Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cells respond to environmental stimuli by fine-tuned regulation of gene expression. Here we investigated the dose-dependent modulation of gene expression at high temporal resolution in response to nutrient and stress signals in yeast. The GAL1 activity in cell populations is modulated in a well-defined range of galactose concentrations, correlating with a dynamic change of histone remodeling and RNA polymerase II (RNAPII) association. This behavior is the result of a heterogeneous induction delay caused by decreasing inducer concentrations across the population. Chromatin remodeling appears to be the basis for the dynamic GAL1 expression, because mutants with impaired histone dynamics show severely truncated dose-response profiles. In contrast, the GRE2 promoter operates like a rapid off/on switch in response to increasing osmotic stress, with almost constant expression rates and exclusively temporal regulation of histone remodeling and RNAPII occupancy. The Gal3 inducer and the Hog1 mitogen-activated protein (MAP) kinase seem to determine the different dose-response strategies at the two promoters. Accordingly, GAL1 becomes highly sensitive and dose independent if previously stimulated because of residual Gal3 levels, whereas GRE2 expression diminishes upon repeated stimulation due to acquired stress resistance. Our analysis reveals important differences in the way dynamic signals create dose-sensitive gene expression outputs.
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PMID:Different Mechanisms Confer Gradual Control and Memory at Nutrient- and Stress-Regulated Genes in Yeast. 2628 30

Meloidogyne incognita is a major plant parasite that causes root-knot disease in numerous agricultural crops. This nematode has severely affected greenhouse crops in China. Chemical insecticides are generally used to control this pest, but they have adverse environmental and human toxicity effects; hence, safe and effective strategies for controlling the root-knot nematode (RKN) are necessary. FMRFamide-like peptides (FLPs) have diverse physiological and biological effects on the locomotory, feeding, and reproductive functions of nematodes, and mitogen-activated protein (MAP) kinase plays an important role in the regulation of transcription factors and protein kinases. These candidates are the common targets of RKN control. They are encoded by Mi-flp-18 and Mi-mpk-1 genes, respectively, in M. incognita . In this study, we used the RNA interference (RNAi) method to silence the transcription of these genes and determined the effects on the pathogenicity of RKN in potted plants. Real-time quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) revealed that Mi-mpk-1 gene expression could be reduced by 33% by RNAi. The RNAi-treated infective nematodes were inoculated with dsRNAs of Mi-flp-18 and Mi-mpk-1 in pot experiments. The root-knot numbers were reduced by 51% after Mi-flp-18 RNAi treatment. Further, the relative abundance of Mi-flp-18 was downregulated by 79% in the endoparasitic M. incognita . Mi-flp-18 RNAi treatment decreased egg masses by 92% and egg numbers by 58%. Mi-mpk-1 RNAi treatment reduced the root-knot numbers by 32% and, remarkably, lowered the relative abundance of Mi-mpk-1 in the endoparasitic M. incognita . Egg masses and numbers were reduced by 42 and 22%, respectively, after RKN was inoculated for 35 days with Mi-mpk-1 RNAi. Therefore, Mi-flp-18 and Mi-mpk-1 genes are susceptible to RNAi and can be used as potential targets for RKN control by regulating nematode infection, parasitism, and reproduction.
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PMID:Mi-flp-18 and Mi-mpk-1 Genes are Potential Targets for Meloidogyne incognita Control. 2678 73

Aberrant profiles of pre-mRNA splicing are frequently observed in cancer. At the molecular level, an altered profile results from a complex interplay between chromatin modifications, the transcriptional elongation rate of RNA polymerase, and effective binding of the spliceosome to the generated transcripts. Key players in this interplay are regulatory splicing factors (SFs) that bind to gene-specific splice-regulatory sequence elements. Although mutations in genes of some SFs were described, a major driver of aberrant splicing profiles is oncogenic signal transduction pathways. Signaling can affect either the transcriptional expression levels of SFs or the post-translational modification of SF proteins, and both modulate the ratio of nuclear versus cytoplasmic SFs in a given cell. Here, we will review currently known mechanisms by which cancer cell signaling, including the mitogen-activated protein kinases (MAPK), phosphatidylinositol 3 (PI3)-kinase pathway (PI3K) and wingless (Wnt) pathways but also signals from the tumor microenvironment, modulate the activity or subcellular localization of the Ser/Arg rich (SR) proteins and heterogeneous nuclear ribonucleoproteins (hnRNPs) families of SFs.
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PMID:Signaling Pathways Driving Aberrant Splicing in Cancer Cells. 2928 7


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