한빛사논문
- 조회203
Sung-Yeon Hwang 1,2,3,11, Hyewon Kim 1,2,3,11, Danielle Denisko 4,5,11, Boxun Zhao 4,6,7,11, Dohoon Lee 8,9, Jiseok Jeong 1,2,3, Jinuk Kim 2, Kiwon Park 1,2,3, Junhyun Park 1,2,3, Dongjoon Jeong 1,2,3, Sehong Park 1,2,3, Hee-Jung Choi 2, Sun Kim 10, Eunjung Alice Lee 4,5,6,7,* & Kwangseog Ahn 1,2,3,*
1Center for RNA Research, Institute for Basic Science, Seoul 08826, Republic of Korea.
2School of Biological Sciences, Seoul National University, Seoul 08826, Republic of Korea.
3SNU Institute for Virus Research, Seoul National University, Seoul 08826, Republic of Korea.
4Division of Genetics and Genomics, Boston Children’s Hospital and Harvard Medical School, Boston, MA 02115, USA.
5Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA.
6Broad Institute of MIT and Harvard, Cambridge, MA 02115, USA.
7Manton Center for Orphan Disease Research, Boston Children’s Hospital, Boston, MA 02115, USA.
8Bioinformatics Institute, Seoul National University, Seoul 08826, Republic of Korea.
9BK21 FOUR Intelligence Computing, Seoul National University, Seoul 08826, Republic of Korea.
10Department of Computer Science and Engineering, Seoul National University, Seoul 08826, Republic of Korea.
11These authors contributed equally: Sung-Yeon Hwang, Hyewon Kim, Danielle Denisko, Boxun Zhao.
*Corresponding authors: correspondence to Eunjung Alice Lee or Kwangseog Ahn
Abstract
Genetic parasites, including viruses and transposons, exploit components from the host for their own replication. However, little is known about virus-transposon interactions within host cells. Here, we discover a strategy where human cytomegalovirus (HCMV) hijacks L1 retrotransposon encoded protein during its replication cycle. HCMV infection upregulates L1 expression by enhancing both the expression of L1-activating transcription factors, YY1 and RUNX3, and the chromatin accessibility of L1 promoter regions. Increased L1 expression, in turn, promotes HCMV replicative fitness. Affinity proteomics reveals UL44, HCMV DNA polymerase subunit, as the most abundant viral binding protein of the L1 ribonucleoprotein (RNP) complex. UL44 directly interacts with L1 ORF2p, inducing DNA damage responses in replicating HCMV compartments. While increased L1-induced mutagenesis is not observed in HCMV for genetic adaptation, the interplay between UL44 and ORF2p accelerates viral DNA replication by alleviating replication stress. Our findings shed light on how HCMV exploits host retrotransposons for enhanced viral fitness.
논문정보
- Research article
- 2024년 09월 (BRIC 등록일 2024-09-04)
- 국내(교신)+국외 연구진
- 생명과학 > 감염생물학
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