XIST

The human Xist RNA gene is located on the long (q) arm of the X chromosome. The Xist RNA gene contains conserved repeats within its structure. Its gene product is largely localized in the nucleus. The Xist RNA gene features a conserved A region, which contains 8 repeats separated by U-rich spacers. The A region appears to encode two long stem-loop RNA structures that each include four repeats.{{cite journal | vauthors = Maenner S, Blaud M, Fouillen L, Savoye A, Marchand V, Dubois A, Sanglier-Cianférani S, Van Dorsselaer A, Clerc P, Avner P, Visvikis A, Branlant C | title = 2-D structure of the A region of Xist RNA and its implication for PRC2 association | journal = PLOS Biology | volume = 8 | issue = 1 | pages = e1000276 | date = January 2010 | pmid = 20052282 | pmc = 2796953 | doi = 10.1371/journal.pbio.1000276 | veditors = Hall K | doi-access = free }} An ortholog of the Xist RNA gene in humans has been identified in mice.{{cite journal | vauthors = Borsani G, Tonlorenzi R, Simmler MC, Dandolo L, Arnaud D, Capra V, Grompe M, Pizzuti A, Muzny D, Lawrence C, Willard HF, Avner P, Ballabio A | title = Characterization of a murine gene expressed from the inactive X chromosome | journal = Nature | volume = 351 | pages = 325–9 | date = May 1991 | issue = 6324 | pmid = 2034278 | doi = 10.1038/351325a0| bibcode = 1991Natur.351..325B | s2cid = 4239301 }}{{cite journal | vauthors = Brockdorff N, Ashworth A, Kay GF, Cooper P, Smith S, McCabe VM, Norris DP, Penny GD, Patel D, Rastan S | title = Conservation of position and exclusive expression of mouse Xist from the inactive X chromosome | journal = Nature | volume = 351 | pages = 329–31 | date = May 1991 | issue = 6324 | pmid = 2034279 | doi = 10.1038/351329a0| bibcode = 1991Natur.351..329B | s2cid = 4342551 }} This ortholog encodes a 15 kb Xist transcript that is also localized in the nucleus. However, the ortholog does not feature conserved repeats.{{cite journal | vauthors = Brockdorff N, Ashworth A, Kay GF, McCabe VM, Norris DP, Cooper PJ, Swift S, Rastan S | title = The product of the mouse Xist gene is a 15 kb inactive X-specific transcript containing no conserved ORF and located in the nucleus | journal = Cell | volume = 71 | issue = 3 | pages = 515–26 | year= 1992 | pmid = 1423610 | doi = 10.1016/0092-8674(92)90519-I | s2cid = 19889657 }} The Xist RNA gene is located within the Xist Inactivation Center (XIC), which plays a major role in X-inactivation.{{cite journal | vauthors = Lee JT, Davidow LS, Warshawsky D | title = Tsix, a gene antisense to Xist at the X-inactivation centre | journal = Nature Genetics | volume = 21 | issue = 4 | pages = 400–4 | date = April 1999 | pmid = 10192391 | doi = 10.1038/7734 | s2cid = 30636065 }}

File:RepA Model Xist.png

The Xist RNA contains a region of conservation called the repeat A (repA) region that contains up to nine repeated elements. It was initially suggested that repA repeats could fold back on themselves to form local intra-repeat stem-loop structures. Later work using in vitro biochemical structure probing proposed several inter-repeat stem-loop structures. A recent study using in vivo biochemical probing and comparative sequence analysis proposed a revision of the repA structure model that includes both intra-repeat and inter-repeat folding found in previous models as well as novel features (see Figure). In addition to its agreement with the in vivo data, this revised model is highly conserved in rodents and mammals (including humans) suggesting functional importance for repA structure. Although the exact function of the repA region is uncertain, it was shown that the entire region is needed for efficient binding to the Suz12 protein.

The Xist RNA directly binds to the inactive X-chromosome through a chromatin binding region of the RNA transcript. The Xist chromatin binding region was first elucidated in female mouse fibroblastic cells. The primary chromatin binding region was shown to localize to the C-repeat region. The chromatin-binding region was functionally mapped and evaluated by using an approach for studying noncoding RNA function in living cells called peptide nucleic acid (PNA) interference mapping. In the reported experiments, a single 19-bp antisense cell-permeating PNA targeted against a particular region of Xist RNA caused the disruption of the Xi. The association of the Xi with macro-histone H2A is also disturbed by PNA interference mapping.

The Xist RNA gene lies within the X-inactivation centre (XIC), which plays a major role in Xist expression and X-inactivation.{{cite journal | vauthors = Herzing LB, Romer JT, Horn JM, Ashworth A | title = Xist has properties of the X-chromosome inactivation centre | journal = Nature | volume = 386 | issue = 6622 | pages = 272–5 | date = March 1997 | pmid = 9069284 | doi = 10.1038/386272a0 | bibcode = 1997Natur.386..272H | s2cid = 4371247 }} The XIC is located on the q arm of the X chromosome (Xq13). XIC regulates Xist in cis X-inactivation, where Tsix, an antisense of Xist, downregulates the expression of Xist. The Xist promoter of XIC is the master regulator of X-inactivation. X-inactivation plays a key role in dosage compensation.

The Tsix antisense gene is a transcript of the Xist gene at the XIC center.{{cite journal | vauthors = Lee JT, Davidow LS, Warshawsky D | title = Tsix, a gene antisense to Xist at the X-inactivation centre | journal = Nature Genetics | volume = 21 | issue = 4 | pages = 400–4 | date = April 1999 | pmid = 10192391 | doi = 10.1038/7734 | s2cid = 30636065 }} The Tsix antisense transcript acts in cis to repress the transcription of Xist, which negatively regulates its expression. The mechanism behind how Tsix modulates Xist activity in cis is poorly understood; however, there are a few theories on its mechanism. One theory is that Tsix is involved in chromatin modification at the Xist locus and another is that transcription factors of pluripotent cells play a role in Xist repression.{{cite journal | vauthors = Senner CE, Brockdorff N | title = Xist gene regulation at the onset of X inactivation | journal = Current Opinion in Genetics & Development | volume = 19 | issue = 2 | pages = 122–6 | date = April 2009 | pmid = 19345091 | doi = 10.1016/j.gde.2009.03.003 }}

The Tsix antisense is believed to activate DNA methyl transferases that methylate the Xist promoter, in return resulting in inhibition of the Xist promoter and thus the expression of the Xist gene.{{cite journal | vauthors = Nesterova TB, Popova BC, Cobb BS, Norton S, Senner CE, Tang YA, Spruce T, Rodriguez TA, Sado T, Merkenschlager M, Brockdorff N | title = Dicer regulates Xist promoter methylation in ES cells indirectly through transcriptional control of Dnmt3a | journal = Epigenetics & Chromatin | volume = 1 | issue = 1 | pages = 2 | date = October 2008 | pmid = 19014663 | pmc = 257704 | doi = 10.1186/1756-8935-1-2 | doi-access = free }} In contrast to Tsix acting, which is an inhibitor to Xist, the methylation of histone 3 lysine 4 (H3K4) up regulates the transcription by opening the chromatin structure. The open chromatin enables the recruitment of transcription factors and thus allows for transcription to occur.{{cite journal | vauthors = Navarro P, Pichard S, Ciaudo C, Avner P, Rougeulle C | title = Tsix transcription across the Xist gene alters chromatin conformation without affecting Xist transcription: implications for X-chromosome inactivation | journal = Genes & Development | volume = 19 | issue = 12 | pages = 1474–84 | date = June 2005 | pmid = 15964997 | pmc = 1151664 | doi = 10.1101/gad.341105 }}

A dsRNA and RNAi pathway have been also proposed to play a role in regulation of the Xist Promoter. Dicer is an RNAi enzyme and it is believed to cleave the duplex of Xist and Tsix at the beginning of X-inactivation, to small ~30 nucleotide RNAs, which have been termed xiRNAs, These xiRNAs are believed to be involved in repressing Xist on the probable active X chromosome based upon studies. A study was conducted where normal endogenous Dicer levels were decreased to 5%, which led to an increase in Xist expression in undifferentiated cells, thus supporting the role of xiRNAs in Xist repression.{{cite journal | vauthors = Ogawa Y, Sun BK, Lee JT | title = Intersection of the RNA interference and X-inactivation pathways | journal = Science | volume = 320 | issue = 5881 | pages = 1336–41 | date = June 2008 | pmid = 18535243 | pmc = 2584363 | doi = 10.1126/science.1157676 | bibcode = 2008Sci...320.1336O }} The role and mechanism of xiRNAs is still under examination and debate.{{Citation needed|date=April 2011}}

Pluripotent stem cells express transcription factors Nanog, Oct4 and Sox2 that seem to play a role in repressing Xist. In the absence of Tsix in pluripotent cells, Xist is repressed, where a mechanism has been proposed that these transcription factors cause splicing to occur at intron 1 at the binding site of these factors on the Xist gene, which inhibits Xist expression A study was conducted where Nanog or Oct4 transcription factors were depleted in pluripotent cells, which resulted in the upregulation of Xist. From this study, it is proposed that Nanog and Oct4 are involved in the repression of Xist expression.{{cite journal | vauthors = Navarro P, Chambers I, Karwacki-Neisius V, Chureau C, Morey C, Rougeulle C, Avner P | title = Molecular coupling of Xist regulation and pluripotency | journal = Science | volume = 321 | issue = 5896 | pages = 1693–5 | date = September 2008 | pmid = 18802003 | doi = 10.1126/science.1160952 | bibcode = 2008Sci...321.1693N | s2cid = 42703823 }}

Polycomb repressive complex 2 (PRC2) consist of a class of polycomb group proteins that are involved in catalyzing the trimethylation of histone H3 on lysine 27 (K27), which results in chromatin repression, and thus leads to transcriptional silencing. Xist RNA recruits polycomb complexes to the inactive X chromosome at the onset of XCI.{{cite journal | vauthors = Zhao J, Sun BK, Erwin JA, Song JJ, Lee JT | title = Polycomb proteins targeted by a short repeat RNA to the mouse X chromosome | journal = Science | volume = 322 | issue = 5902 | pages = 750–6 | date = October 2008 | pmid = 18974356 | pmc = 2748911 | doi = 10.1126/science.1163045 | bibcode = 2008Sci...322..750Z }} SUZ12 is a component of the PRC2 and contains a zinc finger domain. The zinc finger domain is believed to bind to the RNA molecule.{{cite journal | vauthors = de Napoles M, Mermoud JE, Wakao R, Tang YA, Endoh M, Appanah R, Nesterova TB, Silva J, Otte AP, Vidal M, Koseki H, Brockdorff N | title = Polycomb group proteins Ring1A/B link ubiquitylation of histone H2A to heritable gene silencing and X inactivation | journal = Developmental Cell | volume = 7 | issue = 5 | pages = 663–76 | year = 2004 | pmid = 15525528 | doi = 10.1016/j.devcel.2004.10.005 | doi-access = free }} The PRC2 has been observed to repress Xist expression independent of the Tsix antisense transcript, although the definite mechanism is still not known.

X-inactivation plays a key role in dosage compensation mechanisms that allow for equal expression of the X and autosomal chromosomes.{{cite journal | vauthors = Nguyen DK, Disteche CM | title = Dosage compensation of the active X chromosome in mammals | journal = Nature Genetics | volume = 38 | issue = 1 | pages = 47–53 | date = January 2006 | pmid = 16341221 | doi = 10.1038/ng1705 | s2cid = 2898893 }} Different species have different dosage compensation methods, with all of the methods involving the regulation of an X chromosome from one of the either sexes. Some methods involved in dosage compensation to inactivate one of the X chromosomes from one of the sexes are Tsix antisense gene, DNA methylation and DNA acetylation;{{cite journal | vauthors = Csankovszki G, Nagy A, Jaenisch R | title = Synergism of Xist RNA, DNA methylation, and histone hypoacetylation in maintaining X chromosome inactivation | journal = The Journal of Cell Biology | volume = 153 | issue = 4 | pages = 773–84 | date = May 2001 | pmid = 11352938 | pmc = 2192370 | doi = 10.1083/jcb.153.4.773 }} however, the definite mechanism of X-inactivation is still poorly understood. If one of the X chromosomes is not inactivated or is partially expressed, it could lead to over expression of the X chromosome and it could be lethal in some cases.

Turner syndrome is one example of where dosage compensation does not equally express the X chromosome, and in females one of the X chromosomes is missing or has abnormalities, which leads to physical abnormalities and also gonadal dysfunction in females due to the one missing or abnormal X chromosome. Turner syndrome is also referred to as a monosomy X condition.{{cite journal |vauthors=Chenga MK, Nguyena KD, Disteche CM |year=2006 |title=Dosage compensation of the X chromosome and Turner syndrome=International-Congress-series|journal=International Congress Series |volume=1298|pages=3–8 |doi=10.1016/j.ics.2006.06.012}}

Xist expression and X-inactivation change throughout embryonic development. In early embryogenesis, the oocyte and sperm do not express Xist and the X chromosome remains active. After fertilization, when the cells are in the 2 to 4 cell stage, Xist transcripts are expressed from paternal X chromosome(Xp) in every cell, causing that X chromosome to become imprinted and inactivated. Some cells develop into pluripotent cells (the inner cell mass) when the blastocyte forms. There, the imprint is removed, leading to the downregulation of Xist and thus reactivation of the inactive X chromosome. Recent data suggests that Xist activity is regulated by an anti-sense transcript.{{cite journal | vauthors = Mak W, Nesterova TB, de Napoles M, Appanah R, Yamanaka S, Otte AP, Brockdorff N | title = Reactivation of the paternal X chromosome in early mouse embryos | journal = Science | volume = 303 | issue = 5658 | pages = 666–9 | date = January 2004 | pmid = 14752160 | doi = 10.1126/science.1092674 | bibcode = 2004Sci...303..666M | s2cid = 37749083 }} The epiblast cells are then formed and they begin to be differentiated, and the Xist is upregulated from either of the two X chromosomes and at random in ICM, but the Xist is maintained in epiblast, an X is inactivated and the Xist allele is turned off in the active X chromosome. In maturing XX primordial germ cells, Xist is downregulated and X reactivation occurs once again.{{cite journal | vauthors = Nesterova TB, Mermoud JE, Hilton K, Pehrson J, Surani MA, McLaren A, Brockdorff N | title = Xist expression and macroH2A1.2 localisation in mouse primordial and pluripotent embryonic germ cells | journal = Differentiation; Research in Biological Diversity | volume = 69 | issue = 4–5 | pages = 216–25 | date = January 2002 | pmid = 11841480 | doi = 10.1046/j.1432-0436.2002.690415.x | s2cid = 32840485 }}

Mutations in the XIST promoter cause familial skewed X-inactivation.

XIST has been shown to interact with BRCA1.{{cite journal | vauthors = Ganesan S, Silver DP, Drapkin R, Greenberg R, Feunteun J, Livingston DM | title = Association of BRCA1 with the inactive X chromosome and XIST RNA | journal = Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences | volume = 359 | issue = 1441 | pages = 123–8 | date = January 2004 | pmid = 15065664 | pmc = 1693294 | doi = 10.1098/rstb.2003.1371 }}{{cite journal | vauthors = Ganesan S, Silver DP, Greenberg RA, Avni D, Drapkin R, Miron A, Mok SC, Randrianarison V, Brodie S, Salstrom J, Rasmussen TP, Klimke A, Marrese C, Marahrens Y, Deng CX, Feunteun J, Livingston DM | title = BRCA1 supports XIST RNA concentration on the inactive X chromosome | journal = Cell | volume = 111 | issue = 3 | pages = 393–405 | date = November 2002 | pmid = 12419249 | doi = 10.1016/S0092-8674(02)01052-8 | s2cid = 372211 | doi-access = free }}

• X-inactivation
• Dosage compensation
• Tsix

{{Reflist|33em}}

{{Refbegin|33em}}

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{{Refend}}

• [https://www.ncbi.nlm.nih.gov/nuccore/37704377 NCBI Xist entry]
• [http://www.lncrnadb.org/xist/ lncRNAdb Xist entry] {{Webarchive|url=https://web.archive.org/web/20151222120604/http://www.lncrnadb.org/xist/ |date=2015-12-22 }}

Category:Non-coding RNA

Category:Sex-determination systems