Dosage compensation

About: Dosage compensation is a research topic. Over the lifetime, 1920 publications have been published within this topic receiving 124589 citations.

X-chromosome replication patterns in adult, newborn and prenatal opossums

Abstract: Somatic cells from the opossums Monodelphis domestica and Didelphis virginiana were labelled with 5-bromodeoxyuridine (BrdU), treated with colchicine, stained with acridine orange and examined using fluorescence microscopy. BrdU-incorporated metaphase spreads from females of M. domestica at developmental stages from late bilaminar blastocysts to adults showed replication asynchrony of the two (acrocentric) X chromosomes. The long arm of one X chromosome was the latest replicating region in the entire chromosome complement and is presumed to represent transcriptional inactivation and X dosage compensation. The minute short arm of the same X, which contains a nucleolar organizer region, was earlier replicating and synchronous with the short arm of its homologue and is thus assumed to escape inactivation. BrdU-incorporated spreads from cells of fetuses, neonates and adults of D. virginiana also showed a late replicating (submetacentric) X chromosome. The pattern was different from that of M. domestica because of the different morphology and the presence of large blocks of constitutive heterochromatin in both homologues. The timing and pattern of replication of the single X in males of both species resembled the earlier replicating X in females. The array of molecular techniques now available offers the best means for investigating X-chromosome replication and activity states of X-linked genes in the earliest stages of marsupial embryogenesis.

Dosage Compensation of Sex Chromosome Genes in Eukaryotes

Abstract: Sex chromosome evolution is accompanied by significant divergence in morphology and gene content and results in most genes of one of the sex chromosomes being present in two dosages in one sex and in one dos- age in the other. To eliminate the difference in the expression levels of these genes between sexes and to restore equal expression levels of the genes between sex chromosomes and autosomes, mechanisms of dosage compensa- tion have appeared. Studies of three classical objects, Drosophila melanogaster, Caenorhabditis elegans, and mam- mals, have shown that dosage compensation of X-linked genes can be achieved through completely different chromosome-wide mechanisms. New data on sex chromosome gene expression demonstrating that many sex chromosome genes can be expressed at different levels in males and females were recently obtained from birds and butterflies. In this review, dosage compensation mechanisms in D. melanogaster, C. elegans, and mammals are considered and the data on sex chromosome gene expression in birds and butterflies, and their influence on our view of dosage compensation, are discussed.

An evaluation of the inactive mouse X chromosome in somatic cell hybrids.

Abstract: The expression of mouse Zfx, Rps4, Ube1x, and Xist was evaluated in hamster-mouse somatic cell hybrids containing either an active or an inactive mouse X chromosome using polymerase chain reaction of reverse transcribed RNA (RT-PCR). The results showed that Zfx, Rps4, and Ube1x are expressed exclusively from the active mouse X, while Xist is expressed exclusively from the inactive X. These findings confirm the pattern of X inactivation for these mouse genes reported previously based on expression in somatic tissues of F1 females from interspecific crosses. These results demonstrate the existence of differences between human and mouse X inactivation, as the corresponding human genes, ZFX, RPS4X, and UBE1 escape X inactivation.

Is X-chromosome inactivation a homology effect?

Abstract: Homology effect is defined as any effect on gene expression or chromosome behavior relating to the presence of homologous sequences. Using this definition, imprinted X inactivation probably does not qualify as a homology effect, since paternal silencing is strictly the result of gametic imprinting and occurs without regard to total X-chromosome number. In contrast, random X inactivation could however qualify as a homology effect for three reasons. First, X inactivation depends on the presence of more than one X homolog, or more specifically, more than one Xic sequence. Second, some form of trans-sensing must be operative at the onset of X inactivation, specifically during the process of choice, so that an XX cell does not inadvertantly designate one X as both the future active and inactive X. And finally, the fact that Xist and Tsix produce noncoding homologous RNAs conjures up an analogy to posttranscriptional gene silencing in other organisms. In this class of silencing mechanisms, the action of a transcriptionally active gene is nullified by homologous double-stranded RNA molecules produced at ectopic loci in a process referred to as “RNAi” for RNA-inhibition.