Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DNA fragments comprising each of the promoter regions from the geminivirus African cassava mosaic virus (ACMV) were cloned into the pUC18-based vector, pG1, producing transcriptional fusions with the beta-glucuronidase gene (GUS) and nopaline synthase terminator sequence. The relative activity of each promoter construct was analyzed by a GUS expression assay of extracts from Nicotiana clevelandii protoplasts coelectroporated with the GUS reporter constructs and constructs in which individual ACMV open reading frames (ORFs) were placed under control of a cauliflower mosaic virus 35 S promoter. Results suggest repression of the AC1 gene by its gene product, which is required for ACMV DNA synthesis. The promoter activity observed for the single promoter for the DNA A genes encoding functions of spread and the regulation of replication (AC2 and AC3 ORFs) was unaffected by coelectroporation with any of the ACMV ORF constructs. Promoters for the AV1 (coat protein) gene and the two DNA B genes (BV1 and BC1) were activated by electroporation of the AC2 ORF construct. To a lesser extent promoters for the AV1 and BV1 genes were activated with the AC3 ORF construct. The same pattern of promoter repression and activation was observed when transgenic N. benthamiana plants expressing the GUS reporter constructions were inoculated with ACMV DNA A.
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PMID:Regulation of the activities of African cassava mosaic virus promoters by the AC1, AC2, and AC3 gene products. 158 57

Fragments of the African cassava mosaic virus (ACMV) genome, cloned upstream of the beta-glucuronidase (GUS) reporter gene in an expression cassette, were analysed for their ability to direct complementary-sense gene expression in tobacco protoplasts by measuring GUS activity. Five arbitrary domains (A-E) have been designated that contribute to the expression of AC1 (replication-associated protein) and AC4. Consistent with earlier reports, AC1 gene expression was negatively regulated (80% reduction in activity) by its own protein product, and suppression was mimicked by truncated versions of AC1 comprising the N-terminal 57 amino acids. AC1 also suppressed AC4 gene expression to a similar extent. Nucleotide sequences responsible for suppression were mapped to domain A, a 92 bp fragment located immediately upstream of the AC1 initiation codon encompassing the consensus TATA box and transcription start point. Complementary-sense gene expression also decreased by 30-40% in the presence of AV1 (coat protein) although other DNA A-encoded proteins (AV2, AC2, AC3 and AC4) had no effect. The results are discussed in the light of recent advances concerning the initiation of viral DNA replication and the control of gene expression.
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PMID:Regulation of African cassava mosaic virus complementary-sense gene expression by N-terminal sequences of the replication-associated protein AC1. 759 45