Professor Sungshin University Seongbuk-Gu, United States
Abstract Authors: Jeong Bin Jo1, Željko M Svedružić2, Yong-Pil Cheon1
1Division of Developmental Biology and Physiology, Department of Biotechnology, Institute for Basic Sciences, Sungshin University, Seoul 02844, Korea
2Department of Biotechnology, University of Rijeka, 51000 Rijeka, Croatia
Abstract Text: The products of Prnp gene are the functional molecule in development and disease. One of the possible reasons of prion disease is the amount of PrPC in a tissue, and controlling the expression levels of PrPC is suspected as a way of protection the prion. DNA methylation is a major epigenetic mechanism and plays critical roles in the silencing of retrotransposons, genomic imprinting, and cell differentiation. So far, the epigenic modification is happened during early embryonic stage, but it is not fully unmasked the epigenic regulation during cleavage. In this study the expression of the Prnp was examined in the cleavage stage and the evaluation the changes of developmental genes was did by DNMT1 modifying molecules, S-adenosylhomocysteine (SAH), N-phthalyl-L-tryptophan (RG108), and maybridge (Myb1). Development to the blastocyst stage was significantly higher in 10 mM Myb but lower in 1 mM SAH than the control. The expression profiles of Prnp were modified by the inhibitors and the patterns were different between them. The expression of the potency related genes and lineage related genes were also modified with the inhibitor specific patterns. RNAseq results showed the high expression of carbohydrate metabolic genes in Myb1 treated embryos, immune related genes in SAH, and cell proliferation related genes in RG108. Myb1 treated embryos were transferred into the uteri of pseudopregnant mice and got the normal pubs. Put together it is suggested that the gene expression is modified with the DNMT1 inhibitor specific manner and Myb1 is a useful DNMT1 inhibitor for the early stage embryo development along with the regulation of Prnp expression.
Grants: This study was supported by the NRF-2021K1A4A7A02098794 and NRF-2023R1A2C3007223