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Journal articles on the topic 'X-chromosome inactivation'

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Published: 4 June 2021

Last updated: 25 July 2025

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1

Sado, Takashi, and Takehisa Sakaguchi. "Species-specific differences in X chromosome inactivation in mammals." REPRODUCTION 146, no. 4 (2013): R131—R139. http://dx.doi.org/10.1530/rep-13-0173.

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In female mammals, the dosage difference in X-linked genes between XX females and XY males is compensated for by inactivating one of the two X chromosomes during early development. Since the discovery of the X inactive-specific transcript (XIST) gene in humans and its subsequent isolation of the mouse homolog, Xist, in the early 1990s, the molecular basis of X chromosome inactivation (X-inactivation) has been more fully elucidated using genetically manipulated mouse embryos and embryonic stem cells. Studies on X-inactivation in other mammals, although limited when compared with those in the mi

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2

Cattanach, Bruce M., and Colin V. Beechey. "Autosomal and X-chromosome imprinting." Development 108, Supplement (1990): 63–72. http://dx.doi.org/10.1242/dev.108.supplement.63.

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Mouse genetic studies using Robertsonian and reciprocal translations have shown that certain autosomal regions of loci are subject to a parental germ line imprint, which renders maternal and paternal copies functionally inequivalent in the embryo or later stages of development. Duplication of maternal or paternal copies with corresponding paternal/maternal deficiencies in chromosomally balanced zygotes causes various effects. These range from early embryonic lethalities through to mid-fetal and neonatal lethalities, and in some instances viable young with phenotypic effects are obtained. Eight

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3

Rastan, Sohaila, and Elizabeth J. Robertson. "X-chromosome deletions in embryo-derived (EK) cell lines associated with lack of X-chromosome inactivation." Development 90, no. 1 (1985): 379–88. http://dx.doi.org/10.1242/dev.90.1.379.

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The predictions of a model for the initiation of X-chromosome inactivation based on a single inactivation centre were tested in a cytogenetic study using six different embryo-derived (EK) stem cell lines, each with a different-sized deletion of the distal part of one of the X-chromosomes. Metaphase chromosomes were prepared by the Kanda method from each cell line in the undifferentiated state and after induction of differentiation, and cytogenetic evidence sought for a dark-staining inactive X-chromosome. The results confirm the predictions of the model in that when the inactivation centre is

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4

Malcore, Rebecca M., and Sundeep Kalantry. "A Comparative Analysis of Mouse Imprinted and Random X-Chromosome Inactivation." Epigenomes 8, no. 1 (2024): 8. http://dx.doi.org/10.3390/epigenomes8010008.

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The mammalian sexes are distinguished by the X and Y chromosomes. Whereas males harbor one X and one Y chromosome, females harbor two X chromosomes. To equalize X-linked gene expression between the sexes, therian mammals have evolved X-chromosome inactivation as a dosage compensation mechanism. During X-inactivation, most genes on one of the two X chromosomes in females are transcriptionally silenced, thus equalizing X-linked gene expression between the sexes. Two forms of X-inactivation characterize eutherian mammals, imprinted and random. Imprinted X-inactivation is defined by the exclusive

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5

Shevchenko, A. I. "The phenomenon of X chromosome inactivation and human diseases." Genes & Cells 11, no. 2 (2016): 61–69. http://dx.doi.org/10.23868/gc120579.

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In early development, one of the two X chromosomes is randomly inactivated in each somatic cell of female embryos. As a result, women are mosaics that means about a half of their cells bear the active X chromosome inherited from the father, while the genes of the maternally inherited X chromosome are expressed in the other half. Disturbance in the inactivation process during embryogenesis leads to fetal death. Reactivation of the inactive X chromosome in female cells can cause a number of diseases, including cancer and autoimmune disorders. Changes in randomness of X-chromosome inactivation an

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6

Migeon, Barbara R. "X chromosome inactivation." Genome 31, no. 1 (1989): 464. http://dx.doi.org/10.1139/g89-083.

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7

Lyon, Mary F. "X-chromosome inactivation." Current Biology 9, no. 7 (1999): R235—R237. http://dx.doi.org/10.1016/s0960-9822(99)80151-1.

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8

Shevchenko, Alexander I., Elena V. Dementyeva, Irina S. Zakharova, and Suren M. Zakian. "Diverse developmental strategies of X chromosome dosage compensation in eutherian mammals." International Journal of Developmental Biology 63, no. 3-4-5 (2019): 223–33. http://dx.doi.org/10.1387/ijdb.180376as.

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In eutherian mammals, dosage compensation arose to balance X-linked gene expression between sexes and relatively to autosomal gene expression in the evolution of sex chromosomes. Dosage compensation occurs in early mammalian development and comprises X chromosome upregulation and inactivation that are tightly coordinated epigenetic processes. Despite a uniform principle of dosage compensation, mechanisms of X chromosome inactivation and upregulation demonstrate a significant variability depending on sex, developmental stage, cell type, individual, and mammalian species. The review focuses on r

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9

Shevchenko, A. I., I. S. Zakharova, and S. M. Zakian. "The Evolutionary Pathway of X Chromosome Inactivation in Mammals." Acta Naturae 5, no. 2 (2013): 40–53. http://dx.doi.org/10.32607/20758251-2013-5-2-40-53.

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X chromosome inactivation is a complex process that occurs in marsupial and eutherian mammals. The process is thought to have arisen during the differentiation of mammalian sex chromosomes to achieve an equal dosage of X chromosome genes in males and females. The differences in the X chromosome inactivation processes in marsupial and eutherian mammals are considered, and the hypotheses on its origin and evolution are discussed in this review.

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10

Lyon, M. F. "X Chromosome Inactivation and Imprinting." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (1996): 85. http://dx.doi.org/10.1017/s0001566000001148.

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In contrast to the random inactivation of either maternal or paternal X-chromosome in the somatic cells of eutherian mammals, in marsupials the paternal X-chromosome is preferentially inactivated in all cells. Similar exclusively paternal X-inactivation occurs in two extraembryonic cell lineages of mice and rats. Thus, genetic imprinting is an important feature of X-inactivation. In embryonic development the initiation of X-inactivation is thought to occur through the X-inactivation centre, located on the X-Chromosome, and thus imprinting probably acts through this centre. A candidate gene for

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11

Watson, JM. "Monotreme Genetics and Cytology and a Model for Sex-Chromosome Evolution." Australian Journal of Zoology 37, no. 3 (1989): 385. http://dx.doi.org/10.1071/zo9890385.

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The protherian mammals consist of three species: the platypus, the Australian echidna and the Niugini echidna. These mammals diverged from the therian line of descent about 150-200 million years ago; hence comparisons of gene arrangements and gene control mechanisms between prototherian and therian mammals may yield significant data about gene rearrangements during mammalian evolution and about the evolution of complex genetic control systems. The chromosome complements of the three monotreme species are highly conserved. In particular, the X (or X1) chromosomes are G-band identical and share

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12

Monk, Marilyn, and Mark Grant. "Preferential X-chromosome inactivation, DNA methylation and imprinting." Development 108, Supplement (1990): 55–62. http://dx.doi.org/10.1242/dev.108.supplement.55.

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Non-random X-chromosome inactivation in mammals was one of the first observed examples of differential expression dependent on the gamete of origin of the genetic material. The paternally-inherited X chromosome is preferentially inactive in all cells of female marsupials and in the extra-embryonic tissues of developing female rodents. Some form of parental imprinting during male and female gametogenesis must provide a recognition signal that determines the nonrandomness of X-inactivation but its nature is thus far unknown. In the mouse, the imprint distinguishing the X chromosomes in the extra

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13

Clemson, Christine Moulton, Jennifer C. Chow, Carolyn J. Brown, and Jeanne Bentley Lawrence. "Stabilization and Localization of Xist RNA are Controlled by Separate Mechanisms and are Not Sufficient for X Inactivation." Journal of Cell Biology 142, no. 1 (1998): 13–23. http://dx.doi.org/10.1083/jcb.142.1.13.

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These studies address whether XIST RNA is properly localized to the X chromosome in somatic cells where human XIST expression is reactivated, but fails to result in X inactivation (Tinker, A.V., and C.J. Brown. 1998. Nucl. Acids Res. 26:2935–2940). Despite a nuclear RNA accumulation of normal abundance and stability, XIST RNA does not localize in reactivants or in naturally inactive human X chromosomes in mouse/ human hybrid cells. The XIST transcripts are fully stabilized despite their inability to localize, and hence XIST RNA localization can be uncoupled from stabilization, indicating that

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14

Tukiainen, Taru, Alexandra-Chloé Villani, Angela Yen, et al. "Landscape of X chromosome inactivation across human tissues." Nature 550, no. 7675 (2017): 244–48. http://dx.doi.org/10.1038/nature24265.

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Abstract X chromosome inactivation (XCI) silences transcription from one of the two X chromosomes in female mammalian cells to balance expression dosage between XX females and XY males. XCI is, however, incomplete in humans: up to one-third of X-chromosomal genes are expressed from both the active and inactive X chromosomes (Xa and Xi, respectively) in female cells, with the degree of ‘escape’ from inactivation varying between genes and individuals1,2. The extent to which XCI is shared between cells and tissues remains poorly characterized3,4, as does the degree to which incomplete XCI manifes

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15

Viera, Alberto, María Teresa Parra, Sara Arévalo, Carlos García de la Vega, Juan Luis Santos, and Jesús Page. "X Chromosome Inactivation during Grasshopper Spermatogenesis." Genes 12, no. 12 (2021): 1844. http://dx.doi.org/10.3390/genes12121844.

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Regulation of transcriptional activity during meiosis depends on the interrelated processes of recombination and synapsis. In eutherian mammal spermatocytes, transcription levels change during prophase-I, being low at the onset of meiosis but highly increased from pachytene up to the end of diplotene. However, X and Y chromosomes, which usually present unsynapsed regions throughout prophase-I in male meiosis, undergo a specific pattern of transcriptional inactivation. The interdependence of synapsis and transcription has mainly been studied in mammals, basically in mouse, but our knowledge in

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16

Lyon, Mary F. "Do LINEs Have a Role in X-Chromosome Inactivation?" Journal of Biomedicine and Biotechnology 2006 (2006): 1–6. http://dx.doi.org/10.1155/jbb/2006/59746.

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There is longstanding evidence that X-chromosome inactivation (XCI) travels less successfully in autosomal than in X-chromosomal chromatin. The interspersed repeat elements LINE1s (L1s) have been suggested as candidates for “boosters” which promote the spread of XCI in the X-chromosome. The present paper reviews the current evidence concerning the possible role of L1s in XCI. Recent evidence, accruing from the human genome sequencing project and other sources, confirms that mammalian X-chromosomes are indeed rich in L1s, except in regions where there are many genes escaping XCI. The density of

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17

Zlotorynski, Eytan. "X-chromosome inactivation unravelled." Nature Reviews Molecular Cell Biology 16, no. 6 (2015): 325. http://dx.doi.org/10.1038/nrm3998.

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18

Rougeulle, Claire. "Inactivation du chromosome X." médecine/sciences 25, no. 3 (2009): 234–35. http://dx.doi.org/10.1051/medsci/2009253234.

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Zlotorynski, Eytan. "X chromosome inactivation unravelled." Nature Reviews Genetics 16, no. 6 (2015): 315. http://dx.doi.org/10.1038/nrg3955.

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20

Augui, Sandrine, and Edith Heard. "Inactivation du chromosome X." médecine/sciences 24, no. 6-7 (2008): 584–85. http://dx.doi.org/10.1051/medsci/20082467584.

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SCIALDONE, ANTONIO, and MARIO NICODEMI. "STATISTICAL MECHANICS MODELS FOR X-CHROMOSOME INACTIVATION." Advances in Complex Systems 13, no. 03 (2010): 367–76. http://dx.doi.org/10.1142/s0219525910002566.

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We present statistical mechanics models to understand the physical and molecular mechanisms of X-Chromosome Inactivation (XCI), the process whereby a female mammal cell inactivates one of its two X-chromosomes. During XCI, X-chromosomes undergo a series of complex regulatory processes. At the beginning of XCI, the X's recognize and pair, then only one X which is randomly chosen is inactivated. Afterwards, the two X's move to different positions in the cell nucleus according to their different status (active/silenced). Our models illustrate about the still mysterious physical bases underlying a

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22

Sarel-Gallily, Roni, and Nissim Benvenisty. "Large-Scale Analysis of X Inactivation Variations between Primed and Naïve Human Embryonic Stem Cells." Cells 11, no. 11 (2022): 1729. http://dx.doi.org/10.3390/cells11111729.

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X chromosome inactivation is a mammalian dosage compensation mechanism, where one of two X chromosomes is randomly inactivated in female cells. Previous studies have suggested that primed human embryonic stem cells (hESCs) maintain an eroded state of the X chromosome and do not express XIST, while in naïve transition, both XIST and the eroded X chromosome are reactivated. However, the pattern of chromosome X reactivation in naïve hESCs remains mainly unknown. In this study, we examine the variations in the status of X chromosome between primed and naïve hESCs by analyzing RNA sequencing sample

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23

Goto, Tetsuya, and Marilyn Monk. "Regulation of X-Chromosome Inactivation in Development in Mice and Humans." Microbiology and Molecular Biology Reviews 62, no. 2 (1998): 362–78. http://dx.doi.org/10.1128/mmbr.62.2.362-378.1998.

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SUMMARY Dosage compensation for X-linked genes in mammals is accomplished by inactivating one of the two X chromosomes in females. X-chromosome inactivation (XCI) occurs during development, coupled with cell differentiation. In somatic cells, XCI is random, whereas in extraembryonic tissues, XCI is imprinted in that the paternally inherited X chromosome is preferentially inactivated. Inactivation is initiated from an X-linked locus, the X-inactivation center (Xic), and inactivity spreads along the chromosome toward both ends. XCI is established by complex mechanisms, including DNA methylation,

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Debrand, E., C. Chureau, D. Arnaud, P. Avner, and E. Heard. "Functional Analysis of the DXPas34Locus, a 3′ Regulator of Xist Expression." Molecular and Cellular Biology 19, no. 12 (1999): 8513–25. http://dx.doi.org/10.1128/mcb.19.12.8513.

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ABSTRACT X inactivation in female mammals is controlled by a key locus on the X chromosome, the X-inactivation center (Xic). The Xic controls the initiation and propagation of inactivation in cis. It also ensures that the correct number of X chromosomes undergo inactivation (counting) and determines which X chromosome becomes inactivated (choice). The Xist gene maps to the Xic region and is essential for the initiation of X inactivation in cis. Regulatory elements of X inactivation have been proposed to lie 3′ toXist. One such element, lying 15 kb downstream ofXist, is the DXPas34 locus, which

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Lu, Zhipeng, Ava C. Carter, and Howard Y. Chang. "Mechanistic insights in X-chromosome inactivation." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1733 (2017): 20160356. http://dx.doi.org/10.1098/rstb.2016.0356.

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X-chromosome inactivation (XCI) is a critical epigenetic mechanism for balancing gene dosage between XY males and XX females in eutherian mammals. A long non-coding RNA (lncRNA), XIST, and its associated proteins orchestrate this multi-step process, resulting in the inheritable silencing of one of the two X-chromosomes in females. The XIST RNA is large and complex, exemplifying the unique challenges associated with the structural and functional analysis of lncRNAs. Recent technological advances in the analysis of macromolecular structure and interactions have enabled us to systematically disse

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26

AI, Ibraimov. "X-chromosome inactivation: dosage compensation of genes or heterochromatin?" International Journal Of Biology And Medicine 1, no. 1 (2019): 75–87. https://doi.org/10.36811/ijbm.2019.110010.

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X-chromosome inactivation (XCI) is the process by which one of two X chromosomes in mammalian female cells is inactivated. The DNA of the inactive X chromosome is packaged in transcriptionally inactive heterochromatin. It is generally accepted that XCI have evolved to enable dosage compensation in mammals as a way to equalize X-linked gene expression between XX and XY individuals. However, there remain several controversial issues regarding the causes of XCI. The most important of them, why dosage compensation of genes? An alternative hypothesis is discussed that XCI is caused by dose compensa

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Cooper, DW, PG Johnston, JL Vandeberg, and ES Robinson. "X-Chromosome Inactivation in Marsupials." Australian Journal of Zoology 37, no. 3 (1989): 411. http://dx.doi.org/10.1071/zo9890411.

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Marsupial (metatherian) mammals resemble their eutherian ('placental') counterparts in having inacti- vation of one of the two X chromosomes in the soma and premeiotic germ cells of their females. The marsupial X-inactivation system differs from the eutherian system in two respects: firstly, inactivation occurs for the paternally derived allele, i.e. it is not random, and secondly it is often incomplete. Data are available for four X-linked loci, all controlling enzyme structure: glucose-6- phosphate dehydrogenase (G6PD), phosphoglycerate kinase 1 (PGKl), alpha-galactosidase (GLA) and hypoxant

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Panova, A. V., E. D. Nekrasov, M. A. Lagarkova, S. L. Kiselev, and A. N. Bogomazova. "Late Replication of the Inactive X Chromosome Is Independent of the Compactness of Chromosome Territory in Human Pluripotent Stem Cells." Acta Naturae 5, no. 2 (2013): 54–61. http://dx.doi.org/10.32607/20758251-2013-5-2-54-61.

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Dosage compensation of the X chromosomes in mammals is performed via the formation of facultative heterochromatin on extra X chromosomes in female somatic cells. Facultative heterochromatin of the inactivated X (Xi), as well as constitutive heterochromatin, replicates late during the S-phase. It is generally accepted that Xi is always more compact in the interphase nucleus. The dense chromosomal folding has been proposed to define the late replication of Xi. In contrast to mouse pluripotent stem cells (PSCs), the status of X chromosome inactivation in human PSCs may vary significantly. Fluores

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Tada, T., Y. Obata, M. Tada, et al. "Imprint switching for non-random X-chromosome inactivation during mouse oocyte growth." Development 127, no. 14 (2000): 3101–5. http://dx.doi.org/10.1242/dev.127.14.3101.

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In mammals, X-chromosome inactivation occurs in all female cells, leaving only a single active X chromosome. This serves to equalise the dosage of X-linked genes in male and female cells. In the mouse, the paternally derived X chromosome (X(P)) is imprinted and preferentially inactivated in the extraembryonic tissues whereas in the embryonic tissues inactivation is random. To investigate how X(P) is chosen as an inactivated X chromosome in the extraembryonic cells, we have produced experimental embryos by serial nuclear transplantation from non-growing (ng) oocytes and fully grown (fg) oocytes

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Chaumeil, Julie, and Céline Morey. "Régulation du chromosome X et spécificités fonctionnelles des cellules femelles." médecine/sciences 40, no. 12 (2024): 935–46. https://doi.org/10.1051/medsci/2024179.

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Et si posséder deux chromosomes X conférait aux cellules femelles des spécificités exclusives et expliquait les différences de susceptibilité des hommes et des femmes à certaines maladies ? Pourtant, l’un des chromosomes X est réprimé aléatoirement dans chaque cellule femelle dès le stade embryonnaire, ce qui, théoriquement, remet les sexes à égalité. Cette inactivation du chromosome X est un processus épigénétique unique : elle agit à l’échelle d’un chromosome entier et aboutit à un mosaïcisme d’expression des gènes du chromosome X au niveau de l’organisme. Cependant certains gènes échappent

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Jayaweera, Sanduni, Lakmal Gonawala, Nalaka Wijekoon, and Ranil de Silva. "Up to Date Discoveries of X Chromosome Inactivation in Humans Leading to Prospective Treatments for Chromosome-linked Disorders." International Journal of Biomedical Science 14, no. 2 (2018): 48–56. http://dx.doi.org/10.59566/ijbs.2018.14048.

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Mammalian dosage compensation is a complex mechanism allowing inactivation of single X chromosome of the female to compensate to that of the X chromosome of the male. The mechanism includes many long non-coding RNA; mainly XIST, a noncoding RNA which coats the X chromosome to be inactivated and TSIX, another noncoding RNA act as a negative regulator of XIST preventing inactivation of the second X chromosome. Both XIST and TSIX and several other transcription factors along with polycomb proteins (PRC) work together in controlling the inactivation of one X chromosome while the other X chromosome

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Furlan, Giulia, and Rafael Galupa. "Mechanisms of Choice in X-Chromosome Inactivation." Cells 11, no. 3 (2022): 535. http://dx.doi.org/10.3390/cells11030535.

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Early in development, placental and marsupial mammals harbouring at least two X chromosomes per nucleus are faced with a choice that affects the rest of their lives: which of those X chromosomes to transcriptionally inactivate. This choice underlies phenotypical diversity in the composition of tissues and organs and in their response to the environment, and can determine whether an individual will be healthy or affected by an X-linked disease. Here, we review our current understanding of the process of choice during X-chromosome inactivation and its implications, focusing on the strategies evo

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Rougeulle, Claire, Julie Chaumeil, Kavitha Sarma, et al. "Differential Histone H3 Lys-9 and Lys-27 Methylation Profiles on the X Chromosome." Molecular and Cellular Biology 24, no. 12 (2004): 5475–84. http://dx.doi.org/10.1128/mcb.24.12.5475-5484.2004.

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ABSTRACT Histone H3 tail modifications are among the earliest chromatin changes in the X-chromosome inactivation process. In this study we investigated the relative profiles of two important repressive marks on the X chromosome: methylation of H3 lysine 9 (K9) and 27 (K27). We found that both H3K9 dimethylation and K27 trimethylation characterize the inactive X in somatic cells and that their relative kinetics of enrichment on the X chromosome as it undergoes inactivation are similar. However, dynamic changes of H3K9 and H3K27 methylation on the inactivating X chromosome compared to the rest o

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Rastan, S., and S. D. M. Brown. "The search for the mouse X-chromosome inactivation centre." Genetics Research 56, no. 2-3 (1990): 99–106. http://dx.doi.org/10.1017/s0016672300035163.

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SummaryThe phenomenon of X-chromosome inactivation in female mammals, whereby one of the two X chromosome present in each cell of the female embryo is inactivated early in development, was first described by Mary Lyon in 1961. Nearly 30 years later, the mechanism of X-chromosome inactivation remains unknown. Strong evidence has accumulated over the years, however, for the involvement of a major switch or inactivation centre on the mouse X chromosome. Identification of the inactivation centre at the molecular level would be an important step in understanding the mechanism of X-inactivation. In

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Homolka, D., R. Ivanek, J. Capkova, P. Jansa, and J. Forejt. "Chromosomal rearrangement interferes with meiotic X chromosome inactivation." Genome Research 17, no. 10 (2007): 1431–37. http://dx.doi.org/10.1101/gr.6520107.

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de Hoon, B., Erik Splinter, B. Eussen, et al. "X chromosome inactivation in a female carrier of a 1.28 Mb deletion encompassing the human X inactivation centre." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1733 (2017): 20160359. http://dx.doi.org/10.1098/rstb.2016.0359.

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X chromosome inactivation (XCI) is a mechanism specifically initiated in female cells to silence one X chromosome, thereby equalizing the dose of X-linked gene products between male and female cells. XCI is regulated by a locus on the X chromosome termed the X-inactivation centre (XIC). Located within the XIC is XIST , which acts as a master regulator of XCI. During XCI, XIST is upregulated on the inactive X chromosome and chromosome-wide cis spreading of XIST leads to inactivation. In mouse, the Xic comprises Xist and all cis -regulatory elements and genes involved in Xist regulation. The act

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Lobo, Nunes, Gillis, et al. "XIST-Promoter Demethylation as Tissue Biomarker for Testicular Germ Cell Tumors and Spermatogenesis Quality." Cancers 11, no. 9 (2019): 1385. http://dx.doi.org/10.3390/cancers11091385.

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Background: The event of X chromosome inactivation induced by XIST, which is physiologically observed in females, is retained in testicular germ cell tumors (TGCTs), as a result of a supernumerary X chromosome constitution. X chromosome inactivation also occurs in male germline, specifically during spermatogenesis. We aimed to analyze the promoter methylation status of XIST in a series of TGCT tissues, representative cell lines, and testicular parenchyma. Methods: Two independent cohorts were included, comprising a total of 413 TGCT samples, four (T)GCT cell lines, and 86 testicular parenchyma

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Chen, George L., and Josef T. Prchal. "X-linked clonality testing: interpretation and limitations." Blood 110, no. 5 (2007): 1411–19. http://dx.doi.org/10.1182/blood-2006-09-018655.

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Abstract Clonality often defines the diseased state in hematology. Clonal cells are genetically homogenous and derived from the same precursor; their detection is based on genotype or phenotype. Genotypic clonality relies on somatic mutations to mark the clonal population. Phenotypic clonality identifies the clonal population by the expression pattern of surrogate genes that track the clonal process. The most commonly used phenotypic clonality methods are based on the X-chromosome inactivation principle. Clonality detection based on X-chromosome inactivation patterns (XCIP) requires discrimina

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Sado, Takashi, and Neil Brockdorff. "Advances in understanding chromosome silencing by the long non-coding RNA Xist." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1609 (2013): 20110325. http://dx.doi.org/10.1098/rstb.2011.0325.

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In female mammals, one of the two X chromosomes becomes genetically silenced to compensate for dosage imbalance of X-linked genes between XX females and XY males. X chromosome inactivation (X-inactivation) is a classical model for epigenetic gene regulation in mammals and has been studied for half a century. In the last two decades, efforts have been focused on the X inactive-specific transcript ( Xist ) locus, discovered to be the master regulator of X-inactivation. The Xist gene produces a non-coding RNA that functions as the primary switch for X-inactivation, coating the X chromosome from w

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Sahakyan, Anna, Kathrin Plath, and Claire Rougeulle. "Regulation of X-chromosome dosage compensation in human: mechanisms and model systems." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1733 (2017): 20160363. http://dx.doi.org/10.1098/rstb.2016.0363.

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The human blastocyst forms 5 days after one of the smallest human cells (the sperm) fertilizes one of the largest human cells (the egg). Depending on the sex-chromosome contribution from the sperm, the resulting embryo will either be female, with two X chromosomes (XX), or male, with an X and a Y chromosome (XY). In early development, one of the major differences between XX female and XY male embryos is the conserved process of X-chromosome inactivation (XCI), which compensates gene expression of the two female X chromosomes to match the dosage of the single X chromosome of males. Most of our

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Heard, Edith, and Claire Rougeulle. "Digging into X chromosome inactivation." Science 374, no. 6570 (2021): 942–43. http://dx.doi.org/10.1126/science.abm1857.

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42

Chang, Samuel, C. "Mechanisms of X-chromosome inactivation." Frontiers in Bioscience 11, no. 1 (2006): 852. http://dx.doi.org/10.2741/1842.

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43

Kay, Graham F. "Xist and X chromosome inactivation." Molecular and Cellular Endocrinology 140, no. 1-2 (1998): 71–76. http://dx.doi.org/10.1016/s0303-7207(98)00032-x.

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44

Brooks, Wesley H. "X Chromosome Inactivation and Autoimmunity." Clinical Reviews in Allergy & Immunology 39, no. 1 (2009): 20–29. http://dx.doi.org/10.1007/s12016-009-8167-5.

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DISTECHE, CHRISTINE M., and JOEL B. BERLETCH. "X-chromosome inactivation and escape." Journal of Genetics 94, no. 4 (2015): 591–99. http://dx.doi.org/10.1007/s12041-015-0574-1.

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46

Heard, Edith, Philippe Clerc, and Philip Avner. "X-CHROMOSOME INACTIVATION IN MAMMALS." Annual Review of Genetics 31, no. 1 (1997): 571–610. http://dx.doi.org/10.1146/annurev.genet.31.1.571.

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47

Liehr, Thomas, Monika Ziegler, Sharon Löhmer, and Anja Weise. "Assessing Skewed X-Chromosome Inactivation." Current Protocols in Human Genetics 98, no. 1 (2018): e66. http://dx.doi.org/10.1002/cphg.66.

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48

McBurney, Michael W. "X chromosome inactivation: A hypothesis." BioEssays 9, no. 2-3 (1988): 85–88. http://dx.doi.org/10.1002/bies.950090211.

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49

Basrur, P. K., L. E. L. Pinheiro, N. A. Berepubo, E. R. Reyes, and P. C. Popescu. "X chromosome inactivation in X autosome translocation carrier cows." Genome 35, no. 4 (1992): 667–75. http://dx.doi.org/10.1139/g92-101.

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The pattern of X chromosome inactivation in X autosome translocation carriers in a herd of Limousin–Jersey crossbred cattle was studied using the reverse banding technique consisting of 5-bromodeoxyuridine incorporation and acridine orange staining and autoradiography on cultures of solid tissues and blood samples exposed to tritiated thymidine. The late-replicating X chromosome was noted to be the normal X in strikingly high proportions of cells in cultures of different tissues from all translocation carriers. It is suggested that the predominance of cells in which the normal X is inactivated

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50

O'Neill, Laura P., Hugh T. Spotswood, Milan Fernando, and Bryan M. Turner. "Differential loss of histone H3 isoforms mono-, di- and tri-methylated at lysine 4 during X-inactivation in female embryonic stem cells." Biological Chemistry 389, no. 4 (2008): 365–70. http://dx.doi.org/10.1515/bc.2008.046.

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Abstract Silencing of genes on one of the two female X chromosomes early in development helps balance expression of X-linked genes between XX females and XY males and involves chromosome-wide changes in histone variants and modifications. Mouse female embryonic stem (ES) cells have two active Xs, one of which is silenced on differentiation, and provide a powerful model for studying the dynamics of X inactivation. Here, we use immunofluorescence microscopy of metaphase chromosomes to study changes in H3 mono-, di- or tri-methylated at lysine 4 (H3K4me1, -2 or -3) on the inactivating X (Xi) in f

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