Skewed X-inactivation in cloned mice

Sho Senda; Teruhiko Wakayama; Yukiko Yamazaki; Jun Ohgane; Naka Hattori; Satoshi Tanaka; Ryuzo Yanagimachi; Kunio Shiota

doi:10.1016/j.bbrc.2004.06.096

Skewed X-inactivation in cloned mice

Sho Senda, Teruhiko Wakayama, Yukiko Yamazaki, Jun Ohgane, Naka Hattori, Satoshi Tanaka, Ryuzo Yanagimachi, Kunio Shiota

Research output: Contribution to journal › Article › peer-review

30 Citations (Scopus)

Abstract

In female mammals, dosage compensation for X-linked genes is accomplished by inactivation of one of two X chromosomes. The X-inactivation ratio (a percentage of the cells with inactivated maternal X chromosomes in the whole cells) is skewed as a consequence of various genetic mutations, and has been observed in a number of X-linked disorders. We previously reported that phenotypically normal full-term cloned mouse fetuses had loci with inappropriate DNA methylation. Thus, cloned mice are excellent models to study abnormal epigenetic events in mammalian development. In the present study, we analyzed X-inactivation ratios in adult female cloned mice (B6C3F1). Kidneys of eight naturally produced controls and 11 cloned mice were analyzed. Although variations in X-inactivation ratio among the mice were observed in both groups, the distributions were significantly different (Ansary-Bradley test, P

Original language	English
Pages (from-to)	38-44
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	321
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2004.06.096
Publication status	Published - 2004 Aug 13
Externally published	Yes

Keywords

Cloned mouse
DNA methylation
Epigenetics
Skewed X-inactivation
X-chromosome inactivation

ASJC Scopus subject areas

Biochemistry
Biophysics
Molecular Biology

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title = "Skewed X-inactivation in cloned mice",

abstract = "In female mammals, dosage compensation for X-linked genes is accomplished by inactivation of one of two X chromosomes. The X-inactivation ratio (a percentage of the cells with inactivated maternal X chromosomes in the whole cells) is skewed as a consequence of various genetic mutations, and has been observed in a number of X-linked disorders. We previously reported that phenotypically normal full-term cloned mouse fetuses had loci with inappropriate DNA methylation. Thus, cloned mice are excellent models to study abnormal epigenetic events in mammalian development. In the present study, we analyzed X-inactivation ratios in adult female cloned mice (B6C3F1). Kidneys of eight naturally produced controls and 11 cloned mice were analyzed. Although variations in X-inactivation ratio among the mice were observed in both groups, the distributions were significantly different (Ansary-Bradley test, P",

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AU - Senda, Sho

AU - Wakayama, Teruhiko

AU - Yamazaki, Yukiko

AU - Ohgane, Jun

AU - Hattori, Naka

AU - Tanaka, Satoshi

AU - Yanagimachi, Ryuzo

AU - Shiota, Kunio

PY - 2004/8/13

Y1 - 2004/8/13

N2 - In female mammals, dosage compensation for X-linked genes is accomplished by inactivation of one of two X chromosomes. The X-inactivation ratio (a percentage of the cells with inactivated maternal X chromosomes in the whole cells) is skewed as a consequence of various genetic mutations, and has been observed in a number of X-linked disorders. We previously reported that phenotypically normal full-term cloned mouse fetuses had loci with inappropriate DNA methylation. Thus, cloned mice are excellent models to study abnormal epigenetic events in mammalian development. In the present study, we analyzed X-inactivation ratios in adult female cloned mice (B6C3F1). Kidneys of eight naturally produced controls and 11 cloned mice were analyzed. Although variations in X-inactivation ratio among the mice were observed in both groups, the distributions were significantly different (Ansary-Bradley test, P

AB - In female mammals, dosage compensation for X-linked genes is accomplished by inactivation of one of two X chromosomes. The X-inactivation ratio (a percentage of the cells with inactivated maternal X chromosomes in the whole cells) is skewed as a consequence of various genetic mutations, and has been observed in a number of X-linked disorders. We previously reported that phenotypically normal full-term cloned mouse fetuses had loci with inappropriate DNA methylation. Thus, cloned mice are excellent models to study abnormal epigenetic events in mammalian development. In the present study, we analyzed X-inactivation ratios in adult female cloned mice (B6C3F1). Kidneys of eight naturally produced controls and 11 cloned mice were analyzed. Although variations in X-inactivation ratio among the mice were observed in both groups, the distributions were significantly different (Ansary-Bradley test, P

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Skewed X-inactivation in cloned mice

Abstract

Keywords

ASJC Scopus subject areas

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