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SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression
SIN3A is the central scaffold protein of the SIN3/histone deacetylase (HDAC) transcriptional repressor complex. SIN3A participates in the mouse preimplantation development by fine-tuning HDAC1 expression. However, it remains unresolved if this functional significance of SIN3A was conserved in other...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937639/ https://www.ncbi.nlm.nih.gov/pubmed/33692994 http://dx.doi.org/10.3389/fcell.2021.604232 |
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author | Luo, Lei Dang, Yanna Shi, Yan Zhao, Panpan Zhang, Yunhai Zhang, Kun |
author_facet | Luo, Lei Dang, Yanna Shi, Yan Zhao, Panpan Zhang, Yunhai Zhang, Kun |
author_sort | Luo, Lei |
collection | PubMed |
description | SIN3A is the central scaffold protein of the SIN3/histone deacetylase (HDAC) transcriptional repressor complex. SIN3A participates in the mouse preimplantation development by fine-tuning HDAC1 expression. However, it remains unresolved if this functional significance of SIN3A was conserved in other mammals. Herein, RNA-seq results show a large amount of SIN3A mRNA is present in oocytes and early embryos prior to embryonic genome activation and a low amount thereafter, suggesting a maternal origin of SIN3A in pigs, cattle, mice, and humans. Interestingly, immunofluorescence data show that SIN3A protein level peaks at four-cell stage in pigs compared with morula stage in cattle. SIN3A depletion in early embryos causes a developmental arrest at two-cell stage in pigs but does not affect bovine early embryonic development. In contrast with mouse data, SIN3A depletion results in only a slight decrease and even no difference in HDAC1 expression in porcine and bovine early embryos, respectively. In addition, HDAC1 knockdown does not cause two-cell block but leads to a reduced blastocyst rate. By using unbiased RNA-seq approach, we found that Cyclin B1 (CCNB1) transcript level is dramatically reduced. Moreover, CCNB1 knockdown results in a similar phenotype as SIN3A depletion. Injection of exogenous CCNB1 mRNA into SIN3A-depleted embryos could partly rescue embryonic development to pass two-cell stage. In conclusion, our results indicate SIN3A plays an essential role in porcine early embryonic development, which probably involves the regulation of CCNB1 expression. |
format | Online Article Text |
id | pubmed-7937639 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-79376392021-03-09 SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression Luo, Lei Dang, Yanna Shi, Yan Zhao, Panpan Zhang, Yunhai Zhang, Kun Front Cell Dev Biol Cell and Developmental Biology SIN3A is the central scaffold protein of the SIN3/histone deacetylase (HDAC) transcriptional repressor complex. SIN3A participates in the mouse preimplantation development by fine-tuning HDAC1 expression. However, it remains unresolved if this functional significance of SIN3A was conserved in other mammals. Herein, RNA-seq results show a large amount of SIN3A mRNA is present in oocytes and early embryos prior to embryonic genome activation and a low amount thereafter, suggesting a maternal origin of SIN3A in pigs, cattle, mice, and humans. Interestingly, immunofluorescence data show that SIN3A protein level peaks at four-cell stage in pigs compared with morula stage in cattle. SIN3A depletion in early embryos causes a developmental arrest at two-cell stage in pigs but does not affect bovine early embryonic development. In contrast with mouse data, SIN3A depletion results in only a slight decrease and even no difference in HDAC1 expression in porcine and bovine early embryos, respectively. In addition, HDAC1 knockdown does not cause two-cell block but leads to a reduced blastocyst rate. By using unbiased RNA-seq approach, we found that Cyclin B1 (CCNB1) transcript level is dramatically reduced. Moreover, CCNB1 knockdown results in a similar phenotype as SIN3A depletion. Injection of exogenous CCNB1 mRNA into SIN3A-depleted embryos could partly rescue embryonic development to pass two-cell stage. In conclusion, our results indicate SIN3A plays an essential role in porcine early embryonic development, which probably involves the regulation of CCNB1 expression. Frontiers Media S.A. 2021-02-22 /pmc/articles/PMC7937639/ /pubmed/33692994 http://dx.doi.org/10.3389/fcell.2021.604232 Text en Copyright © 2021 Luo, Dang, Shi, Zhao, Zhang and Zhang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cell and Developmental Biology Luo, Lei Dang, Yanna Shi, Yan Zhao, Panpan Zhang, Yunhai Zhang, Kun SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression |
title | SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression |
title_full | SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression |
title_fullStr | SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression |
title_full_unstemmed | SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression |
title_short | SIN3A Regulates Porcine Early Embryonic Development by Modulating CCNB1 Expression |
title_sort | sin3a regulates porcine early embryonic development by modulating ccnb1 expression |
topic | Cell and Developmental Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937639/ https://www.ncbi.nlm.nih.gov/pubmed/33692994 http://dx.doi.org/10.3389/fcell.2021.604232 |
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