Barr body

You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.

In those species (including humans) in which sex is determined by the presence of the Y or W chromosome rather than the diploidy of the X or Z, a Barr body is the inactive X chromosome in a female cell, or the inactive Z in a male (Lyon, 2003), rendered inactive in a process called Lyonization. The Lyon hypothesis states that in cells with multiple X chromosomes, all but one is inactivated during mammalian embryogenesis (Lyon, 1961). This happens early in embryonic development at random in mammals, (Brown, 1997) except in marsupials and in some extra-embryonic tissues of some placental mammals, in which the father's X chromosome is always deactivated (Lee, 2003). Barr bodies are named after their discoverer, Murray Barr (Barr & Bertram, 1949).

The inactivation state of chromosomes is passed on to daughter cells during mitosis (Hall et al., 2003). Since random chromosomes are selected for inactivation early in embryonic development, this results in different regions of the adult body having different chromosomes inactivated. This can be significant if different alleles of a gene are present on the different chromosomes; in some regions of the body one allele will be active, and in other regions the other will. This is what results in the coloration pattern of female calico cats; pigmentation genes on the X chromosome are activated in different patches of skin based on which chromosome is condensed in those regions (Alberts et al., 2002).

The Barr body chromosome is generally considered to be inert, but in fact a small number of genes remain active and expressed in some species. These genes are generally those which are present on the other sex chromosome (Y or W) (Lyon, 2003).

Mechanism

Mammalian X-chromosome inactivation is initiated from the X inactivation centre or Xic, usually found near the centromere (Rougeulle et al., 2003). The centre contains twelve genes, seven of which code for proteins, five for untranslated RNAs, of which only two are known to play an active role in the X inactivation process, Xist and Tsix (Rougeulle et al., 2003). The centre also appears to be important in chromosome counting: ensuring that random inactivation only takes place when two X-chromosomes are present. The provision of an extra artificial Xic in early embryogenesis can induce inactivation of the single X found in male cells (Rougeulle et al., 2003).

The roles of Xist and Tsix appear to be antagonistic. The loss of Tsix expression on the future inactive X chromosome results in an increase in levels of Xist around the Xic. Meanwhile, on the future active X Tsix levels are maintained; thus the levels of Xist remain low. (Lee et al, 1999) This shift allows Xist to begin coating the future inactive chromosome, spreading out from the Xic (Lyon, 2003). In non-random inactivation this choice appears to be fixed and current evidence suggests that the maternally inherited gene may be imprinted (Brown, 1997).

It is thought that this constitutes the mechanism of choice, and allows downstream processes to establish the compact state of the Barr body. These changes include histone modifications, such as histone H3 methylation (Heard et al., 2001) and histone H2A ubiquitination, (de Napoles et al., 2004) as well as direct modification of the DNA itself, via the methylation of CpG sites (Chadwick et al., 2003). These changes help inactivate gene expression on the inactive X-chromosome and to bring about its compaction to form the Barr body.

See also

• X-inactivation
• Sex-determination system
• Demethylation
• Acetylation

References

Links to full text articles are provided where access is free, in other cases only the abstract has been linked.

• Alberts,B., Johnson,A., Lewis,J., Raff,M., Roberts,K., Walter,P., (2002), Molecular Biology of the Cell, Fourth Edition, (428-429) Garland Science, 0-8153-4072-9 (Web Edition, Free access)

• Barr, M. L., Bertram, E. G., (1949), A Morphological Distinction between Neurones of the Male and Female, and the Behaviour of the Nucleolar Satellite during Accelerated Nucleoprotein Synthesis. Nature. 163 (4148): 676-7.

• Brown,C.J., Robinson,W.P., (1997), XIST Expression and X-Chromosome Inactivation in Human Preimplantation Embryos. Am. J. Hum. Genet. 61, 5-8 (Full Text PDF)

• Chadwick,B.P., Willard,H.F., (2003), Barring gene expression after XIST: maintaining faculative heterochromatin on the inactive X. j.semcdb 14, 359-367 (Abstract)

• de Napoles,M., Mermoud,J.E., Wakao,R., Tang,Y.A., Endoh,M., Appanah,R., Nesterova,T.B., Silva,J., Otte,A.P., Vidal,M., Koseki,H., Brockdorff,N., (2004), Polycomb Group Proteins Ring1A/B Link Ubiquitylation of Histone H2A to Heritable Gene Silencing and X Inactivation. Dev. Cell 7, 663-676 (Abstract)

• Hall,L.L., Lawrence,J.B., (2003), The Cell Biology of a Novel Chromosomal RNA: Chromosome Painting By XIST/Xist RNA Initiates a remodeling cascade. j.semcdb 14, 369-378 (Abstract)

• Heard, E., Rougeulle, C., Arnaud, D., Avner, P., Allis, C. D. (2001), Methylation of Histone H3 at Lys-9 Is an Early Mark on the X Chromosome during X Inactivation. Cell 107, 727-738. (Full Text)

• Lee, J. T., Davidow, L. S., Warshawsky, D., (1999), Tisx, a gene antisense to Xist at the X-inactivation centre. Nat. Genet. 21, 400-404. Full Text

• Lee, J. T., (2003), X-chromosome inactivation: a multi-disciplinary approach. j.semcdb 14, 311-312. (doi:10.1016/j.semcdb.2003.09.025 Abstract)

• Lyon, M. F. (1961), Gene Action in the X-chromosome of the Mouse (Mus musculus L.) Nature. 190 (4773): 372-3. PMID 13764598 (Abstract)

• Lyon, M. F., (2003), The Lyon and the LINE hypothesis. j.semcdb 14, 313-318. (Abstract)

• Rougeulle, C., Avner, P. (2003), Controlling X-inactivationin mammals: what does the centre hold?. j.semcdb 14, 331-340. (Abstract)de:Geschlechts-Chromatin

et:Barri kehakefr:Corpuscule de Barr hu:Barr-test ja:バー小体sr:Барово тело sv:Barrkropp

WikiDoc Help Menu Quick Start.. Get Started Here! How to Login How to Search Pages How to Start a New Page How to Edit a Page Cheat Sheet Editing basics Learning Basic Formatting How to make Links in WikiDoc & to External Sites How to Make Lists How to Ignoring Formatting Adding References or Footnotes to Articles Tracking Changes You Have Made How to Put an Article Into a Category When Multiple Topics Should Go To The Same Page (MI, Acute MI, AMI) Using Redirection Advanced editing How to Make Tables How to Insert Images and Other Media How to Add Video Help:How to Make Columns Web Colors How To Make Templates How to Move Pages Inserting Dynamic Dates and Times Inserting WikiDoc Statistics Editing the Table of Contents Communicating your edits Let others know what you changed: The importance of Edit Summaries Minor Edits Edit Conflicts Help Videos You Can Watch Getting Started Video

Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .