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Dosage Compensation (dosage + compensation)

Distribution by Scientific Domains
Life Sciences100%

Selected Abstracts

Form and function of dosage-compensated chromosomes , a chicken-and-egg relationship

BIOESSAYS, Issue 8 2010
Charlotte Grimaud
Abstract Does the three-dimensional (3D) conformation of interphase chromosomes merely reflect their function or does it actively contribute to gene regulation? The analysis of sex chromosomes that are subject to chromosome-wide dosage compensation processes promises new insight into this question. Chromosome conformations are dynamic and largely determined by association of distant chromosomal loci in the nuclear space or by their anchoring to the nuclear envelope, effectively generating chromatin loops. The type and extent of such interactions depend on chromatin-bound transcription regulators and therefore reflects function. Dosage compensation adjusts the overall transcription activity of X chromosomes to assure balanced expression in the two sexes. Initial analyses of mammalian and Drosophila X chromosomes have led to the hypothesis that their conformations may not only reflect their functional state but may in turn contribute to the coordination of chromosome-wide tuning of transcription. [source]

SEXUAL ANTAGONISM AND THE EVOLUTION OF X CHROMOSOME INACTIVATION

EVOLUTION, Issue 8 2008
Jan Engelstädter
In most female mammals, one of the two X chromosomes is inactivated early in embryogenesis. Expression of most genes on this chromosome is shut down, and the inactive state is maintained throughout life in all somatic cells. It is generally believed that X-inactivation evolved as a means of achieving equal gene expression in males and females (dosage compensation). Following degeneration of genes on the Y chromosome, gene expression on X chromosomes in males and females is upregulated. This results in closer to optimal gene expression in males, but deleterious overexpression in females. In response, selection is proposed to favor inactivation of one of the X chromosomes in females, restoring optimal gene expression. Here, we make a first attempt at shedding light on this intricate process from a population genetic perspective, elucidating the sexually antagonistic selective forces involved. We derive conditions for the process to work and analyze evolutionary stability of the system. The implications of our results are discussed in the light of empirical findings and a recently proposed alternative hypothesis for the evolution of X-inactivation. [source]

An embryonic story: Analysis of the gene regulative network controlling Xist expression in mouse embryonic stem cells

BIOESSAYS, Issue 7 2010
Pablo Navarro
Abstract In mice, dosage compensation of X-linked gene expression is achieved through the inactivation of one of the two X-chromosomes in XX female cells. The complex epigenetic process leading to X-inactivation is largely controlled by Xist and Tsix, two non-coding genes of opposing function. Xist RNA triggers X-inactivation by coating the inactive X, while Tsix is critical for the designation of the active X-chromosome through cis -repression of Xist RNA accumulation. Recently, a plethora of trans -acting factors and cis -regulating elements have been suggested to act as key regulators of either Xist, Tsix or both; these include ubiquitous factors such as Yy1 and Ctcf, developmental proteins such as Nanog, Oct4 and Sox2, and X-linked regulators such as Rnf12. In this paper we summarise recent advances in our knowledge of the regulation of Xist and Tsix in embryonic stem (ES) and differentiating ES cells. [source]

X-chromosome upregulation and inactivation: two sides of the dosage compensation mechanism in mammals

BIOESSAYS, Issue 1 2009
Elena V. Dementyeva
Abstract Mammals have a very complex, tightly controlled, and developmentally regulated process of dosage compensation. One form of the process equalizes expression of the X-linked genes, present as a single copy in males (XY) and as two copies in females (XX), by inactivation of one of the two X-chromosomes in females. The second form of the process leads to balanced expression between the X-linked and autosomal genes by transcriptional upregulation of the active X in males and females. However, not all X-linked genes are absolutely balanced. This review is focused on the recent advances in studying the dosage compensation phenomenon in mammals. [source]

Chromosome chains and platypus sex: kinky connections

BIOESSAYS, Issue 7 2005
Terry Ashley
Mammal sex determination depends on an XY chromosome system, a gene for testis development and a means of activating the X chromosome. The duckbill platypus challenges these dogmas.1,2 Gutzner et al.1 find no recognizable SRY sequence and question whether the mammalian X was even the original sex chromosome in the platypus. Instead they suggest that the original platypus sex chromosomes were derived from the ZW chromosome system of birds and reptiles. Unraveling the puzzles of sex determination and dosage compensation in the platypus has been complicated by the fact that it has a surplus of sex chromosomes. Rather than a single X and Y chromosome, the male platypus has five Xs and five Ys. BioEssays 27:681,684, 2005. © 2005 Wiley Periodicals, Inc. [source]

Silence of the fathers: Early X inactivation

BIOESSAYS, Issue 8 2004
Mimi K. Cheng
X chromosome inactivation is the mammalian answer to the dilemma of dosage compensation between males and females. The study of this fascinating form of chromosome-wide gene regulation has yielded surprising insights into early development and cellular memory. In the past few months, three papers1,3 reported unexpected findings about the paternal X chromosome (Xp). All three studies agree that the Xp is imprinted to become inactive earlier than ever suspected during embryonic development. Although apparently incomplete, this early form of inactivation insures dosage compensation throughout development. Silencing of the Xp persists in cells of extraembryonic tissues, but it is erased and followed by random X inactivation in cells of the embryo proper. These findings challenge several aspects of the current view of X inactivation during early development and may have profound impact on studies of pluripotency and epigenetics. BioEssays 26:821,824, 2004. © 2004 Wiley Periodicals, Inc. [source]