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Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice.

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Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice. / Shin, Jongdae; Bossenz, Michael; Chung, Young; Ma, Hong; Byron, Meg; Taniguchi-Ishigaki, Naoko; Zhu, Xiaochun; Jiao, Baowei; Hall, Lisa L; Green, Michael R; Jones, Stephen N; Hermans-Borgmeyer, Irmgard; Lawrence, Jeanne B; Bach, Ingolf.

In: NATURE, Vol. 467, No. 7318, 7318, 2010, p. 977-981.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Shin, J, Bossenz, M, Chung, Y, Ma, H, Byron, M, Taniguchi-Ishigaki, N, Zhu, X, Jiao, B, Hall, LL, Green, MR, Jones, SN, Hermans-Borgmeyer, I, Lawrence, JB & Bach, I 2010, 'Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice.', NATURE, vol. 467, no. 7318, 7318, pp. 977-981. <http://www.ncbi.nlm.nih.gov/pubmed/20962847?dopt=Citation>

APA

Shin, J., Bossenz, M., Chung, Y., Ma, H., Byron, M., Taniguchi-Ishigaki, N., Zhu, X., Jiao, B., Hall, L. L., Green, M. R., Jones, S. N., Hermans-Borgmeyer, I., Lawrence, J. B., & Bach, I. (2010). Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice. NATURE, 467(7318), 977-981. [7318]. http://www.ncbi.nlm.nih.gov/pubmed/20962847?dopt=Citation

Vancouver

Shin J, Bossenz M, Chung Y, Ma H, Byron M, Taniguchi-Ishigaki N et al. Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice. NATURE. 2010;467(7318):977-981. 7318.

Bibtex

@article{997ff5a00b6a412799b8f04149d43124,
title = "Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice.",
abstract = "Two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Imprinted XCI begins with the detection of Xist RNA expression on the paternal X?chromosome (Xp) at about the four-cell stage of embryonic development. In the embryonic tissues of the inner cell mass, a random form of XCI occurs in blastocysts that inactivates either Xp or the maternal X?chromosome (Xm). Both forms of XCI require the non-coding Xist RNA that coats the inactive X?chromosome from which it is expressed. Xist has crucial functions in the silencing of X-linked genes, including Rnf12 (refs 3, 4) encoding the ubiquitin ligase RLIM (RING finger LIM-domain-interacting protein). Here we show, by targeting a conditional knockout of Rnf12 to oocytes where RLIM accumulates to high levels, that the maternal transmission of the mutant X?chromosome (?m) leads to lethality in female embryos as a result of defective imprinted XCI. We provide evidence that in ?m female embryos the initial formation of Xist clouds and Xp silencing are inhibited. In contrast, embryonic stem cells lacking RLIM are able to form Xist clouds and silence at least some X-linked genes during random XCI. These results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted XCI.",
keywords = "Animals, Male, Female, Mice, Mice, Transgenic, Cell Line, Animals, Congenic, Blastocyst metabolism, Chromosomes, Mammalian genetics, Embryo Loss genetics, Fathers, Gene Silencing, Genomic Imprinting, Mothers, RNA, Untranslated genetics, Repressor Proteins deficiency, X Chromosome genetics, X Chromosome Inactivation genetics, Animals, Male, Female, Mice, Mice, Transgenic, Cell Line, Animals, Congenic, Blastocyst metabolism, Chromosomes, Mammalian genetics, Embryo Loss genetics, Fathers, Gene Silencing, Genomic Imprinting, Mothers, RNA, Untranslated genetics, Repressor Proteins deficiency, X Chromosome genetics, X Chromosome Inactivation genetics",
author = "Jongdae Shin and Michael Bossenz and Young Chung and Hong Ma and Meg Byron and Naoko Taniguchi-Ishigaki and Xiaochun Zhu and Baowei Jiao and Hall, {Lisa L} and Green, {Michael R} and Jones, {Stephen N} and Irmgard Hermans-Borgmeyer and Lawrence, {Jeanne B} and Ingolf Bach",
year = "2010",
language = "English",
volume = "467",
pages = "977--981",
journal = "NATURE",
issn = "0028-0836",
publisher = "NATURE PUBLISHING GROUP",
number = "7318",

}

RIS

TY - JOUR

T1 - Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice.

AU - Shin, Jongdae

AU - Bossenz, Michael

AU - Chung, Young

AU - Ma, Hong

AU - Byron, Meg

AU - Taniguchi-Ishigaki, Naoko

AU - Zhu, Xiaochun

AU - Jiao, Baowei

AU - Hall, Lisa L

AU - Green, Michael R

AU - Jones, Stephen N

AU - Hermans-Borgmeyer, Irmgard

AU - Lawrence, Jeanne B

AU - Bach, Ingolf

PY - 2010

Y1 - 2010

N2 - Two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Imprinted XCI begins with the detection of Xist RNA expression on the paternal X?chromosome (Xp) at about the four-cell stage of embryonic development. In the embryonic tissues of the inner cell mass, a random form of XCI occurs in blastocysts that inactivates either Xp or the maternal X?chromosome (Xm). Both forms of XCI require the non-coding Xist RNA that coats the inactive X?chromosome from which it is expressed. Xist has crucial functions in the silencing of X-linked genes, including Rnf12 (refs 3, 4) encoding the ubiquitin ligase RLIM (RING finger LIM-domain-interacting protein). Here we show, by targeting a conditional knockout of Rnf12 to oocytes where RLIM accumulates to high levels, that the maternal transmission of the mutant X?chromosome (?m) leads to lethality in female embryos as a result of defective imprinted XCI. We provide evidence that in ?m female embryos the initial formation of Xist clouds and Xp silencing are inhibited. In contrast, embryonic stem cells lacking RLIM are able to form Xist clouds and silence at least some X-linked genes during random XCI. These results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted XCI.

AB - Two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Imprinted XCI begins with the detection of Xist RNA expression on the paternal X?chromosome (Xp) at about the four-cell stage of embryonic development. In the embryonic tissues of the inner cell mass, a random form of XCI occurs in blastocysts that inactivates either Xp or the maternal X?chromosome (Xm). Both forms of XCI require the non-coding Xist RNA that coats the inactive X?chromosome from which it is expressed. Xist has crucial functions in the silencing of X-linked genes, including Rnf12 (refs 3, 4) encoding the ubiquitin ligase RLIM (RING finger LIM-domain-interacting protein). Here we show, by targeting a conditional knockout of Rnf12 to oocytes where RLIM accumulates to high levels, that the maternal transmission of the mutant X?chromosome (?m) leads to lethality in female embryos as a result of defective imprinted XCI. We provide evidence that in ?m female embryos the initial formation of Xist clouds and Xp silencing are inhibited. In contrast, embryonic stem cells lacking RLIM are able to form Xist clouds and silence at least some X-linked genes during random XCI. These results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted XCI.

KW - Animals

KW - Male

KW - Female

KW - Mice

KW - Mice, Transgenic

KW - Cell Line

KW - Animals, Congenic

KW - Blastocyst metabolism

KW - Chromosomes, Mammalian genetics

KW - Embryo Loss genetics

KW - Fathers

KW - Gene Silencing

KW - Genomic Imprinting

KW - Mothers

KW - RNA, Untranslated genetics

KW - Repressor Proteins deficiency

KW - X Chromosome genetics

KW - X Chromosome Inactivation genetics

KW - Animals

KW - Male

KW - Female

KW - Mice

KW - Mice, Transgenic

KW - Cell Line

KW - Animals, Congenic

KW - Blastocyst metabolism

KW - Chromosomes, Mammalian genetics

KW - Embryo Loss genetics

KW - Fathers

KW - Gene Silencing

KW - Genomic Imprinting

KW - Mothers

KW - RNA, Untranslated genetics

KW - Repressor Proteins deficiency

KW - X Chromosome genetics

KW - X Chromosome Inactivation genetics

M3 - SCORING: Journal article

VL - 467

SP - 977

EP - 981

JO - NATURE

JF - NATURE

SN - 0028-0836

IS - 7318

M1 - 7318

ER -