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Human Endogenous Retrovirus K (HERV-K) can drive gene expression as a promoter in Caenorhabditis elegans.
Serpen Durnaoglu1,2 (Post-Doc), Heui-Soo Kim3 (Professor), Joohong Ahnn 1,2,# (Professor), Sun-Kyung Lee 1,2,*,# (Research Professor)
1Dept. of Life Science, Hanyang University,
2Research Institute for Natural Sciences, Hanyang Univerisity,
33Department of Biological Sciences, College of Natural Sciences,, Pusan National University
Abstract
Endogenous retroviruses (ERVs) are retrotransposons present in various metazoan genomes, and have been implicated in metazoan evolution but also in that of nematodes and humans. The long terminal repeat (LTR) retrotransposons contain several regulatory sequences including promoters and enhancers that regulate endogenous gene expression and thereby control organismal development. ERVs including the LTR retrotransposons constitute 8% of the human genome, and less than 0.6% of the Caenorhabditis elegans (C. elegans) genome, a nematode genetic model system. To investigate the evolutionarily conserved mechanism in the transcriptional activity of retrotransposons, we generated a transgenic worm model driving green fluorescent protein (GFP) expression using Human endogenous retroviruses (HERV)-K LTR as a promoter. The promoter activity of HERV-K LTR was robust and fluorescence was observed in various tissues throughout development. Interestingly, persistent GFP expression was specifically detected in the adult vulva muscle. Using deletion constructs, we found that the region from positions 675 to 868 containing the TATA box was necessary for promoter activity driving gene expression in the vulva. Interestingly, we found that the promoter activity of the LTR was dependent on che-1 transcription factor, a sensory neuron driver, and lin-15b, a negative regulator of RNAi and germline gene expression. These results suggest an evolutionary conservation of the LTR retrotransposon activity in transcriptional regulation as well as the possibility of che-1 function in non-neuronal tissues.
Abstract, Accepted Manuscript(in press) [Submitted on July 15, 2020, Accepted on August 20, 2020]
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