The University of Tokyo · Medicine
Professor Jumpei Ito's research lab focuses on the evolutionary and molecular interactions between host defense systems and retroelements, particularly endogenous retroviruses (ERVs) and APOBEC3 antiviral factors. The lab investigates how endogenous retroviral sequences shape host gene regulation and immune defense, with a strong emphasis on epigenetic regulation, viral restriction mechanisms, and the coevolutionary dynamics between host restriction factors and retroviruses. Recent work explores the role of HERV-derived regulatory elements in cancer gene expression aberrations and the convergent evolution of SARS-CoV-2 spike protein mutations in Omicron subvariants. The lab integrates genomics, evolutionary biology, and virology to uncover fundamental principles of host-pathogen coevolution.
Figures are computed from collected data and may differ slightly.
Human endogenous retroviruses (HERVs) and other long terminal repeat (LTR)-type retrotransposons (HERV/LTRs) have regulatory elements that possibly influence the transcription of host genes. We systematically identified and characterized these regulatory elements based on publicly available datasets of ChIP-Seq of 97 transcription factors (TFs) provided by ENCODE and Roadmap Epigenomics projects. We determined transcription factor-binding sites (TFBSs) using the ChIP-Seq datasets and identified
In late 2022, various Omicron subvariants emerged and cocirculated worldwide. These variants convergently acquired amino acid substitutions at critical residues in the spike protein, including residues R346, K444, L452, N460, and F486. Here, we characterize the convergent evolution of Omicron subvariants and the properties of one recent lineage of concern, BQ.1.1. Our phylogenetic analysis suggests that these five substitutions are recurrently acquired, particularly in younger Omicron lineages.
<i>APOBEC3</i> (<i>A3</i>) genes are members of the <i>AID/APOBEC</i> gene family that are found exclusively in mammals. <i>A3</i> genes encode antiviral proteins that restrict the replication of retroviruses by inducing G-to-A mutations in their genomes and have undergone extensive amplification and diversification during mammalian evolution. Endogenous retroviruses (ERVs) are sequences derived from ancient retroviruses that are widespread mammalian genomes. In this study we characterize the <i
Gene expression aberration is a hallmark of cancers, but the mechanisms underlying such aberrations remain unclear. Human endogenous retroviruses (HERVs) are genomic repetitive elements that potentially function as enhancers. Since numerous HERVs are epigenetically activated in tumors, their activation could cause global gene expression aberrations in tumors. Here, we show that HERV activation in tumors leads to the up-regulation of hundreds of transcriptional suppressors, namely, Krüppel-associ
The host defense against viral infection is acquired during the coevolution or symbiosis of the host and pathogen. Several cellular factors that restrict retroviral infection have been identified in the hosts. Feline leukemia virus (FeLV) is a gammaretrovirus that is classified into several receptor interference groups, including a novel FeLV-subgroup D (FeLV-D) that we recently identified. FeLV-D is generated by transduction of the env gene of feline endogenous gammaretrovirus of the domestic c
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