Background: Recent research results strongly suggest that certain genetic variants of grapevine virus A (GVA) and grapevine virus B (GVB), two members of the Vitivirus genus of the family Betaflexiviridae, are the cause of Shiraz disease and corky bark disease of grapevines in South Africa, respectively. To investigate this hypothesis, work was undertaken to construct DNA clones of these viruses.
Findings And Conclusions: Biologically viable and stable DNA clones of genetic variants of GVA and GVB B from South Africa were constructed. The clones share 76.3, 73.2 and 85.2, 77.6 % nt sequence similarity with corresponding clones constructed in Italy and Israel. The results suggest that a derivative of a mini binary vector pCB302 is superior to pCAMBIA1305.1 for the construction of infectious and stable DNA clones of vitiviruses. Successful construction of such DNA clones of GVA and GVB reported in this study is a clear step towards fulfilling Koch's 3rd postulate in investigating the aetiology of Shiraz disease and corky bark disease.
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http://dx.doi.org/10.1186/s40064-015-1517-2 | DOI Listing |
J Transl Med
January 2025
Department of Radiation Oncology, State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Background: Drug resistance constitutes one of the principal causes of poor prognosis in breast cancer patients. Although cancer cells can maintain viability independently of mitochondrial energy metabolism, they remain reliant on mitochondrial functions for the synthesis of new DNA strands. This dependency underscores a potential link between mitochondrial energy metabolism and drug resistance.
View Article and Find Full Text PDFWe lack tools to edit DNA sequences at scales necessary to study 99% of the human genome that is noncoding. To address this gap, we applied CRISPR prime editing to insert recombination handles into repetitive sequences, up to 1697 per cell line, which enables generating large-scale deletions, inversions, translocations, and circular DNA. Recombinase induction produced more than 100 stochastic megabase-sized rearrangements in each cell.
View Article and Find Full Text PDFMol Cancer Res
January 2025
Weill Cornell Medicine, New York, NY, United States.
Kaposi Sarcoma (KS) is a frequently aggressive malignancy caused by Kaposi sarcoma herpesvirus (KSHV/HHV-8). People with immunodeficiencies, including HIV, are at increased risk for developing KS, but our understanding of the contributions of the cellular genome to KS pathogenesis remains limited. To determine if there are cellular genetic alterations in KS that might provide biological or therapeutic insights, we performed whole exome sequencing on 78 KS tumors and matched normal control skin from 59 adults with KS (46 with HIV-associated KS and 13 with HIV-negative KS) receiving treatment at the Uganda Cancer Institute in Kampala, Uganda.
View Article and Find Full Text PDFNucleic Acids Res
January 2025
Department of Pharmaceutical Sciences, University of California, Irvine, CA 92697-3958, United States.
Growth in the development of engineered polymerases for synthetic biology has led to renewed interest in assays that can measure the fidelity of polymerases that are capable of synthesizing artificial genetic polymers (XNAs). Conventional approaches require purifying the XNA intermediate of a replication cycle (DNA → XNA → DNA) by denaturing polyacrylamide gel electrophoresis, which is a slow, costly, and inefficient process that requires a large-scale transcription reaction and careful extraction of the XNA strand from the gel slice. In an effort to streamline the assay, we developed a purification-free approach in which the XNA transcription and reverse transcription steps occur inside the matrix of a hydrogel-coated magnetic particle.
View Article and Find Full Text PDFNat Rev Cancer
January 2025
Translational Oncogenomics Laboratory, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UK.
Intratumour hypoxia is a feature of all heterogenous solid tumours. Increased levels or subregions of tumour hypoxia are associated with an adverse clinical prognosis, particularly when this co-occurs with genomic instability. Experimental evidence points to the acquisition of DNA and chromosomal alterations in proliferating hypoxic cells secondary to inhibition of DNA repair pathways such as homologous recombination, base excision repair and mismatch repair.
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