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 | |
| Publication status | Published - 2004 Aug 13 |
| Externally published | Yes |
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Keywords
- Cloned mouse
- DNA methylation
- Epigenetics
- Skewed X-inactivation
- X-chromosome inactivation
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Skewed X-inactivation in cloned mice. / Senda, Sho; Wakayama, Teruhiko; Yamazaki, Yukiko; Ohgane, Jun; Hattori, Naka; Tanaka, Satoshi; Yanagimachi, Ryuzo; Shiota, Kunio.
In: Biochemical and Biophysical Research Communications, Vol. 321, No. 1, 13.08.2004, p. 38-44.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Skewed X-inactivation in cloned mice
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
KW - Cloned mouse
KW - DNA methylation
KW - Epigenetics
KW - Skewed X-inactivation
KW - X-chromosome inactivation
UR - http://www.scopus.com/inward/record.url?scp=3542996285&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3542996285&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2004.06.096
DO - 10.1016/j.bbrc.2004.06.096
M3 - Article
C2 - 15358212
AN - SCOPUS:3542996285
VL - 321
SP - 38
EP - 44
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 1
ER -