Trichostatin A specifically improves the aberrant expression of transcription factor genes in embryos produced by somatic cell nuclear transfer

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作者
Kimiko Inoue
Mami Oikawa
Satoshi Kamimura
Narumi Ogonuki
Toshinobu Nakamura
Toru Nakano
Kuniya Abe
Atsuo Ogura
机构
[1] Bioresource Center,Department of Pathology
[2] RIKEN,Department of Animal Bioscience
[3] Graduate School of Life and Environmental Sciences,undefined
[4] University of Tsukuba,undefined
[5] Medical School and Graduate School of Frontier Biosciences,undefined
[6] Osaka University,undefined
[7] Nagahama Institute of Bio-Science and Technology,undefined
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Scientific Reports | / 5卷
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摘要
Although mammalian cloning by somatic cell nuclear transfer (SCNT) has been established in various species, the low developmental efficiency has hampered its practical applications. Treatment of SCNT-derived embryos with histone deacetylase (HDAC) inhibitors can improve their development, but the underlying mechanism is still unclear. To address this question, we analysed gene expression profiles of SCNT-derived 2-cell mouse embryos treated with trichostatin A (TSA), a potent HDAC inhibitor that is best used for mouse cloning. Unexpectedly, TSA had no effect on the numbers of aberrantly expressed genes or the overall gene expression pattern in the embryos. However, in-depth investigation by gene ontology and functional analyses revealed that TSA treatment specifically improved the expression of a small subset of genes encoding transcription factors and their regulatory factors, suggesting their positive involvement in de novo RNA synthesis. Indeed, introduction of one of such transcription factors, Spi-C, into the embryos at least partially mimicked the TSA-induced improvement in embryonic development by activating gene networks associated with transcriptional regulation. Thus, the effects of TSA treatment on embryonic gene expression did not seem to be stochastic, but more specific than expected, targeting genes that direct development and trigger zygotic genome activation at the 2-cell stage.
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