Homologous ribosomal protein genes on the human X and Y chromosomes: escape from X inactivation and possible implications for Turner syndrome

Fisher, Emc

doi:10.1016/0168-9525(91)90058-x

Cited by 52 publications

(75 citation statements)

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“…RPS4X is not dosage compensated, and is known to escape X inactivation (Fisher et al, 1990). The present microarray results confirm that RPS4X is found in equal levels between normal male and female brain samples, which may be due to the close similarity between RPS4X and RPS4Y genes (Skaletsky et al, 2003).…”

Section: Sex Chromosome Linked Gene Expressionsupporting

confidence: 74%

“…Both RPS4Y and RPS4X encode ribosomal protein S4. Fisher et al (1990) demonstrated that the RPS4Y and RPS4X proteins differ at 19 of 263 amino acids. Since these genes are ubiquitously expressed in human tissues, it was suggested that the ribosome of human males and females Gene symbols shown with * were found to be differentially expressed by microarray analysis of male and female brain samples.…”

Section: Sex Chromosome Linked Gene Expressionmentioning

confidence: 99%

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Gender-Specific Gene Expression in Post-Mortem Human Brain: Localization to Sex Chromosomes

Vawter

Evans

Choudary

et al. 2003

Neuropsychopharmacol

198

151

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Gender differences in brain development and in the prevalence of neuropsychiatric disorders such as depression have been reported. Gender differences in human brain might be related to patterns of gene expression. Microarray technology is one useful method for investigation of gene expression in brain. We investigated gene expression, cell types, and regional expression patterns of differentially expressed sex chromosome genes in brain. We profiled gene expression in male and female dorsolateral prefrontal cortex, anterior cingulate cortex, and cerebellum using the Affymetrix oligonucleotide microarray platform. Differentially expressed genes between males and females on the Y chromosome (DBY, SMCY, UTY, RPS4Y, and USP9Y) and X chromosome (XIST) were confirmed using real-time PCR measurements. In situ hybridization confirmed the differential expression of gender-specific genes and neuronal expression of XIST, RPS4Y, SMCY, and UTY in three brain regions examined. The XIST gene, which silences gene expression on regions of the X chromosome, is expressed in a subset of neurons. Since a subset of neurons express gender-specific genes, neural subpopulations may exhibit a subtle sexual dimorphism at the level of differences in gene regulation and function. The distinctive pattern of neuronal expression of XIST, RPS4Y, SMCY, and UTY and other sex chromosome genes in neuronal subpopulations may possibly contribute to gender differences in prevalence noted for some neuropsychiatric disorders. Studies of the protein expression of these sexchromosome-linked genes in brain tissue are required to address the functional consequences of the observed gene expression differences.

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Section: Sex Chromosome Linked Gene Expressionsupporting

confidence: 74%

Section: Sex Chromosome Linked Gene Expressionmentioning

confidence: 99%

Gender-Specific Gene Expression in Post-Mortem Human Brain: Localization to Sex Chromosomes

Vawter

Evans

Choudary

et al. 2003

Neuropsychopharmacol

198

151

View full text Add to dashboard Cite

show abstract

“…This can then be confirmed by quantitation of the relevant transcripts from XO, XX, XXX or XXXX human cell lines. 7,8 We present an independent RT-PCR based approach using cDNA from cloned human cell lines. In a clonal female cell line, only one of either paternal or maternally derived X-chromosomes is active in every cell.…”

Section: Introductionmentioning

confidence: 99%

A novel expression based approach for assessing the inactivation status of human X-linked genes

Benjamin

Bakel

Craig³

2000

Eur J Hum Genet

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We present a novel RT-PCR-based approach for determining the inactivation status of X-linked genes. Using cDNA from cloned female cell lines in which only the maternal or paternally derived X chromosome is active, we are able to demonstrate expression from only one allele in genes known to be inactivated. Following reverse transcription, amplification across a polymorphism will yield a product from a single allele if the gene of interest is inactivated, and products from both alleles in a gene escaping inactivation. We have verified this approach using the human androgen receptor and FMR1 loci which have been shown to be subjected to normal inactivation. The potential for widespread application of this approach was shown by the successful demonstration of inactivation at the MAOA and HPRT loci using intronic polymorphisms.

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“…Most of the genes that avoid inactivation have a Y-linked homologue. The human X-linked genes known to have Y-linked homologous sequences and that probably avoid inactivation presently number at least nine: AMGX, KALIGJ, GSJ, ANT3, XG, MIC2, STSX, RPS4X, ZFX (Goodfellow & Tippett, 1981;Migeon et at., 1982;Goodfellow et al, 1984;Schneider-Gädicke et at., 1989;Fisher et at., 1990;; Slim et at., 1993;Schiebel et at., 1993; reviewed in Ballabio & Willard, 1992) (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

“…This appears generally to be the case (SchneiderGadicke et at., 1989;Fisher et aL, 1990 and above references) (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

Embryonic growth and the evolution of the mammalian Y chromosome. II. Suppression of selfish Y-linked growth factors may explain escape from X-inactivation and rapid evolution of Sry

Hurst¹

1994

Heredity

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The mammalian Y chromosome may be an attractor for selfish growth factors. A suppressor of the selfish growth effects would be expected to spread were it to have an appropriate parent-specific expression rule. A suppressor could act by boosting the resource demands of competing female embryos. This possibility may explain incidences of the escape from X-inactivation and provides a rationale for why these genes typically have Y-linked homologues. Alternatively, a suppressor could act to decrease the resource demands of males with the selfish Y. This possibility is supported by the finding that the size of male, but not female, human infants is negatively correlated to the number of X chromosomes. A protracted arms race between a selfish gene and its suppressor may ensue. Both the variation in copy number of Zfyand the unusually fast sequence evolution of Siy may be explained by such an arms race. As required by the model, human S#y is known to have an X-linked suppressor. Preliminary evidence suggests that, as predicted, rapid sequence evolution of Sry may be correlated with female promiscuity. The case for fast sequence evolution as the product of maternal/foetal conflict is strengthened by consideration of the rapid evolution of placental lactogens in both ruminants and rodents.

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Homologous ribosomal protein genes on the human X and Y chromosomes: escape from X inactivation and possible implications for Turner syndrome

Cited by 52 publications

References 0 publications

Gender-Specific Gene Expression in Post-Mortem Human Brain: Localization to Sex Chromosomes

Gender-Specific Gene Expression in Post-Mortem Human Brain: Localization to Sex Chromosomes

A novel expression based approach for assessing the inactivation status of human X-linked genes

Embryonic growth and the evolution of the mammalian Y chromosome. II. Suppression of selfish Y-linked growth factors may explain escape from X-inactivation and rapid evolution of Sry

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