Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 15, Pages -Publisher
MDPI
DOI: 10.3390/ijms22158187
Keywords
SCNT embryos; transcription pathways; gene regulatory networks; abnormal gene expression; molecular barriers
Funding
- National Natural Science Foundation of China [62061034, 61861036]
- Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region [NJYT-18-B01]
- Science and Technology Major Project of Inner Mongolia Autonomous Region of China [2019ZD031]
- Fund for Excellent Young Scholars of Inner Mongolia [2017JQ04]
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The incomplete activation of transcription pathways in nuclear transfer arrest embryos can hinder the development process by causing massive dysregulation of genes. This potential molecular barrier, alongside incomplete reprogramming of epigenetic modifications, broadens the understanding of SCNT embryonic development at a molecular level.
Somatic cell nuclear transfer (SCNT) technology can reprogram terminally differentiated cell nuclei into a totipotent state. However, the underlying molecular barriers of SCNT embryo development remain incompletely elucidated. Here, we observed that transcription-related pathways were incompletely activated in nuclear transfer arrest (NTA) embryos compared to normal SCNT embryos and in vivo fertilized (WT) embryos, which hinders the development of SCNT embryos. We further revealed the transcription pathway associated gene regulatory networks (GRNs) and found the aberrant transcription pathways can lead to the massive dysregulation of genes in NTA embryos. The predicted target genes of transcription pathways contain a series of crucial factors in WT embryos, which play an important role in catabolic process, pluripotency regulation, epigenetic modification and signal transduction. In NTA embryos, however, these genes were varying degrees of inhibition and show a defect in synergy. Overall, our research found that the incomplete activation of transcription pathways is another potential molecular barrier for SCNT embryos besides the incomplete reprogramming of epigenetic modifications, broadening the understanding of molecular mechanism of SCNT embryonic development.
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