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Liu, H.-P.

Publications and source records attributed to Liu, H.-P..

2 recordsLinked to original sources

Amur grape genome sequence

To date, there is no high-quality sequence for genomes of the East Asian grape species, hindering biological and breeding research efforts to improve grape cultivars. This study presents a [~]522 Mb of the Vitis amurensis (Va) genome sequence containing 27,635 coding genes. Phylogenetic analysis indicated that V. riparia (Vr) may firstly split from the other two species, Va, V. Vinifera (Vv; Pinot Noir: PN40024 and Cabernet Sauvignon). Much divergent gene reservation among three grape duplicated gene sets suggests that the core eudicot common hexaploidy (ECH), 130 million years ago (Mya), has still played a non-negligible role in grape species divergence and biological innovation. Prominent accumulation of sequence variants might have improved cold resistance in Va, resulting in a more robust cold resistance gene regulatory network than those in Vv and Vr. In contrast, Va preserved much fewer NBS disease resistance genes than the other grapes. Notably, multi-omics analysis identified one trans-cinnamate 4-monooxygenase gene positively correlated to the resveratrol accumulated during Va berry development. A selective sweep analysis revealed a hypothetical Va sex-determination region (SDR). Besides, a PPR-containing protein-coding gene in the hypothetical SDR may be related with sex determination in Va. The content and arrangement order of genes in the putative SDR of female Va were similar to the SDR of female Vv. However, the putative SDR of female Va lost one Flavin-containing monooxygenases (FMO) and contained one extra uncharacterized protein-coding gene. These findings will improve the understanding of Vitis biology and contribute to the improvement of grape breeding.

genomics↗

Adenosine Deaminase Acting on RNA 1 Associates with Orf Virus OV20.0 and Enhances Viral Replication

Orf virus (ORFV) infects sheep and goats and is also an important zoonotic pathogen. The viral protein OV20.0 has been shown to suppress innate immunity by targeting the double-stranded RNA (dsRNA)-activated protein kinase (PKR) by multiple mechanisms. These mechanisms include a direct interaction with PKR and binding with two PKR activators, dsRNA and the cellular PKR activator (PACT), which ultimately leads to the inhibition of PKR activation. In the present study, we identified a novel association between OV20.0 and adenosine deaminase acting on RNA 1 (ADAR1). OV20.0 bound directly to the dsRNA binding domains (RBDs) of ADAR1 in the absence of dsRNA. Additionally, OV20.0 preferentially interacted with RBD1 of ADAR1, which was essential for its dsRNA binding ability and for the homodimerization that is critical for intact adenosine (A)-to-inosine (I) editing activity. Finally, the association with OV20.0 suppressed the A-to-I editing ability of ADAR1, while ADAR1 played a proviral role during ORFV infection by inhibiting PKR phosphorylation. These observations revealed a new strategy used by OV20.0 to evade antiviral responses via PKR.\n\nImportanceViruses evolve specific strategies to counteract host innate immunity. ORFV, an important zoonotic pathogen, encodes OV20.0 to suppress PKR activation via multiple mechanisms, including interactions with PKR and two PKR activators. In this study, we demonstrated that OV20.0 interacts with ADAR1, a cellular enzyme responsible for converting adenosine (A) to inosine (I) in RNA. The RNA binding domains, but not the catalytic domain, of ADAR1 are required for this interaction. The OV20.0-ADAR1 association affects the functions of both proteins; OV20.0 suppressed the A-to-I editing of ADAR1, while ADAR1 elevated OV20.0 expression. The proviral role of ADAR1 is likely due to the inhibition of PKR phosphorylation. As RNA editing by ADAR1 contributes to the stability of the genetic code and the structure of RNA, these observations suggest that in addition to serving as a PKR inhibitor, OV20.0 might modulate ADAR1-dependent gene expression to combat antiviral responses or achieve efficient viral infection.

microbiology↗