I. INTRODUCTION
Human males and females behave and react to various situations differently, which has been thought to be caused by differences in hormones secreted by the gonads of each gender. In mammals, the male’s testes secrete testosterone from the Leydig cells, which acts on the brain to cause masculine patterns of development and to differentiate the brain from that of the female. The effectiveness of these effects could give the impression that all meaningful sex differences in the brain and in brain diseases are induced by gonadal secretions (Arnold 2004).
At the gross level, the brain is highly dimorphic between the sexes in terms of size and structure. The average male brain weighs about 11% more, as this difference remains significant when controlling for males’ overall greater physical size. The female brain, however, is simply not a downsized version of the male brain; the volumes of specific regions, relative to the cerebrum are known to differ between males and females. For instance, the volumes of the frontal and medial paralimbic cortices are larger in women; the fronto-medial cortex, amygdale and hypothalamus, on the other hand, are larger in men. These differences in sizes can be substantial (Craig et al 2004).
Taken altogether, the evidence suggests that men’s and women’s brain development follows significantly different trajectories from very early in life. During development, sex hormone may direct such differentiation, and this is discussed in detail later; however, genetic, non-hormonal signals may also trigger specific examples of sexual differentiation of the brain. This thesis is supported by two arguments: first, direct genetic control of sexual differentiation in behavior may be as likely to evolve as hormonal control; second, neural and non-neural sexual dimorphisms have been reported that are not well explained by classical theories of steroid-dependent sexual differentiation (Arnold 2004).
II. BACKGROUND
The sex chromosomes are unusual in that they are differentially represented in the two sexes and, therefore, have been subject to sex-specific evolutionary pressures. Theses pressures favor X and Y genes that are sexually antagonistic; in other words, which are more adaptive in one sex than in the other. The implications of this sexual bias in X and Y genes are usually discussed with regard to the primary sex organs: the gonads. The brain is also an important sex organ, as it controls functions and behaviors that are advantageous in one sex, and contains structures that are adaptive mostly in one sex (Arnold 2004).
In birds and mammals, the sex chromosomes differ in size and in the type of genes that they contain. The human Y chromosome, for example, is only about one-third of the size of the X chromosome; the Y-chromosome genes only encode 27 proteins as compared to 1500 proteins that are encoded by the X-chromosome genes (Arnold 2004).
When looking for genes with differential expression between the sexes, the obvious starting points are those loci located on the X and Y chromosomes. Apart from its direct role in sex determination, the human Y chromosome has evolved to carry a combination of male-specific fertility genes and a limited range of housekeeping genes with homologues on the human X, while not denying the possibility that differential expression of these in the two sexes may be significant, it is also important to acknowledge that the human X has up to 1,000 genes, some of which could potentially contribute significantly to sexual determination process itself. In particular, an understanding of which genes do and do not escape X-inactivation may be crucial to evaluating their potential contribution to sexually dimorphic characteristics (Arnold 2004).
The genetic differences between XX and XY cells and organs stem from the presence or absence of Y genes, and from X gene dosage, mosaicism and parental imprint. The Y gene that has the strongest masculinizing effect on the brain is the SRY gene. This gene causes testicular development and the consequent production of high levels of testosterone, which causes permanent masculinization during brain development and reversible masculinization of male functions in adulthood. A potentially larger constitutive genetic difference between the XX and XY cells involves X-linked genes. X-inactivation might eliminate sex differences in X-linked gene expression caused by differences in genomic dose, because both male and female cells would express a single dose of X genes. However, several important sex differences probably persist. The first and most obvious difference is that because X inactivation is incomplete and varies according to tissue type and developmental stage, genes that escape inactivation can be expressed at a higher level in females (Arnold 2004; Morris 2004).
X-inactivation is the means by which males and females are rendered more similar in terms of gene expression; however, it also provides an opportunity for sex differences to arise, resulting from expression differentials of genes that escape inactivation. As previously mentioned, estimates of the number of these have increased such that it is now thought that up to one in five genes on the inactive X are expressed. X-linked genes that escape inactivation can be subdivided into two groups: those that have Y homologues and those that do not (Craig et al 2004).
III. CURRENT STATUS
Homosexuality is a common occurrence in humans and other species, yet its genetic and evolutionary basis is poorly understood. Gavrilets and Rice (2006) had formulated and studied a series of simple mathematical models for the purpose of predicting empirical patterns that can be used to determine the form of selection that leads to polymorphism of genes that influence homosexuality. Specifically, they had developed a theory to make contrasting predictions about the genetic characteristics of genes that influence homosexuality including: (i) chromosomal location, (ii) dominance among segregating alleles and (iii) effect sizes that distinguish between the two major models for their polymorphism: the overdominance and sexual antagonism models. Their study had concluded that the measurement of the genetic characteristics of quantitative trait loci (QTLs) found in genomic screens for genes influencing homosexuality can be highly informative in resolving the form of natural selection maintaining their polymorphism.
Additional research by Blanchard (2004) sought to analyze the relation between older brothers and homosexuality in men. Meta-analysis of aggregate data from 14 samples representing 10,143 male subjects had showed that homosexuality in human males is predicted by higher numbers of older brothers, but not by higher numbers of older sisters, younger brothers, or younger sisters. The relation between number of older brothers and sexual orientation holds only for males. This phenomenon has therefore been called the fraternal birth order effect.
Research on birth order, birth weight, and sexual orientation suggested that the developmental pathway to homosexuality initiated by older brothers operates during prenatal life. Calculations assuming a causal relation between older brothers and sexual orientation have estimated the proportion of homosexual men who owe their sexual orientation to fraternal birth order at 15% in one study and 29% in another. The maternal immune hypothesis proposes that the fraternal birth order effect reflects the progressive immunization of some mothers to male-specific antigens by each succeeding male fetus and the increasing effects of such immunization on sexual differentiation of the brain in each succeeding male fetus. There was found to be at least three possible mechanisms by which the mother’s immune response could influence the fetus: (1) the transfer of anti-male antibodies across the placenta from the maternal into the fetal compartment; (2) the transfer of maternal cytokines across the placenta; and (3) maternal immune reactions affecting the placenta itself. This hypothesis was found to be consistent with recent studies showing that the quantity of fetal cells that enter the maternal circulation is greater than previously thought, and that the number of male-specific proteins encoded by Y-chromosome genes is greater than previously thought.
IV. SUMMARY ; CONCLUSION
The differentiation in development of a fetus greatly relies on the presence and/or absence of certain genes in its environment. One of these genes is the SRY gene. The SRY gene is contained in the Y chromosome, which induces the undifferentiated gonads to form as testes rather than ovaries. The testes then secrete hormones to masculinize the rest of the body, while suppressing the development of the female reproductive tract at the same time. The absence of this SRY gene, on the other hand, results in the gonads’ development as an ovary and the body forms a feminine configuration.
Despite these seemingly straight-forward reactions that are due to the presence and/or absence of the gene, polymorphism (homosexuality) still occurs. Continuous years of research still have to be done in order to understand the underlying genetic variations that occur in the DNA level.
V. REFERENCES
Arnold AP. 2004. Sex Chromosomes and Brain Gender. Nature Reviews: Neuroscience. 5: 1-8.
Blanchard R. 2004. Quantitative and theoretical analyses of the relation between older brothers and homosexuality in men. Journal of Theoretical Biology. 230(2):173-187.
Craig IW, E Harper and CS Loat. 2004. The Genetic Basis for Sex Differences in Human Behaviour: Role of the Sex Chromosomes. Annals of Human Genetics 68, 269-284.
Gavrilets S, WR Rice. 2006. Genetic models of homosexuality: generating testable predictions. Proceedings of the Royal Society of Biological Sciences 273(1605):3031-3038.
Morris JA, CL Jordan and SM Breedlove. 2004. Sexual differentiation of the vertebrate nervous system. Nature Reviews: Neuroscience 7(10): 1034-1040.
