Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas
Somatic cell nuclear transfer (SCNT) frequently results in abnormal placenta development in cloned mice. Here the authors show that loss of histone methylation (H3K27me3) imprinting in clustered Sfmbt2 miRNAs contributes to SCNT placenta defect.
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2020-05-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-020-16044-8 |
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doaj-9a90abcae67c4e6d8be26b81b3d9af932021-05-11T08:52:36ZengNature Publishing GroupNature Communications2041-17232020-05-0111111210.1038/s41467-020-16044-8Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentasKimiko Inoue0Narumi Ogonuki1Satoshi Kamimura2Hiroki Inoue3Shogo Matoba4Michiko Hirose5Arata Honda6Kento Miura7Masashi Hada8Ayumi Hasegawa9Naomi Watanabe10Yukiko Dodo11Keiji Mochida12Atsuo Ogura13Bioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENBioresource Engineering Division, Bioresource Research Center, RIKENSomatic cell nuclear transfer (SCNT) frequently results in abnormal placenta development in cloned mice. Here the authors show that loss of histone methylation (H3K27me3) imprinting in clustered Sfmbt2 miRNAs contributes to SCNT placenta defect.https://doi.org/10.1038/s41467-020-16044-8 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Kimiko Inoue Narumi Ogonuki Satoshi Kamimura Hiroki Inoue Shogo Matoba Michiko Hirose Arata Honda Kento Miura Masashi Hada Ayumi Hasegawa Naomi Watanabe Yukiko Dodo Keiji Mochida Atsuo Ogura |
spellingShingle |
Kimiko Inoue Narumi Ogonuki Satoshi Kamimura Hiroki Inoue Shogo Matoba Michiko Hirose Arata Honda Kento Miura Masashi Hada Ayumi Hasegawa Naomi Watanabe Yukiko Dodo Keiji Mochida Atsuo Ogura Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas Nature Communications |
author_facet |
Kimiko Inoue Narumi Ogonuki Satoshi Kamimura Hiroki Inoue Shogo Matoba Michiko Hirose Arata Honda Kento Miura Masashi Hada Ayumi Hasegawa Naomi Watanabe Yukiko Dodo Keiji Mochida Atsuo Ogura |
author_sort |
Kimiko Inoue |
title |
Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas |
title_short |
Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas |
title_full |
Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas |
title_fullStr |
Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas |
title_full_unstemmed |
Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas |
title_sort |
loss of h3k27me3 imprinting in the sfmbt2 mirna cluster causes enlargement of cloned mouse placentas |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2020-05-01 |
description |
Somatic cell nuclear transfer (SCNT) frequently results in abnormal placenta development in cloned mice. Here the authors show that loss of histone methylation (H3K27me3) imprinting in clustered Sfmbt2 miRNAs contributes to SCNT placenta defect. |
url |
https://doi.org/10.1038/s41467-020-16044-8 |
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