Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.48 (transcriptase)
9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phytohormone abscisic acid (ABA) regulates plant growth and development as well as stress tolerance. To gain more insights into ABA signalling, a population of chemical-inducible activation-tagged Arabidopsis mutants was screened on the basis of the ABA effect on the inhibition of seed germination. Two novel ABA supersensitive mutants ABA supersensitive during germination1 (absg1) and absg2 were characterized as alleles of Dicer-like1 (DCL1) and HEN1, respectively, as microRNA biogenesis genes, and accordingly, these two mutants were renamed dcl1-11 and hen1-16. The dcl1-11 mutant was an ABA hypersensitive mutant for seed germination and root growth. Reverse transcriptase polymerase chain reaction assays revealed that the expression of ABA- and stress-responsive genes was increased in dcl1-11, as compared with the wild type (WT). Furthermore, the germination assay showed that dcl1-11 was also more sensitive to salt and osmotic stress. The hen1-16 mutant also showed supersensitive to ABA during seed germination. Further analysis showed that, among the microRNA biogenesis genes, all the other mutants were not only enhanced in sensitivity to ABA, salt and osmotic stress, but also enhanced the expression of ABA-responsive genes. In addition to the mutants in the microRNA biogenesis, the interruption of the production of crucial components of other small RNA pathways such as dcl2, dcl3 and dcl4 also caused ABA supersensitive during germination.
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PMID:The disturbance of small RNA pathways enhanced abscisic acid response and multiple stress responses in Arabidopsis. 1820 12

Plant microRNAs (miRNAs) and small interfering RNAs (siRNAs) bear a 2'-O-methyl group on the 3'-terminal nucleotide. This methyl group is post-synthetically added by the methyltransferase protein HEN1 and protects small RNAs from enzymatic activities that target the 3'-OH. A mutagenesis screen for suppressors of the partial loss-of-function hen1-2 allele in Arabidopsis identified second-site mutations that restore miRNA methylation. These mutations affect two subunits of the DNA-dependent RNA polymerase IV (Pol IV), which is essential for the biogenesis of 24 nt endogenous siRNAs. A mutation in RNA-dependent RNA polymerase 2, another essential gene for the biogenesis of endogenous 24-nt siRNAs, also rescued the defects in miRNA methylation of hen1-2, revealing a previously unsuspected, negative influence of siRNAs on HEN1-mediated miRNA methylation. In addition, our findings imply the existence of a negative modifier of HEN1 activity in the Columbia genetic background.
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PMID:siRNAs compete with miRNAs for methylation by HEN1 in Arabidopsis. 2044 24

Tobamoviral replicase possesses an RNA-dependent RNA polymerase (RDR) domain and is translated from genomic (g)RNA via a stop codon readthrough mechanism at a one-to-ten ratio relative to a shorter protein lacking the RDR domain. The two proteins share methyltransferase and helicase domains and form a heterodimer implicated in gRNA replication. The shorter protein is also implicated in suppressing RNA silencing-based antiviral defenses. Using a stop codon mutant of Oilseed rape mosaic tobamovirus (ORMV), we demonstrate that the readthrough replicase (p182) is sufficient for gRNA replication and for subgenomic RNA transcription during systemic infection in Nicotiana benthamiana and Arabidopsis thaliana. However, the mutant virus displays milder symptoms and does not interfere with HEN1-mediated methylation of viral short interfering (si)RNAs or plant small (s)RNAs. The mutant virus tends to revert the stop codon, thereby restoring expression of the shorter protein (p125), even in the absence of plant Dicer-like activities that generate viral siRNAs. Plant RDR activities that generate endogenous siRNA precursors do not prevent replication or movement of the mutant virus, and double-stranded precursors of viral siRNAs representing the entire virus genome are likely synthesized by p182. Transgenic expression of p125 partially recapitulates the ORMV disease symptoms associated with overaccumulation of plant sRNAs. Taken together, the readthrough replicase p182 is sufficient for viral replication and transcription but not for silencing suppression. By contrast, the shorter p125 protein suppresses silencing, provokes severe disease symptoms, causes overaccumulation of unmethylated viral and plant sRNAs but it is not an essential component of the viral replicase complex.
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PMID:Revisiting the Roles of Tobamovirus Replicase Complex Proteins in Viral Replication and Silencing Suppression. 2914 Jan 68