Showing papers on "X hyperactivation published in 1995"

Equality for X Chromosomes

Abstract: In many species, females possess two X chromosomes and males have one X chromosome. This difference is critical for the initial determination of sex. However, the X encodes many functions required equally in males and females; thus, X chromosome expression must be adjusted to compensate for the difference in dosage between the sexes. Distinct dosage compensation mechanisms have evolved in different species. A common theme in the Drosophila melanogaster and Caenorhabditis elegans systems is that a subtle alteration of chromatin structure may impose this modest, but vital adjustment of the X chromosome transcription level.

X inactivation of the FMR1 fragile X mental retardation gene.

Abstract: X chromosome inactivation has been hypothesised to play a role in the aetiology and clinical expression of the fragile X syndrome. The identification of the FMR1 gene involved in fragile X syndrome allows testing of the assumption that the fragile X locus is normally subject to X inactivation. We studied the expression of the FMR1 gene from inactive X chromosomes by reverse transcription of RNA followed by PCR (RT-PCR), both in somatic cell hybrids which retain an active or inactive human X chromosome and in a female patient with a large deletion surrounding the FMR1 gene. In both analyses, the data indicate that FMR1 is not normally expressed from the inactive X chromosome and is, therefore, subject to X chromosome inactivation. This finding is consistent with the results of previous studies of DNA methylation of FMR1 on active and inactive X chromosomes, verifies previous assumptions about the fragile X locus, and supports the involvement of X inactivation in the variable phenotype of females with full mutations of the FMR1 gene.

The hyperactive X chromosome is not early replicating in mitotically active somatic cells of Drosophila nasuta males.

Abstract: The temporal order of replication of the X chromosome(s) in mitotically dividing male and female cells in early embryos and in brain ganglia of Drosophila nasuta larvae was examined using [3H]thymidine pulse labelling and autoradiography. Both the X chromosomes in female cells and the single X chromosome in male cells replicated in complete synchrony with the autosome set in the nucleus. Thus, unlike the well-known early completion of replication by the hemizygous X chromosome in polytene nuclei in the salivary glands of male Drosophila larvae, the single X chromosome in mitotically dividing cells does not replicate earlier than the autosomes. We conclude that transcriptional hyperactivity of the single X chromosome required for dosage compensation in somatic cells of male Drosophila is not dependent upon its early replication.