Browsing by Subject "ATCV-1"
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Publication Wirt-Virus Wechselwirkungen bei der Infektion durch Acanthocystis turfacea Chlorella Virus 1 : Regulation der Genexpression früher Gene und des Ubiquitin-Systems(2021) Lindner, Kamila; Pfitzner, Artur J. P.Acanthocystis turfacea Chlorella Virus 1 (ATCV-1) is a virus of the genus Chloroviruses that infects the unicellular green alga Chlorella heliozoae. The infection with ATCV-1 is lethal for the algae and requires the correct expression of the 860 hypothetical virus genes. These genes are divided into early, early/late and late genes which are expressed at different times, depending on their protein function. Gene expression is regulated by their corresponding viral promoters and can be controlled by viral or host-specific transcription factors. The stability of proteins is regulated by the host’s ubiquitin system. This study investigated the expression of early viral genes and the ubiquitin- mediated protein degradation regulated by ATCV-1. By investigating the promoters of the early genes of ATCV-1 Z174L, Z765R and Z798L respectively, consensus sequences were identified including a Hex motif and a TATA box that can be bound by viral, but most importanly, host transcription factors. By in vivo interactions with G-box binding factors, a direct regulation of the early promoters, including aforementioned Hex motif, could be demonstrated. Along with this new regulatory mechanism for the expression of early viral genes, evidence for additional mechanisms for the regulation of early genes with different consensus sequences, such as AATGACA, were found. In the second part of this study, three novel viral proteins were identified as proteins of the ubiquitin system: a viral ubiquitin (Z203L), a viral RING E3 ligase (Z292L) and a viral SKP1 protein (Z339L). Experiments have shown that ATCV-1 is able to interfere with the host’s ubiquitin system using these proteins. Although the E3 ligases are responsible for the specific ubiquitination of the target proteins (e.g. Z292L in the case of enolase), the additional expression of a viral ubiquitin ensures a sufficient amount of the signal protein is present. The results of this study demonstrate a wide range of host-virus interactions at the level of gene regulation and protein degradation. ATCV-1 can use host factors to initiate its own gene expression and, with the help of the components of the ubiquitin system encoded in the viral genome, reprogram the host’s protein degradation.