ArticleProceedings of the National Academy of Sciences of the United States of America2015
Xist imprinting is promoted by the hemizygous (unpaired) state in the male germ line.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Imprinted X chromosome inactivation at the gamete-to-embryo transition.Molecular cell · 2024Article
- The compleX balancing act of controlling X-chromosome dosage and how it impacts mammalian germline development.The Biochemical journal · 2023Article
- Linking Chromosomal Silencing WithFrontiers in cell and developmental biology · 2021Article
- FUS ALS-causative mutations impair FUS autoregulation and splicing factor networks through intron retention.Nucleic acids research · 2020Article
- LncRNA Jpx induces Xist expression in mice using both trans and cis mechanisms.PLoS genetics · 2018Article
- Understanding the Role of lncRNAs in Nervous System Development.Advances in experimental medicine and biology · 2017Review
- Round Spermatid Injection Rescues Female Lethality of a Paternally Inherited Xist Deletion in Mouse.PLoS genetics · 2016Article
- Parent-of-origin effects of A1CF and AGO2 on testicular germ-cell tumors, testicular abnormalities, and fertilization bias.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Pairing and anti-pairing: a balancing act in the diploid genome.Current opinion in genetics & development · 2016Review
- QnAs with Jeannie T. Lee.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Imprinted X chromosome inactivation offers up a double dose of epigenetics.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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8 authors at 5 institutions in 1 country.
Funding
Abstract
The long noncoding X-inactivation-specific transcript (Xist gene) is responsible for mammalian X-chromosome dosage compensation between the sexes, the process by which one of the two X chromosomes is inactivated in the female soma. Xist is essential for both the random and imprinted forms of X-chromosome inactivation. In the imprinted form, Xist is paternally marked to be expressed in female embryos. To investigate the mechanism of Xist imprinting, we introduce Xist transgenes (Tg) into the male germ line. Although ectopic high-level Xist expression on autosomes can be compatible with viability, transgenic animals demonstrate reduced fitness, subfertility, defective meiotic pairing, and other germ-cell abnormalities. In the progeny, paternal-specific expression is recapitulated by the 200-kb Xist Tg. However, Xist imprinting occurs efficiently only when it is in an unpaired or unpartnered state during male meiosis. When transmitted from a hemizygous father (+/Tg), the Xist Tg demonstrates paternal-specific expression in the early embryo. When transmitted by a homozygous father (Tg/Tg), the Tg fails to show imprinted expression. Thus, Xist imprinting is directed by sequences within a 200-kb X-linked region, and the hemizygous (unpaired) state of the Xist region promotes its imprinting in the male germ line.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.