Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
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The genomic DNA of Helicoverpa armigera single-nucleocapsid nucleopolyhedrovirus (C1 clone) was digested with BamHI, EcoRV, HindIII, KpnI, PstI and XbaI, respectively, and formed 11, 31, 13, 6, 7, and 25 fragments larger than 400 bp, respectively. The size of genome was estimated to be about 130.7 kb. A detailed physical map was constructed for the six restriction enzymes. The five homologous region, hr1, hr2, hr3, hr4 and hr5, and the ten genes including polyhedrin gene (ph), immediate-early gene(ie1), p74, p10, chitinase gene, DNA directed DNA polymerase gene (DNApol), helicase gene, superoxide dismutase gene (sod), alkaline-exonuclease gene (alk-exo), ecdysteroid UDP-glucosyltransferase gene (egt) were identified and their locations in the genome were determined. The genome organization of HaSNPV is quite different from those of other NPVs ever determined. The p10 gene was located in the fragment BamHI-I(1.89 kb) with the transcriptional direction opposite to the polyhedrin gene. Upstream and downstream of the p10 gene were p26 and p74 gene, respectively. The transcriptional direction of p26 is the same as that of p10 gene, and opposite to that of the p74 gene. The ORF encoding p10 was 261 nucleotide long and encoding a putative 87 amino acid polypeptide of 9.3 kD. The immediate upsteam region of the p10 was an A-rich region, and aconserved TAAG motif, associated with transcriptional start sites in other p10 genes, was identified at a site 52 nucleotides upstream of the start codon ATG. A putative polyadenylation signal, AATAAA, was found 20 nucleotides downstream of the termination codon.
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PMID:Genome Structure and the p10 Gene of the Helicoverpa armigera Nucleopolyhedrovirus. 1205 Aug 7

Strains of the yeast Pichia inositovora that carry the linear plasmids pPin1-1 (18 kb) and pPin1-3 (10 kb) display a killer activity towards Saccharomyces cerevisiae. Cloning and sequencing of the smaller plasmid, pPin1-3, revealed that it is 9683 bp long and has 154-bp terminal inverted repeats. Comparison of pPin1-3 with the only other completely sequenced killer plasmid, pGKL1 of Kluyveromyces lactis, revealed differences in genome organization. The Pichia element has four ORFs that account for 95% of the sequence. ORF1 is homologous to the putative immunity gene of the K. lactis system. A viral B-type DNA polymerase is encoded by ORF2. The predicted product of ORF3 displays similarities to the alpha- and beta-subunits of the heterotrimeric K. lactis killer toxin, also known as zymocin. A cysteine-rich chitin-binding site and a chitinase signature, characteristic for the alpha-subunit of zymocin were identified in Orf3p. Chitin affinity chromatography and Western analysis confirmed the plasmid specific expression and secretion of a protein that cross-reacts with an antibody raised against the alpha-subunit of K. lactis zymocin. Disruption of the major chitin synthase-gene ( CHS3) renders S. cerevisiae resistant to the toxin, providing further evidence that chitin is the cellular receptor for the P. inositovora toxin. Orf4p of pPin1-3 displays only weak similarities to the gamma-subunit of zymocin, which causes a G1 cell-cycle arrest in S. cerevisiae. However, disruption of the S. cerevisiae gene ELP3/TOT3, which encodes a histone-acetyltransferase that is essential for zymocin action, resulted in reduced sensitivity to the P. inositovora toxin also. Thus, despite obvious differences in genome organization and protein architecture, both killer systems very probably have similar modes of action.
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PMID:Structural and functional analysis of the killer element pPin1-3 from Pichia inositovora. 1368 Mar 68

The multicapsid nucleopolyhedroviruses (NPVs) of Spodoptera exigua (SeMNPV), Spodoptera frugiperda (SfMNPV), and Spodoptera littoralis (SpliNPV) are genetically similar (78 % similarity) but differ in their degree of host specificity. Infection by each of the three NPVs in these three Spodoptera host species was determined by oral inoculation of larvae with occlusion bodies (OBs) or intrahaemocoelic injection with occlusion derived virions (ODVs). RT-PCR analysis of total RNA from inoculated insects, targeted at immediate early (ie-0), early (egt, DNA polymerase), late (chitinase) and very late genes (polyhedrin), indicated that each of the NPVs initiated an infection in all three host species tested. SpliMNPV produced a fatal NPV disease in both heterologous hosts, S. frugiperda and S. exigua, by oral inoculation or injection. SfMNPV was lethal to heterologous hosts, S. exigua and S. littoralis, but infected larvae did not melt and disintegrate, and progeny OBs were not observed. SeMNPV was able to replicate in heterologous hosts and all genes required for replication were present in the genome, as the virus primary infection cycle was observed. However, gene expression was significantly lower in heterologous hosts. SeMNPV pathogenesis in S. frugiperda and S. littoralis was blocked at the haemocoel transmission stage and very nearly cleared. SeMNPV mixtures with SpliMNPV or SfMNPV did not extend the host range of SeMNPV; in all cases, only the homologous virus was observed to proliferate. It is concluded that entry and the primary virus infection cycle are not the only, or the major determinants, for SeMNPV infection of heterologous Spodoptera species.
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PMID:Virus entry or the primary infection cycle are not the principal determinants of host specificity of Spodoptera spp. nucleopolyhedroviruses. 1544 46