Unreprogrammed H3K9me3 prevents minor zygotic genome activation and lineage commitment in SCNT embryos
© 2023. Springer Nature Limited..
Somatic cell nuclear transfer (SCNT) can be used to reprogram differentiated somatic cells to a totipotent state but has poor efficiency in supporting full-term development. H3K9me3 is considered to be an epigenetic barrier to zygotic genomic activation in 2-cell SCNT embryos. However, the mechanism underlying the failure of H3K9me3 reprogramming during SCNT embryo development remains elusive. Here, we perform genome-wide profiling of H3K9me3 in cumulus cell-derived SCNT embryos. We find redundant H3K9me3 marks are closely related to defective minor zygotic genome activation. Moreover, SCNT blastocysts show severely indistinct lineage-specific H3K9me3 deposition. We identify MAX and MCRS1 as potential H3K9me3-related transcription factors and are essential for early embryogenesis. Overexpression of Max and Mcrs1 significantly benefits SCNT embryo development. Notably, MCRS1 partially rescues lineage-specific H3K9me3 allocation, and further improves the efficiency of full-term development. Importantly, our data confirm the conservation of deficient H3K9me3 differentiation in Sertoli cell-derived SCNT embryos, which may be regulated by alternative mechanisms.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:14 |
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| Enthalten in: |
Nature communications - 14(2023), 1 vom: 09. Aug., Seite 4807 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Xu, Ruimin [VerfasserIn] |
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| Anmerkungen: |
Date Completed 11.08.2023 Date Revised 19.11.2023 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1038/s41467-023-40496-3 |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Somatic cell nuclear transfer (SCNT) can be used to reprogram differentiated somatic cells to a totipotent state but has poor efficiency in supporting full-term development. H3K9me3 is considered to be an epigenetic barrier to zygotic genomic activation in 2-cell SCNT embryos. However, the mechanism underlying the failure of H3K9me3 reprogramming during SCNT embryo development remains elusive. Here, we perform genome-wide profiling of H3K9me3 in cumulus cell-derived SCNT embryos. We find redundant H3K9me3 marks are closely related to defective minor zygotic genome activation. Moreover, SCNT blastocysts show severely indistinct lineage-specific H3K9me3 deposition. We identify MAX and MCRS1 as potential H3K9me3-related transcription factors and are essential for early embryogenesis. Overexpression of Max and Mcrs1 significantly benefits SCNT embryo development. Notably, MCRS1 partially rescues lineage-specific H3K9me3 allocation, and further improves the efficiency of full-term development. Importantly, our data confirm the conservation of deficient H3K9me3 differentiation in Sertoli cell-derived SCNT embryos, which may be regulated by alternative mechanisms | ||
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| 700 | 1 | |a Zhu, Qianshu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Yuyan |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Mo |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Lingyue |e verfasserin |4 aut | |
| 700 | 1 | |a Shen, Shijun |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Guang |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Zhifei |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Xiaolei |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Qi |e verfasserin |4 aut | |
| 700 | 1 | |a Kou, Xiaochen |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Yanhong |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Hong |e verfasserin |4 aut | |
| 700 | 1 | |a Jiang, Cizhong |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Chong |e verfasserin |4 aut | |
| 700 | 1 | |a Gao, Shaorong |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Xiaoyu |e verfasserin |4 aut | |
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