual behavior; counter intuitively individuals with two X-chromosomes displayed more behavior than mice with one X-chromosome. The X-chromosome effect did not generalize to sexually dimorphic resident–intruder aggression, or dimorphic vasopressin (AVP) density in the lateral septum of Y* mice. Our data indicate that two X-chromosomes increase male sexual behavior in mice, but the Y-chromosome may increase aggression and AVP immunoreactivity in the lateral septum.