Expression of Xist in mouse germ cells correlates with X–chromosome inactivation

McCarrey, John R.; Dilworth, Donald D.

doi:10.1038/ng1192-200

Cited by 135 publications

(58 citation statements)

References 26 publications

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“…Ectopic expression of the H19 gene resulted in prenatal lethality (10), suggesting that H19 may play a role in mammalian development. The Xist RNA is involved in X-chromosome inactivation (8,9,32,44,52,54,57,58), possibly as a component in a nonchromatin nuclear structure that associates specifically with the inactive X chromosome (13). Moreover, recent data have emerged which showed that untranslated RNAs can play a role in cell growth and differentiation, as well as transformation and oncogenesis.…”

Section: Discussionmentioning

confidence: 99%

bic, a Novel Gene Activated by Proviral Insertions in Avian Leukosis Virus-Induced Lymphomas, Is Likely To Function through Its Noncoding RNA

Tam

Ben‐Yehuda

Hayward

1997

Molecular and Cellular Biology

269

200

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The bic locus is a common retroviral integration site in avian leukosis virus (ALV)-induced B-cell lymphomas originally identified by infection of chickens with ALVs of two different subgroups (Clurman and Hayward, Mol. Cell. Biol. 9:2657-2664, 1989). Based on its frequent association with c-myc activation and its preferential activation in metastatic tumors, the bic locus is thought to harbor a gene that can collaborate with c-myc in lymphomagenesis and presumably plays a role in late stages of tumor progression. In the present study, we have cloned and characterized two novel genes, bdw and bic, at the bic locus. bdw encoded a putative novel protein of 345 amino acids. However, its expression did not appear to be altered in tumor tissues, suggesting that it is not involved in oncogenesis. The bic gene consisted of two exons and was expressed as two spliced and alternatively polyadenylated transcripts at low levels in lymphoid/hematopoietic tissues. In tumors harboring bic integrations, proviruses drove bic gene expression by promoter insertion, resulting in high levels of expression of a chimeric RNA containing bic exon 2. Interestingly, bic lacked an extensive open reading frame, implying that it may function through its RNA. Computer analysis of RNA from small exon 2 of bic predicted extensive double-stranded structures, including a highly ordered RNA duplex between nucleotides 316 and 461. The possible role of bic in cell growth and differentiation is discussed in view of the emerging evidence that untranslated RNAs play a role in growth control.The proto-oncogene c-myc plays a critical role in the development of lymphomas in birds and mammals (16,48). Experiments in both the murine and avian systems indicate that activation of c-myc alone is not sufficient for full malignancy. In E-c-myc transgenic mice, monoclonal lymphomas develop only after a variable and relatively long latency (2), suggesting that additional genetic alterations besides c-myc are required to induce full-blown lymphomas. Consistent with this notion, c-Myc (or the viral homolog v-Myc) is able to cooperate with a number of other proto-oncogene products in lymphomagenesis in rodents (1). These include the nuclear protein 27,71), Ras G protein (3,40,60), the serine/threonine kinases Pim-1 (70, 72) and Raf (40), the nonreceptor proteintyrosine kinase Abl (28,41), and the mitochondrial membrane protein 62,63).In birds, studies of avian leukosis virus (ALV)-induced lymphomas have provided strong evidence for the requirement of multiple genetic events in lymphomagenesis. The development of avian lymphoid leukosis is believed to follow an orderly progression through three distinct clinical stages (15, 49). (i) Transformed follicles, which are hyperplastic follicles consisting of abnormally proliferating lymphoblasts, appear within 4 to 8 weeks postinfection, and an estimated 10 to 100 transformed follicles can be found in a single bursa. (ii) From 10 to 14 weeks postinfection onwards, macroscopic tumor nodules appear in the bursa. If present at ...

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Section: Discussionmentioning

confidence: 99%

bic, a Novel Gene Activated by Proviral Insertions in Avian Leukosis Virus-Induced Lymphomas, Is Likely To Function through Its Noncoding RNA

Tam

Ben‐Yehuda

Hayward

1997

Molecular and Cellular Biology

269

200

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“…Xist recruits an array of chromatin-modifying enzymes to the future inactive X chromosome that induce gene silencing by catalysing methylation, ubiquitylation and deacetylation of defined histone residues (Heard and Disteche, 2006). In males, Xist is expressed exclusively in the testis (McCarrey and Dilworth, 1992;Salido et al, 1992;Richler et al, 1992;Ayoub et al, 1997) and has been reported to coat the sex body in a manner analogous to that in female somatic cells. The presence of Xist on the Y as well as on the X chromosome in the sex body spawned the 'quasi-cis' model of MSCI, in which X chromosome-derived Xist transcripts spread from the X chromosome to the Y chromosome via the region of X-Y synapsis (Ayoub et al, 1997).…”

Section: An Introduction To Sex Chromosome Activity In Spermatogenesismentioning

confidence: 99%

Meiotic sex chromosome inactivation

Turner¹

2007

Development

625

601

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X chromosome inactivation is most commonly studied in the context of female mammalian development, where it performs an essential role in dosage compensation. However, another form of X-inactivation takes place in the male,during spermatogenesis, as germ cells enter meiosis. This second form of X-inactivation, called meiotic sex chromosome inactivation (MSCI) has emerged as a novel paradigm for studying the epigenetic regulation of gene expression. New studies have revealed that MSCI is a special example of a more general mechanism called meiotic silencing of unsynapsed chromatin (MSUC), which silences chromosomes that fail to pair with their homologous partners and, in doing so, may protect against aneuploidy in subsequent generations. Furthermore, failure in MSCI is emerging as an important etiological factor in meiotic sterility.

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“…A cardinal feature that distinguishes male from female meiosis in mammals is the progressive condensation of the X and Y chromosomes during meiotic prophase to form the XY-, or sex body (Solari, 1974). The formation of the XY-body has been considered as a morphological manifestation of meiotic sex chromosome inactivation (MSCI) (Monesi, 1965;KofmanAlfaro and Chandley, 1970;Odartchenko and Pavillard, 1970;Kierszenbaum and Tres, 1974;Latos-Bielenska and Vogel, 1992;McCarrey and Dilworth, 1992). An increasing number of proteins have been identified that locate to the XY-body (Smith and Benavente, 1992;Smith and Benavente, 1995;Calenda et al, 1994;Kralewski et al, 1997;Bauer et al, 1998;Motzkus et al, 1999;Hoyer-Fender et al, 2000;Parraga and del Mazo, 2000;Richler et al, 2000;Turner et al, 2000) but their significance if any for MSCI or heterochromatinisation are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Localisation of histone macroH2A1.2 to the XY-body is not a response to the presence of asynapsed chromosome axes

Hoyer‐Fender

Czirr

Radde

et al. 2004

Journal of Cell Science

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Expression of Xist in mouse germ cells correlates with X–chromosome inactivation

Cited by 135 publications

References 26 publications

bic, a Novel Gene Activated by Proviral Insertions in Avian Leukosis Virus-Induced Lymphomas, Is Likely To Function through Its Noncoding RNA

bic, a Novel Gene Activated by Proviral Insertions in Avian Leukosis Virus-Induced Lymphomas, Is Likely To Function through Its Noncoding RNA

Meiotic sex chromosome inactivation

Localisation of histone macroH2A1.2 to the XY-body is not a response to the presence of asynapsed chromosome axes

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