Talk:SRY

Voting on proposed merger

Strongly oppose merger; the two genes are distinct, so they should each have their own articles. MrPMonday 07:09, 16 May 2006 (UTC)

• I concur with MrPMonday. I also oppose the merger. While they may be related, they are seperate genes. Epolk 23:57, 30 May 2006 (UTC)

--Grouphug (talk) 03:57, 5 December 2009 (UTC)

Does this help?

I wrote this. I give permission to use it. I'm not sure if any of this is helpful, but if it is, feel free to use it. It is more or less a review of the current research regarding the effect of SrY on the brain.

Review of Current Research It is thought that primarily sex steroids cause sexual differentiation of the mammalian brain.2 However, it appears XY and XX brain cells express different genes independently of sex steroids.3 That is to say, the differences in gene expression between XY and XX brain cells precede the influence of sex steroids.4 SRY is linked to the Y chromosome and thus is only present in XY (male) individuals, where it determines “maleness”. Researchers showed that SRY is also expressed in dopaminergic neurons in the substantia nigra of male rodents. Downregulating SRY in the substantia nigra results in decreased tyrosine hydroxylase expression and this led to motor deficits in the rodents. Tyrosine hydroxylase is an enzyme that catalyzes tyrosine to DOPA, which is a precursor to dopamine. Additionally, dopamine is a precursor to epinephrine and norepinephrine. These neurotransmitters are all catecholamines. The exact mechanism of SRY increasing tyrosine hydroxylase is currently unknown.1 Other researchers investigated the effects of SRY on the midbrain instead of the substantia nigra. They specifically focused on the ventral tegmental area, an area of the midbrain that is important in motivation, reward system, drug addiction, and other processes. They found differences between the sexes, specifically, that the females had more tyrosine hydroxylase in the ventral tegmental area than the males. These results may be due to either the SRY or the SRY and sex steroids.7 In another experiment, the SRY region of mice was deleted and then both XX and XY mice were given a SRY gene on an autosome. Levels of progesterone receptor increased in mice with the SRY transgene in certain areas of the brain regardless of the genetic makeup of the mice (XX or XY). This suggests that in this case, unlike the previous two, it is the sex steroids that control the progesterone receptor expression and not the genetic makeup of the cells.5 Other experiments have used this approach.8 There are two different types of SRY mrNA: linear and circular. Circular transcripts, probably untranslatable, we found in embryonic mouse brains of day 11 through 19. Linear transcripts, which are translatable, were located in the diencephalon, midbrain, and cortex. This change from circular SRY mrNA to linear SRY mrNA suggests the SRY gene is developmentally regulated.6 SOX is a family of transcription factors that regulates the expression sex-determining genes. Interestingly, a SOX protein, SOX13 in mice, is involved in neuronal differentiation, and therefore can be medically important as a possible early warning/test for childhood brain tumors.13, Fig 4(below) Additionally, there is another important SOX related to the brain and behavior; SOX9.19 Campomelic dysplasia is a form of dwarfism that includes brain anomalies such as dilated lateral ventricles, cerebellum defects, and abnormal corpus callosum. SOX9 was expressed where these abnormalities occurred in campomelic dysplasiastic patients.19

1. Direct regulation of adult brain function by the male-specific factor SRY. Dewing P, Chiang CW, Sinchak K, Sim H, Fernagut PO, Kelly S, Chesselet MF, Micevych PE, Albrecht KH, Harley VR, Vilain E. Curr Biol. 2006 Feb 21;16(4):415-20.

2. J.A. Morris, C.L. Jordan and S.M. Breedlove, Sexual differentiation of the vertebrate nervous system, Nat. Neurosci. 7 (2004), pp. 1034–1039.

3. A.P. Arnold and P.S. Burgoyne, Are XX and XY brain cells intrinsically different?, Trends Endocrinol. Metab. 15 (2004), pp. 6–11.

4. P. Dewing, T. Shi, S. Horvath and E. Vilain, Sexually dimorphic gene expression in mouse brain precedes gonadal differentiation, Brain Res. Mol. Brain Res. 118 (2003), pp. 82–90.

5. Neonatal mice possessing an Sry transgene show a masculinized pattern of progesterone receptor expression in the brain independent of sex chromosome status. Wagner CK, Xu J, Pfau JL, Quadros PS, De Vries GJ, Arnold AP. Endocrinology. 2004 Mar;145(3):1046-9. Epub 2003 Nov 26.

6. Developmental profile of Sry transcripts in mouse brain. Mayer A, Mosler G, Just W, Pilgrim C, Reisert I. Neurogenetics. 2000 Sep;3(1):25-30.

7. Morphological analyses of sex differences and age-related changes in C3H mouse midbrain. Tanida T, Warita K, Mitsuhashi T, Ishihara K, Yokoyama T, Kitagawa H, Hoshi N. J Vet Med Sci. 2009 Jul;71(7):855-63.

8. What does the "four core genotypes" mouse model tell us about sex differences in the brain and other tissues? Arnold AP, Chen X. Front Neuroendocrinol. 2009 Jan;30(1):1-9. Epub 2008 Nov 11. Review.

9. Sex chromosome complement and gonadal sex influence aggressive and parental behaviors in mice. Gatewood JD, Wills A, Shetty S, Xu J, Arnold AP, Burgoyne PS, Rissman EF. J Neurosci. 2006 Feb 22;26(8):2335-42.

13. SOX13 is up-regulated in the developing mouse neuroepithelium and identifies a sub-population of differentiating neurons. Wang Y, Bagheri-Fam S, Harley VR. Brain Res Dev Brain Res. 2005 Jun 30;157(2):201-8.

19. Localisation of the SRY-related HMG box protein, SOX9, in rodent brain. Pompolo S, Harley VR. Brain Res. 2001 Jul 6;906(1-2):143-8 —Preceding unsigned comment added by Grouphug (talk • contribs) 03:54, 5 December 2009 (UTC)

Educational assignment group members

BASEDbio (talk) 19:05, 9 October 2013 (UTC)