X chromosome

About: X chromosome is a research topic. Over the lifetime, 9862 publications have been published within this topic receiving 407354 citations. The topic is also known as: GO:0000805 & chrX.

X chromosomes, retrogenes and their role in male reproduction

Abstract: Retrogenes originate from their progenitor genes by retroposition. Several retrogenes reported in recent studies are autosomal, originating from X-linked progenitor genes, and have evolved a testis-specific expression pattern. During male meiosis, sex chromosomes are segregated into a so-called 'XY' body and are silenced transcriptionally. It has been widely hypothesized that the silencing of the X chromosome during male meiosis is the driving force behind the retroposition of X-linked genes to autosomes during evolution. With the advent of sequenced genomes of many species, many retrogenes can be identified and characterized. The testis-specific retrogenes might be associated with human male infertility. My goal here is to integrate recent findings, highlight controversies in the field and identify areas for further study.

Progressive loss of DNA sequences from terminal chromosome deficiencies in Drosophila melanogaster.

Abstract: Terminal deficiencies at the tip of the X chromosome can be induced at a high frequency (0.2-0.3%) by irradiating Drosophila females carrying a homozygous mutator (mu-2) with low doses of X-rays. These terminal deficiencies are unstable, since over a period of 3 1/2 years DNA sequences were lost from their distal ends at a rate of 75 bp per generation, presumably due to the absence of a complete wild-type telomeric structure. Breakpoints of these deletions in the 5' upstream regulatory region of the yellow gene, giving rise to a mosaic cuticle pigmentation pattern typical of the y2 type, were used to define the location of tissue-specific cis-acting regulatory elements that are required for body, wing or bristle pigmentation.

Total aneuploidy and age-related sex chromosome aneuploidy in cultured lymphocytes of normal men and women

Abstract: In PHA-cultured lymphocytes, about 8% of metaphases from 32 women were aneuploid compared to 4% of metaphases from 35 men A significant part of this aneuploidy was characterized by sex chromosome involvement: in women, the loss or gain of X chromosomes; in men, the gain of X chromosomes and the loss or gain of Y chromosomes The incidence of this aneuploidy was positively age-related for both sexes Premature division of the X-chromosome centromere was closely associated with X-chromosome aneuploidy in women and men, and appeared to be the mechanism of nondisjunction causing this aneuploidy Premature centromere division (PCD) indicated a dysfunction of the X-chromosome centromere with aging, and this dysfunction was the basic cause of age-related aneuploidy A similar mechanism of nondisjunction may operate for the Y chromosome of men, but could not be clearly demonstrated because of the low incidence of Y-chromosome aneuploidy

Epigenetic aspects of X-chromosome dosage compensation.

Abstract: The X chromosomes of mammals and fruit flies exhibit unusual properties that have evolved to deal with the different dosages of X-linked genes in males (XY) and females (XX). The X chromosome dosage-compensation mechanisms discovered in these species are evolutionarily unrelated, but exhibit surprising parallels in their regulatory strategies. These features include the importance of noncoding RNAs, and epigenetic spreading of chromatin-modifying activities. Sex chromosomes have posed a fascinating puzzle for biologists. The dissimilar organization, gene content, and regulation of the X and Y chromosomes are thought to reflect selective forces acting on original pairs of identical chromosomes (1–3). The result in many organisms is a male-specific Y chromosome that has lost most of its original genetic content, and a difference in dosage of the X chromosome in males (XY) and females (XX).

Regulation of monoamine oxidase A by the SRY gene on the Y chromosome

Abstract: Monoamine oxidase A (MAO A), encoded by the X chromosome, catalyzes the oxidative deamination of monoamine neurotransmitters, such as serotonin, and plays a critically important role in brain development and functions. Abnormal MAO A activity has been implicated in several neuropsychiatric disorders, such as depression, autism, and attention deficit hyperactivity disorder, which show sexual dimorphism. However, the molecular basis for these disease processes is unclear. Recently, we found that MAO A was a putative target gene directly regulated by a transcription factor encoded by the sex-determining region Y (SRY) gene located on the Y chromosome. We demonstrated that SRY activates both MAO A-promoter and catalytic activities in a human male neuroblastoma BE(2)C cell line. A functional SRY-binding site in the MAO A core promoter was identified and validated by electrophoretic mobility shift and chromatin immunoprecipitation (ChIP) analyses. Coimmunoprecipitation and ChIP assays showed that SRY and Sp1 form a transcriptional complex and synergistically activate MAO A transcription. This is the first study demonstrating that the Y-encoded transcription factor SRY is capable of regulating an X-located gene, suggesting a novel molecular mechanism for sexual dimorphism in neural development, brain functions, and initiation/progression of neural disorders associated with MAO A dysfunction.—Wu, J. B., Chen, K., Li, Y., Lau, Y.-F. C., Shih, J. C. Regulation of monoamine oxidase A by the SRY gene on the Y chromosome.