Relevant bibliographies by topics / X and Y chromosomes

Academic literature on the topic 'X and Y chromosomes'

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Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "X and Y chromosomes"

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McAllister, Bryant F. "Sequence Differentiation Associated With an Inversion on the Neo-X Chromosome of Drosophila americana." Genetics 165, no. 3 (November 1, 2003): 1317–28. http://dx.doi.org/10.1093/genetics/165.3.1317.

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Abstract Sex chromosomes originate from pairs of autosomes that acquire controlling genes in the sex-determining cascade. Universal mechanisms apparently influence the evolution of sex chromosomes, because this chromosomal pair is characteristically heteromorphic in a broad range of organisms. To examine the pattern of initial differentiation between sex chromosomes, sequence analyses were performed on a pair of newly formed sex chromosomes in Drosophila americana. This species has neo-sex chromosomes as a result of a centromeric fusion between the X chromosome and an autosome. Sequences were analyzed from the Alcohol dehydrogenase (Adh), big brain (bib), and timeless (tim) gene regions, which represent separate positions along this pair of neo-sex chromosomes. In the northwestern range of the species, the bib and Adh regions exhibit significant sequence differentiation for neo-X chromosomes relative to neo-Y chromosomes from the same geographic region and other chromosomal populations of D. americana. Furthermore, a nucleotide site defining a common haplotype in bib is shown to be associated with a paracentric inversion [In(4)ab] on the neo-X chromosome, and this inversion suppresses recombination between neo-X and neo-Y chromosomes. These observations are consistent with the inversion acting as a recombination modifier that suppresses exchange between these neo-sex chromosomes, as predicted by models of sex chromosome evolution.
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Gillings, M. R., R. Frankham, J. Speirs, and M. Whalley. "X-Y Exchange and the Coevolution of the X and Y rDNA Arrays in Drosophila melanogaster." Genetics 116, no. 2 (June 1, 1987): 241–51. http://dx.doi.org/10.1093/genetics/116.2.241.

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ABSTRACT The nucleolus organizers on the X and Y chromosomes of Drosophila melanogaster are the sites of 200-250 tandemly repeated genes for ribosomal RNA. As there is no meiotic crossing over in male Drosophila, the X and Y chromosomal rDNA arrays should be evolutionarily independent, and therefore divergent. The rRNAs produced by X and Y are, however, very similar, if not identical. Molecular, genetic and cytological analyses of a series of X chromosome rDNA deletions (bb alleles) showed that they arose by unequal exchange through the nucleolus organizers of the X and Y chromosomes. Three separate exchange events generated compound X·YL chromosomes carrying mainly Y-specific rDNA. This led to the hypothesis that X-Y exchange is responsible for the coevolution of X and Y chromosomal rDNA. We have tested and confirmed several of the predictions of this hypothesis: First, X·YL chromosomes must be found in wild populations. We have found such a chromosome. Second, the X·YL chromosome must lose the YL arm, and/or be at a selective disadvantage to normal X+ chromosomes, to retain the normal morphology of the X chromosome. Six of seventeen sublines founded from homozygous X·YLbb stocks have become fixed for chromosomes with spontaneous loss of part or all of the appended YL. Third, rDNA variants on the X chromosome are expected to be clustered within the X+ nucleolus organizer, recently donated ("Y") forms being proximal, and X-specific forms distal. We present evidence for clustering of rRNA genes containing Type 1 insertions. Consequently, X-Y exchange is probably responsible for the coevolution of X and Y rDNA arrays.
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Uno, Yoshinobu, Chizuko Nishida, Chiyo Takagi, Takeshi Igawa, Naoto Ueno, Masayuki Sumida, and Yoichi Matsuda. "Extraordinary Diversity in the Origins of Sex Chromosomes in Anurans Inferred from Comparative Gene Mapping." Cytogenetic and Genome Research 145, no. 3-4 (2015): 218–29. http://dx.doi.org/10.1159/000431211.

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Sex determination in frogs (anurans) is genetic and includes both male and female heterogamety. However, the origins of the sex chromosomes and their differentiation processes are poorly known. To investigate diversity in the origins of anuran sex chromosomes, we compared the chromosomal locations of sex-linked genes in 4 species: the African clawed frog (Xenopus laevis), the Western clawed frog (Silurana/X. tropicalis), the Japanese bell-ring frog (Buergeria buergeri), and the Japanese wrinkled frog (Rana rugosa). Comparative mapping data revealed that the sex chromosomes of X. laevis, X. tropicalis and R. rugosa are different chromosome pairs; however, the sex chromosomes of X. tropicalis and B. buergeri are homologous, although this may represent distinct evolutionary origins. We also examined the status of sex chromosomal differentiation in B. buergeri, which possesses heteromorphic ZW sex chromosomes, using comparative genomic hybridization and chromosome painting with DNA probes from the microdissected W chromosome. At least 3 rearrangement events have occurred in the proto-W chromosome: deletion of the nucleolus organizer region and a paracentric inversion followed by amplification of non-W-specific repetitive sequences.
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Röpke, Albrecht, and Frank Tüttelmann. "MECHANISMS IN ENDOCRINOLOGY: Aberrations of the X chromosome as cause of male infertility." European Journal of Endocrinology 177, no. 5 (November 2017): R249—R259. http://dx.doi.org/10.1530/eje-17-0246.

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Male infertility is most commonly caused by spermatogenetic failure, clinically noted as oligo- or a-zoospermia. Today, in approximately 20% of azoospermic patients, a causal genetic defect can be identified. The most frequent genetic causes of azoospermia (or severe oligozoospermia) are Klinefelter syndrome (47,XXY), structural chromosomal abnormalities and Y-chromosomal microdeletions. Consistent with Ohno’s law, the human X chromosome is the most stable of all the chromosomes, but contrary to Ohno’s law, the X chromosome is loaded with regions of acquired, rapidly evolving genes, which are of special interest because they are predominantly expressed in the testis. Therefore, it is not surprising that the X chromosome, considered as the female counterpart of the male-associated Y chromosome, may actually play an essential role in male infertility and sperm production. This is supported by the recent description of a significantly increased copy number variation (CNV) burden on both sex chromosomes in infertile men and point mutations in X-chromosomal genes responsible for male infertility. Thus, the X chromosome seems to be frequently affected in infertile male patients. Four principal X-chromosomal aberrations have been identified so far: (1) aneuploidy of the X chromosome as found in Klinefelter syndrome (47,XXY or mosaicism for additional X chromosomes). (2) Translocations involving the X chromosome, e.g. nonsyndromic 46,XX testicular disorders of sex development (XX-male syndrome) or X-autosome translocations. (3) CNVs affecting the X chromosome. (4) Point mutations disrupting X-chromosomal genes. All these are reviewed herein and assessed concerning their importance for the clinical routine diagnostic workup of the infertile male as well as their potential to shape research on spermatogenic failure in the next years.
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Willhoeft, Ute, Jutta Mueller-Navia, and Gerald Franz. "Analysis of the sex chromosomes of the Mediterranean fruit fly by microdissected DNA probes." Genome 41, no. 1 (February 1, 1998): 74–78. http://dx.doi.org/10.1139/g97-102.

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In the Mediterranean fruit fly, Ceratitis capitata, the sex-determining region maps to the long arm of the Y chromosome. DNA from this region of the Y chromosome and, for comparison, from the tip of the long arm of the X chromosome, was isolated by microdissection and amplified by degenerate oligonucleotide primer PCR (DOP-PCR). FISH of the Y-chromosomal microdissection products medY1-medY5 to mitotic chromosomes revealed hybridization signals on most of the long arm of the Y chromosome, including the male-determining region, and on the long arm of the X chromosome, as well as weaker signals on the autosomes, some of which were located in the heterochromatin next to the centromeres. The X-chromosomal microdissected probe medX1 revealed strong signals on the sex chromosomes and randomly distributed signals on the autosomes. Chromosomal in situ suppression hybridization indicates that the Y chromosome contains considerable amounts of Y-enriched and Y-specific sequences and that X-enriched sequences are present on the long arm of the X chromosome. The microdissected probes medY1, medY2, and medX1 hybridize to the sex chromosomes of two closely related species,Ceratitis rosa and Trirhithrum coffeae.
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Mahesh, G., N. B. Ramachandra, and H. A. Ranganath. "Autoradiographic study of transcription and dosage compensation in the sex and neo-sex chromosome of Drosophila nasuta nasuta and Drosophila nasuta albomicans." Genome 44, no. 1 (February 1, 2001): 71–78. http://dx.doi.org/10.1139/g00-100.

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Cellular autoradiography is used to study the transcription patterns of the polytene X chromosomes in Drosophila nasuta nasuta and D. n. albomicans. D. n. nasuta, with 2n = 8, includes a pair of complete heteromorphic sex chromosomes, whereas D. n. albomicans, with 2n = 6, has a pair of metacentric neo-sex chromosomes representing incomplete heteromorphic sex chromosomes. The neo-X chromosome has two euchromatic arms, one representing the ancestral X while the other represents the ancestral autosome 3 chromosomes. The metacentric neo-Y chromosome has one arm with a complete heterochromatic ancestral Y and the other arm with a euchromatic ancestral autosome 3. The transcription study has revealed that the X chromosome in D. n. nasuta is hyperactive, suggesting complete dosage compensation, while in the neo-X chromosome of D. n. albomicans the ancestral X chromosome is hyperactive and the ancestral autosome 3, which is part of the neo-sex chromosome, is similar to any other autosomes. This finding shows dosage compensation on one arm (XLx/–) of the neo-X chromosome, while the other arm (XR3/YR3) is not dosage compensated and has yet to acquire the dosage compensatory mechanism.Key words: Drosophila, chromosomal races, neo-sex chromosome, transcription and dosage compensation.
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England, P. R., H. W. Stokes, and R. Frankham. "Clustering of rDNA containing type 1 insertion sequence in the distal nucleolus organiser of Drosophila melanogaster: implications for the evolution of X and Y rDNA arrays." Genetical Research 51, no. 3 (June 1988): 209–15. http://dx.doi.org/10.1017/s0016672300024307.

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SummaryThe ribosomal RNAs produced by the multigene families on the X and Y chromosomes of Drosophila melanogaster are very similar despite the apparent evolutionary isolation of the X and Y chromosomal rDNA. X–Y exchange through the rDNA is one mechanism that may promote co-evolution of the two gene clusters by transferring Y rDNA copies to the X chromosome. This hypothesis predicts that the proximal rDNA of X chromosomes will be Y-like. Consequently, rDNA variants found only on the X chromosome (such as those interrupted by type 1 insertions) should be significantly clustered in the distal X nucleolus organizer. Proximal and distal portions of the X chromosome nucleolus organizer were separated by recombination between the inverted chromosomes In(1)scv2 (breakpoint in the centre of the rDNA) and In(1)sc4Lsc8R (no rDNA). Molecular analyses of the resulting stocks demonstrated that rRNA genes containing type 1 insertions were predominantly located on the chromosome carrying the distal portion of the X rDNA, thus confirming a prediction of the X–Y exchange hypothesis for the co-evolution of X and Y chromosomal rDNA. Distal clustering is not predicted by the alternative hypotheses of selection or gene conversion.
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Manicardi, G. C., D. C. Gautam, D. Bizzaro, E. Guicciardi, A. M. Bonvicini Pagliai, and U. Bianchi. "Chromosome banding in aphids: G, C, AluI, and HaeIII banding patterns in Megoura viciae (Homoptera, Aphididae)." Genome 34, no. 4 (August 1, 1991): 661–65. http://dx.doi.org/10.1139/g91-101.

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The holocentric mitotic chromosomes of Megoura viciae, a species that has been little studied cytogenetically to date, have been characterized by applying G, C, AluI, and HaeIII banding techniques. C bands have shown the best defined patterns, particularly on the X chromosome. This chromosome, on the other hand, behaved as the most reactive to the various treatments. Uncondensed, prometaphase X chromosomes showed a number of heterochromatic bands, interspersed among the euchromatin, which fused together during metaphase condensation. AluI and HaeIII treatments also produced reproducible banding patterns. These data permit an accurate identification of the X chromosome as well as of the autosomal pairs 1 and 2, and facilitate the construction of nonambiguous karyotypes. They will also stimulate studies on the organization of chromatin in holocentric, holokinetic chromosomes. Finally they could also promote research on chromosomal rearrangements that have occurred during the course of speciation and evolution of aphids, since these kinds of events may be significantly affected by the condition of chromosomal holocentrism.Key words: aphids, holocentric chromosomes, chromosome banding, heterochromatin.
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McAllister, Bryant F., and Brian Charlesworth. "Reduced Sequence Variability on the NeoY Chromosome of Drosophila americana americana." Genetics 153, no. 1 (September 1, 1999): 221–33. http://dx.doi.org/10.1093/genetics/153.1.221.

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Abstract Sex chromosomes are generally morphologically and functionally distinct, but the evolutionary forces that cause this differentiation are poorly understood. Drosophila americana americana was used in this study to examine one aspect of sex chromosome evolution, the degeneration of nonrecombining Y chromosomes. The primary X chromosome of D. a. americana is fused with a chromosomal element that was ancestrally an autosome, causing this homologous chromosomal pair to segregate with the sex chromosomes. Sequence variation at the Alcohol Dehydrogenase (Adh) gene was used to determine the pattern of nucleotide variation on the neo-sex chromosomes in natural populations. Sequences of Adh were obtained for neo-X and neo-Y chromosomes of D. a. americana, and for Adh of D. a. texana, in which it is autosomal. No significant sequence differentiation is present between the neo-X and neo-Y chromosomes of D. a. americana or the autosomes of D. a. texana. There is a significantly lower level of sequence diversity on the neo-Y chromosome relative to the neo-X in D. a. americana. This reduction in variability on the neo-Y does not appear to have resulted from a selective sweep. Coalescent simulations of the evolutionary transition of an autosome into a Y chromosome indicate there may be a low level of recombination between the neo-X and neo-Y alleles of Adh and that the effective population size of this chromosome may have been reduced below the expected value of 25% of the autosomal effective size, possibly because of the effects of background selection or sexual selection.
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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 (June 15, 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. Fluorescence in situ hybridization with a whole X-chromosome-specific DNA probe revealed that late-replicating Xi may occupy either compact or dispersed territory in human PSCs. Thus, the late replication of the Xi does not depend on the compactness of chromosome territory in human PSCs. However, the Xi reactivation and the synchronization in the replication timing of X chromosomes upon reprogramming are necessarily accompanied by the expansion of X chromosome territory.
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Dissertations / Theses on the topic "X and Y chromosomes"

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Morey, Céline. "Caractérisation du rôle de la région en aval du gène Xist lors de l'inactivation du chromosome X murin par mutagenèse ciblée dans les cellules ES." Paris 5, 2004. http://www.theses.fr/2004PA05N040.

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Chez les mammifères, la compensation de dose des gènes liés à l' X entre les sexes est assurée par l' inactivation transcriptionnelle de l' un des deux chromosomes X, au hasard, chez la femelle. Ce processus dépend des fonctions de comptage et de choix et recquiert l' expression du gène Xist localisé sur le chromosome X. Ce gène produit un grand ARN non-codant qui recouvre le chromosome X inactif. La délétion de 65 kb en aval de Xist, incluant le minisatellite DXPas 34 et l' initiation d' une transcription antisens (Tsix), dans des cellules ES-cellules récapitulant l' inactivation lors de leur différenciation in vitro-induit l'altération du choix et du comptage. Par une stratégie de complémentation cre/oxP, nous avons montré que la restitution de Tsix au site de la délétion de 65 kb dans les cellules XX est insuffisante au rétablissement de l' inactivation aléatoire. . .
In mammals, dosage compensation of X-linked genes is ensured by X-chromosome inactivation wherby one X chromosome in each female embryonic cell (ES) is chosen at random to become silenced. X-inactivation depends on the counting of X chromosomes and on the choice of the inactive X, It is mediated by the expression of the Xist non-coding RNA wich coats the inactive X and by the Tsix antisense transcipt, a Tsix antisense transcript, a Xist regulator. A 65 kb deletion extending 3' to Xist and including both Tsix and the DXPas34 minisatellite, disrupts choice and counting. Using a cre/loxP site-specific re-insertion strategy in XX deleted ES cells we showed that targeting back, at the 65 kb mutated locus, the Tsix antisense transcription fails to retore random X-inactivation. In contrast, normal counting can be restored in XO deleted ES cells. .
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Kayserili, Melek A., Dave T. Gerrard, Pavel Tomancak, and Alex T. Kalinka. "An Excess of Gene Expression Divergence on the X Chromosome in Drosophila Embryos: Implications for the Faster-X Hypothesis." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-180730.

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The X chromosome is present as a single copy in the heterogametic sex, and this hemizygosity is expected to drive unusual patterns of evolution on the X relative to the autosomes. For example, the hemizgosity of the X may lead to a lower chromosomal effective population size compared to the autosomes, suggesting that the X might be more strongly affected by genetic drift. However, the X may also experience stronger positive selection than the autosomes, because recessive beneficial mutations will be more visible to selection on the X where they will spend less time being masked by the dominant, less beneficial allele—a proposal known as the faster-X hypothesis. Thus, empirical studies demonstrating increased genetic divergence on the X chromosome could be indicative of either adaptive or non-adaptive evolution. We measured gene expression in Drosophila species and in D. melanogaster inbred strains for both embryos and adults. In the embryos we found that expression divergence is on average more than 20% higher for genes on the X chromosome relative to the autosomes; but in contrast, in the inbred strains, gene expression variation is significantly lower on the X chromosome. Furthermore, expression divergence of genes on Muller's D element is significantly greater along the branch leading to the obscura sub-group, in which this element segregates as a neo-X chromosome. In the adults, divergence is greatest on the X chromosome for males, but not for females, yet in both sexes inbred strains harbour the lowest level of gene expression variation on the X chromosome. We consider different explanations for our results and conclude that they are most consistent within the framework of the faster-X hypothesis.
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Coultas, Susan L. (Susan Lynette). "A comparison of straight-stained, Q-stained, and reverse flourescent-stained cell lines for detection of fragile sites on the human X chromosome." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc798127/.

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Cell cultures were examined for percentage of fragile sites seen in straight-stained, Q-stained and reverse fluorescent-stained preparations. In all cases, percentage of fragile site expression was decreased when compared to straight-stained preparations. However, fragile sites seen in Q- and RF-stain could be identified as on X chromosomes.
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Turner, Caroline. "Cytogenetic and molecular studies of ring (X) chromosomes." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297376.

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Avery, Mina. "Educational development in individuals with extra X chromosomes." abstract and full text PDF (free order & download UNR users only), 2008. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1460746.

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Hussein, Sultana Muhammad School of Pathology UNSW. "Fragile X mental retardation and fragile X chromosomes in the Indonesian population." Awarded by:University of New South Wales. School of Pathology, 1998. http://handle.unsw.edu.au/1959.4/33198.

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The Indonesian archipelago comprises more than 17,000 islands, inhabited by ~200 million people constituting more than 350 recognizable ethnic and tribal groups which can be classified into two broad ethno-linguistic groups [the Austronesian (AN) and non-Austronesian (NAN) speaking peoples] and 3 physical anthropology groups (Deutero Malay, Proto Malay and Papuan). The origins of these groups are of considerable anthropological interest. The anthropology of Indonesia is extremely complex and still controversial. The present populations of Indonesia show very great diversity. The data presented below result from an investigation of the Fragile X A syndrome and the size and distribution of alleles at fragile sites on the X chromosome among Javanese males with developmental disability (DD) and unselected males from 10 major Indonesian ethnic groups. The Fragile X syndrome is caused by expansion of a CGG trinucleotide repeat array in the 5' untranslated region of the FMR-1 gene at Xq27.3. Normal X chromosomes have between 6-54 CGG trinucleotide repeats, whereas premutation alleles have 55-230 and full mutation alleles more than 230 repeats. In a study of predominantly Caucasian males with intellectual disability, the prevalence of Fragile X syndrome is estimated to be approximately 1:4,000. FRAXE mental retardation syndrome is caused by an expansion of a GCC trinucleotide repeat in the 5'UTR of FMR2 gene located 600 kb telomeric to FMR1. The prevalence of FMR2 is 1-2 per 100,000 live births. FMR2 common alleles consist of 11-30 GGC repeats; intermediate alleles between 31-60 GCC repeats; premutation alleles with 61-200 repeats and full mutation alleles have over 200 repeats with attendant methylation of the repeat array The first Indonesian screening program aimed at determining the presence and prevalence of fragile XA syndrome among individuals with mild DD (IQ above 50) from special schools (N=205) and isolated areas (N=50) of Java was undertaken in 1994-1996 by cytogenetic and molecular studies. In this first study 4 fragile X positive children were found among 255 males with DD. The estimated prevalence of fragile-X in males with mild DD from special schools was 1.95% (5/205) and the overall prevalence was 1.57% (4/255). The number of trinucleotide repeats in the 5' untranslated regions of the FMR1 and FMR2 genes were determined by PCR in 254 Fragile XA-negative Javanese male children with DD. The distribution of FMR1 and FMR2 trinucleotide repeat alleles was found to be significantly different in the Indonesian population with DD compared to that in equivalent Caucasian populations. The trimodal distribution of Indonesian FMR1 alleles (29, 30 and 36 repeats) is largely in agreement with findings from other Asian populations). This provides supportive evidence that the origin of Indonesians could be the same as that of the Chinese and Japanese. Sequence analysis was performed on the trinucleotide repeat arrays of the 27 individuals' FMR1 alleles in the 'grey zone' (35-52 repeats). The identification of 16 unrelated individuals with a (CGG)36 allele that also contains a (CGG)6 segment [(CGG)9AGG(CGG)9AGG(CGG)6 AGG(CGG)9 or 9A9A6A9 pattern] is in agreement with earlier observations in the Japanese population. It is proposed that this FMR1 array pattern may be specific for Asian populations and that Javanese and Japanese populations may have arisen from a single progenitor population. The presence of pure 25, 33 and 34 CGGs in FMR1 alleles with 36, 44 and 45 repeats respectively, suggests that these may represent alleles at high risk for instability and may therefore be at early stages of expansion to a premutation. The lack of the characteristic (CGG)6 in all three alleles with ?? 25 pure CGG arrays suggests that the most common Asian 36 repeat allele is not predisposed to slippage expansion. Seven of the 8 alleles with 36 CGG repeats could be sequenced. Seven of 36 CGG repeats FMR1 alleles from the Hiri population has been sequenced and 4 alleles indicated 9A9A6A9 pattern, 1 sample with 10A25 pattern Two of the remaining alleles showed 12A6A6A9 structure, which consisted of a tandem duplication of the (CGG)6 segment. The presence of a tandem duplication of (CGG)6 segments has never been reported in any other population. The other major findings of this study are that FRAXE syndrome is a rare cause of developmental disability in this predominantly-Javanese population. The most common FMR2 (GCC)20 allele in this selected Asian population is significantly longer than that previously reported for Caucasian populations. There was a weak correlation between the overall length of the FMR1 and FMR2 repeat arrays within the normal range (Spearman's Rank Correlation = 0.130, p-value=0.042) in the Indonesian population, which have been no previous associations reported for alleles within the normal range. One approach to studying the origins of the human populations is to study the genetic structure of polymorphic alleles such as those at the FMR1 locus and its linked microsatellite markers DXS548 and FRAXAC1. Length polymorphisms of the FMR1 gene (CGG)n repeat array, DXS548 and FRAXAC1 were studied in a total of 1,008 unselected males from 10 different Indonesian ethnic groups. FMR1 alleles were identified ranging from 8 to 57 CGG repeats. The most common CGG repeat allele was 29 (45.6%) followed by 30 (27.4%) and 36 repeats (8.0%). One hundred and forty four grey zone (3-52 CGG) alleles were found in the study population. Four people of the same ethnic group from an isolated island in Eastern Indonesia (Hiri, Ternate), a representative of the NAN ethnolinguistic group, had CGG repeat lengths of 55-57. The prevalence of these alleles is estimated to be 3.3% (4/120) in the population of Hiri or 0.4% (4/1008) of whole Indonesian population. Thirteen different alleles were found at the DXS548 locus, of which allele numbers 7 [194 bp] (44.1%), 6.5 [195bp] (43.5%) and 6 [196bp] (7.5%) are the most common. Seven rare alleles, some of which have not been previously found in Asian peoples were also identified (190, 191,192, 193, 197,198, 199, 202, 204 and 206) and accounted for 3.9% of the total. The odd number alleles were dominantly found in this study whereas almost none found in Caucasian. The finding of many "odd numbered" alleles DXS548 has never been found in other Asian population and has only been documented extremely rarely in Caucasians and Africans. Five different alleles of FRAXAC1 identified with alleles D [106 bp] (62.2%) and C [108bp] (35.6%) accounting for 97.8% of FRAXAC1 alleles in the population. Three rare alleles (104, 110, 112 bp = 2.2%) were identified that have not been previously found in other Asian populations (1-3). There is a striking linkage disequilibrium of FMR1 alleles with FRAXAC1 (p=0.0001), 88% of 29 (CGG)n repeats alleles associated with FRAXAC1 allele D (106bp) versus only 17% with the 30 (CGG)n repeat alleles, which is in agreement with other studies. The value of D' was calculated to be 0.7. The longer alleles of both DXS548 and FRAXAC1 were found mostly in the NAN ethnolinguistic group. Moreover the Irian Jaya people also showed a higher percentage of people with 30 CGG repeats and the 108 bp FRAXAC1. The Eastern Indonesian NAN groups demonstrate a different genetic background probably due to the contribution of Melanesian peoples. The Analysis of Molecular Variance (AMOVA) identified that the vast majority of genetic diversity occurs within, rather than between, ethnic groups. These data are consistent with a model where there is sufficient migration (~20 per generation) between populations to minimise differentiation of population through genetic drift. The results obtained are consistent with three clusters of populations that share similar allele frequencies at the fragile X locus. The most clearly defined cluster is based in the east of Indonesia and includes the two Irian populations, Minahasans and Hiri. A surprising finding was that the Minahasan who are Deutero-Malay in origin and physical appearance are genetically closer to the Irianese. This may reflect the admixture of Melanesian alleles or other eastern Indonesian alleles as a result of their geographic location in that part of Indonesia. The second major cluster is largely based in the west of the country and is composed of the following Deutero-Malay populations; Javanese, Balinese, Acehnese but which also includes people from Ternate (not including those from Hiri). Using Delta Mu and Nei's genetic distance for FMR1 locus in this study the Javanese were shown to have the closest distance to Balinese which is consistent with anthropological data and with published data. The third group is a "western and central" group composed of Bimanese, Dayak and Sundanese who share some features of the western and eastern clusters but mostly resemble the western Indonesian populations. Bima is located in the lesser Sunda in between west Indonesia and east Indonesia. The Bimanese are of mixed Deutero & Proto Malay origin that is consistent with their geographic location. The Bataks are distinctive and sit somewhat apart in this scheme. In this study, Bataks were found not to resemble the other Proto-Malay group studied (the Dayak). The Dayaks were found to have fewer alleles than the Bataks at FRAXAC1 and DXS548. In all four methods of calculating genetic distance Bataks showed a large genetic distance to almost all other ethnic groups. There are differences in allele frequency between east and west Indonesia as well as other Asian nations, but the genetic similarities between these groups are also very impressive. The findings from this study are consistent with other genetic anthropological evidence that the people of Indonesia have the same origin as North-east Asian groups. This model is referred to as the "express train from Taiwan" in which the Austronesian speakers are proposed to have radiated from Taiwan bringing the Malayo-Polynesian language group to the Philippines, Borneo and Sulawesi around 5000-4500 B.P.E. However Richards et al.(1998) have used the diversity in the mtDNA D Loop to propose an alternative to the "express train" model. The "two train7quot; model proposes that the Austronesian languages originated within eastern Indonesia during the Pleistocene era and spread through Melanesia and into the remote Pacific within the past 6,000 years. Unfortunately the high migration rates between population groups that were demonstrated in this thesis and the known migration patterns of populations through Indonesia preclude determining whether the observed allelic heterogeneity is a function of the original population or due to the admixture of several gene pools in more recent times.
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Holm, Sofia. "Molecular genetic studies of psoriasis susceptibility in 6p21.3 /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-225-X.

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Khalil, Ahmad M. "Histone modifications and chromatin dynamics of the mammalian inactive sex chromosomes title." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0008329.

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Thesis (Ph.D.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 102 pages. Includes Vita. Includes bibliographical references.
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Kayserili, Melek A., Dave T. Gerrard, Pavel Tomancak, and Alex T. Kalinka. "An Excess of Gene Expression Divergence on the X Chromosome in Drosophila Embryos: Implications for the Faster-X Hypothesis." PLOS, 2012. https://tud.qucosa.de/id/qucosa%3A28925.

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The X chromosome is present as a single copy in the heterogametic sex, and this hemizygosity is expected to drive unusual patterns of evolution on the X relative to the autosomes. For example, the hemizgosity of the X may lead to a lower chromosomal effective population size compared to the autosomes, suggesting that the X might be more strongly affected by genetic drift. However, the X may also experience stronger positive selection than the autosomes, because recessive beneficial mutations will be more visible to selection on the X where they will spend less time being masked by the dominant, less beneficial allele—a proposal known as the faster-X hypothesis. Thus, empirical studies demonstrating increased genetic divergence on the X chromosome could be indicative of either adaptive or non-adaptive evolution. We measured gene expression in Drosophila species and in D. melanogaster inbred strains for both embryos and adults. In the embryos we found that expression divergence is on average more than 20% higher for genes on the X chromosome relative to the autosomes; but in contrast, in the inbred strains, gene expression variation is significantly lower on the X chromosome. Furthermore, expression divergence of genes on Muller's D element is significantly greater along the branch leading to the obscura sub-group, in which this element segregates as a neo-X chromosome. In the adults, divergence is greatest on the X chromosome for males, but not for females, yet in both sexes inbred strains harbour the lowest level of gene expression variation on the X chromosome. We consider different explanations for our results and conclude that they are most consistent within the framework of the faster-X hypothesis.
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Fraser, Neil J. "Molecular studies of the human x and y chromosomes." Thesis, University of Oxford, 1987. http://ora.ox.ac.uk/objects/uuid:e22e64bb-64e5-4474-86e2-1c3d5eb6155a.

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The isolation and characterisation of sequences from the X and Y chromosomes will give some insight into the evolutionary relationship between these chromosomes, and may be of use in the study of X-linked disorders. The availability of cDNA and genomic sequences for the human STS locus (associated with the disorder, X-linked ichthyosis) has allowed a preliminary investigation of this locus in man and other species. The localisation of these sequences to Xp22.3, provides confirmation of the sub-regional assignment of the structural gene for STS. STS homologous sequences have been identified on the long arm of the Y chromosome. These sequences also appear present on the X and Y chromosomes of the chimpanzee. In other higher primates, they appear to be X-, but not Y-, linked, suggesting that the situation in man and chimpanzee is the result of a rearrangement between the X and Y chromosomes during the past 15 million years. Another region of X Y homology has been analysed. The locus DXYS27 maps to Yp and Xq21. Restriction enzyme analysis and direct sequence comparison has shown the two loci to be «99% homologous. Phylogenetic studies suggest that the locus is X-, but not Y-, linked in the chimpanzee, suggesting an evolutionarily recent transposition of material from the X to the Y chromosome. The mutations resulting in the X-Y differences appear to have occurred on both the X and Y chromosomes. It has been possible to demonstrate that the Y-specific locus is transferred to the X chromosome in many, but not all, aberrant X-Y interchanges resulting in XX maleness. A sequence has been isolated that detects a hypervariable locus at Xp11.3→Xcen (DXS255) . The hypervariability appears to be due to the presence of a tandemly repeated sequence of variable length. Attempts to clone this repeat have been unsuccessful, as it appears to be unstable in the vector/host systems employed. This sequence will be of value in linkage studies of disease loci known to be present in this region. Hypervariability at this locus has not been identified in other species, suggesting that the repeat sequence is an evolutionarily recent acquisition by the X chromosome. Taken together, the results obtained suggest that the simple model predicting an ancient origin for the bulk of the Y chromosome will have to be reassessed.
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Books on the topic "X and Y chromosomes"

1

Frederick, Hecht, ed. Fragile sites on human chromosomes. New York: Oxford University Press, 1985.

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Miller, James R. X-linked traits: A catalog of loci in nonhuman mammals. Cambridge: Cambridge University Press, 1990.

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Sado, Takashi, ed. X-Chromosome Inactivation. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8766-5.

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Grön, Mathias. Effects of human X and Y chromosomes on oral and craniofacial morphology. Oulu, Finland: Oulun Yliopisto, 1999.

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The X in sex: How the X chromosome controls our lives. Cambridge, Mass: Harvard University Press, 2003.

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Letsche, Curt. Chromosom X: Eine keineswegs phantastische Geschichte. Berlin: Spotless, 1994.

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E, Schwartz Charles, and Schroer Richard J, eds. X-linked mental retardation. New York: Oxford University Press, 2000.

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Veenema, Henk. Clinical, cytogenetic and molecular aspects of the fragile-X syndrome. Amsterdam/Haarlem: Uitgeverij Thesis, 1989.

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McKusick, Victor A. Mendelian inheritance in man: Catalogs of autosomal dominant, autosomal recessive, and X-linked phenotypes. 9th ed. Baltimore: Johns Hopkins University Press, 1990.

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Mendelian inheritance in man: Catalogs of autosomal dominant, autosomal recessive, and x-linked phenotypes. 7th ed. Baltimore: Johns Hopkins University Press, 1986.

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Book chapters on the topic "X and Y chromosomes"

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Dosage Compensation Systems." In Introduction to Epigenetics, 67–89. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_4.

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AbstractThis chapter provides an introduction to chromosome-wide dosage compensation systems. We will examine the evolution of dosage compensation, which is thought to be driven by the appearance of differentiated sex chromosomes. In a subset of species with X chromosomal sex determination or XY sex chromosome systems, expression of X-linked genes is regulated by chromosome-wide modifications that equalize gene expression differences between males and females. The molecular mechanisms of X chromosome-wide dosage compensation have been studied in flies, worms, and mammals. Each of these species uses a distinct dosage compensation strategy with a different molecular mechanism. In the wormCaenorhabditis elegans, gene expression on the two X chromosomes of hermaphrodites is reduced to a level that approximates a single X chromosome in males. The fruit flyDrosophila melanogasterachieves dosage compensation by increased transcription of the single X chromosome in males to a level that is similar to the two X chromosomes in females. Lastly, in mammals, one of the two X chromosomes in female cells is transcriptionally inactive and a single X chromosome is transcribed in both sexes. Studies of dosage compensation systems provide insights into how epigenetic regulation controls gene expression and chromatin organization differentially within a cell.
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Miller, Orlando J., and Eeva Therman. "The X Chromosome, Dosage Compensation, and X Inactivation." In Human Chromosomes, 267–81. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4613-0139-4_18.

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Therman, Eeva. "Human X Chromosome." In Human Chromosomes, 166–75. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-0269-8_18.

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Therman, Eeva, and Millard Susman. "Human X Chromosome." In Human Chromosomes, 210–19. New York, NY: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4684-0529-3_21.

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Therman, Eeva. "Structurally Abnormal X Chromosomes." In Human Chromosomes, 182–93. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-0269-8_20.

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Therman, Eeva, and Millard Susman. "Functional Structure of the Human X Chromosome." In Human Chromosomes, 228–36. New York, NY: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4684-0529-3_23.

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Steinemann, S., and M. Steinemann. "Neo-X and Neo-Y Chromosomes in Drosophila miranda." In Chromosomes Today, 55–63. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-94-017-1033-6_6.

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Kehrer-Sawatzki, Hildegard, and Horst Hameister. "The X Chromosome Plays a Special Role During Speciation." In Chromosomes Today, 65–71. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-94-017-1033-6_7.

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Miller, Orlando J., and Eeva Therman. "Fragile Sites, Trinucleotide Repeat Expansion, and the Fragile X Syndrome." In Human Chromosomes, 295–308. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4613-0139-4_20.

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El-Fishawy, Paul. "X and Y Chromosomes." In Encyclopedia of Autism Spectrum Disorders, 3411. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_101591.

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Conference papers on the topic "X and Y chromosomes"

1

Shinohara, Kunio. "Observation Of Human Chromosomes With Soft X-Ray Contact Microscopy." In 1989 Intl Congress on Optical Science and Engineering, edited by Rene Benattar. SPIE, 1989. http://dx.doi.org/10.1117/12.961823.

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Williams, Shawn P., Chris J. Jacobsen, Janos Kirz, Xiaodong Zhang, Jack Van't Hof, and Susan Lamm. "Radiation damage to chromosomes in the scanning transmission x-ray microscope." In San Diego '92, edited by Chris J. Jacobsen and James E. Trebes. SPIE, 1993. http://dx.doi.org/10.1117/12.138747.

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Bhartiya, Archana. "X-ray Ptychography Imaging of Human Chromosomes After Low-dose Irradiation." In Microscience Microscopy Congress 2021 incorporating EMAG 2021. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.mmc2021.251.

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Fung, Jingly, Heinz-Ulli G. Weier, James D. Goldberg, and Roger A. Pedersen. "Simultaneous scoring of 10 chromosomes (9,13,14,15,16,18,21,22,X, and Y) in interphase nuclei by using spectral imaging." In BiOS '99 International Biomedical Optics Symposium, edited by Daniel L. Farkas, Robert C. Leif, and Bruce J. Tromberg. SPIE, 1999. http://dx.doi.org/10.1117/12.349203.

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Del Vecchio, Carmen, Dimer Bencivenni, and Emanuele Durante Mangoni. "X-chromosome linked recessive diseases model." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5626475.

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Hayden, L. P., M. H. Cho, D. A. Lomas, P. Bakke, A. Gulsvik, E. K. Silverman, T. H. Beaty, N. Laird, C. Lange, and D. L. DeMeo. "X Chromosome Genetic Associations in COPD." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4868.

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"X-chromosome Inactivation in American Mink iPSCs." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-310.

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Chan, Vivian, V. W. S. Liu, A. C. K. Wong, and T. K. Chan. "DNA POLYMORPHISMS IN OR LINKED TO THE FACTOR VIII GENE IN CHINESE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644049.

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78 unrelated X chromosomes from Southern Chinese (56 normal and 22 haemophiliac) were studied. DNA was restricted by Bel I, Bgl I or Taq I and hybridized to 3' factor VIII:C cDNA probe (5 kb, Chiron) or St 14.1 probe(3 kb, Oberle &Mandel) by standard techniques. The intragenic Bel I polymorphic site was positive in 82%, while Bgl I polymorphic site was positive in all. Thus, 29.5%(2 x×0.82 × 0.18) of Chinese females carried the Bel I polymorphism. Asto the Taq I polymorphism in the closely linked DXS52 DNA segment, the incidences for the various alleles were :System I - allele (3) 10.2%, (4) 2.6%, (5) 2.6%,(6) 17.9%, (7) 21.8% and (8) 44.9% System II - α a allele 56%, 6 allele 44%. Approximately 80% of females were heterozygous for two different alleles. Hence the Bel I and Taq I polymorphisms can be used to track the defective factor VIII gene for carrier detection and prenatal diagnosis. Furthermore, their frequencies in the Chinese are different from those previously reported in other ethnic groups.
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Soboleva, E. S., V. S. Fedorova, V. A. Burlak, M. V. Sharakhova, and G. N. Artemov. "INVERSION POLYMORPHISM OF NATURAL POPULATIONS ANOPHELES BEKLEMISHEVI STEGNII ET KABANOVA IN WESTERN SIBERIA." In V International Scientific Conference CONCEPTUAL AND APPLIED ASPECTS OF INVERTEBRATE SCIENTIFIC RESEARCH AND BIOLOGICAL EDUCATION. Tomsk State University Press, 2020. http://dx.doi.org/10.17223/978-5-94621-931-0-2020-35.

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The geographical distribution and inversion polymorphism of malaria mosquitoes Anopheles beklemishevi Stegnii et Kabanova in the West Siberia were investigated. X chromosome homozygous cytotypes were defined by fluorescent in situ hybridization of microdissected DNA-probe, labeling the breakpoints region of X chromosome inversions. For the first time the samples, which are homozygous and hemizygous by inversions X1 и X2 were detected. Cytotypes representation and frequencies have not differences between northern and southern (Altay) population of the malaria mosquitoes.
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Scofield, H., R. Sharma, V. Harris, J. Cavett, J. Harley, B. Kurien, A. Rasmussen, and K. Sivils. "313 Very rare x chromosome aneuploidies in lupus and sjogren’s." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.313.

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Reports on the topic "X and Y chromosomes"

1

Barker, D. F. Molecular mapping of chromosomes 17 and X. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/6697096.

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Barker, D. F. Molecular mapping of chromosomes 17 and X. Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/6659529.

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Barker, D. F. Molecular mapping of chromosomes 17 and X. Progress report. Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/10138536.

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Barker, D. F. Molecular mapping of chromosomes 17 and X. Progress report. Office of Scientific and Technical Information (OSTI), December 1989. http://dx.doi.org/10.2172/10131158.

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Caskey, C., D. Nelson, and D. Ledbetter. Mapping and ordered cloning of the human X chromosome. Office of Scientific and Technical Information (OSTI), October 1989. http://dx.doi.org/10.2172/5518435.

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Caskey, C. T., and D. L. Nelson. Mapping and ordered cloning of the human X chromosome. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/6387495.

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Willard, H. F., F. Cremers, J. L. Mandel, A. P. Monaco, D. L. Nelson, and D. Schlessinger. Report of the fifth international workshop on human X chromosome mapping. Office of Scientific and Technical Information (OSTI), December 1994. http://dx.doi.org/10.2172/304035.

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Schlessinger, D., J. L. Mandel, A. P. Monaco, D. L. Nelson, and H. F. Willard. Report of the Fourth International Workshop on human X chromosome mapping 1993. Office of Scientific and Technical Information (OSTI), December 1993. http://dx.doi.org/10.2172/10142506.

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Panning, Barbara. X Chromosome Inactivation and Breast Cancer: Epigenetic Alteration in Tumor Initiation and Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada474949.

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Caskey, C. T., and D. L. Nelson. Mapping and ordered cloning of the human X chromosome. Progress report, September 1991--November 1992. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/10158585.

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