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

While this Saccharomyces cerevisiae SIN4 gene product is a component of a mediator complex associated with RNA polymerase II, various studies suggest the involvement of Sin4 in the alteration of higher-order chromatin structure. Our previous analysis of a sin4 mutant suggested that the mechanisms of transcriptional repression by Sin4 (mediator) and the Tup1-Ssn6 complex (general repressor) are different. To elucidate the way in which these two repression systems are interrelated, we isolated mutants that exhibit enhanced transcription of a reporter gene harboring the upstream activation sequence (UAS), but still are subject to Tup1-Ssn6-mediated repression. Besides sin4, rgr1, tup1, and ssn6 mutants, we also obtained new mutants that enhance basal transcription even from a core promoter without UAS. Such mutants, designated rbt for regulator of basal transcription, can be classified into at least six complementation groups, i.e., four single (rbt1 to rbt4) and two apparently double (rbt5 rbt6 and rbt7 rbt8) mutations. The phenotype of rbt mutants is dependent on the TATA box and not specific to the integration site or kind of core promoter. No significant difference in micrococcal nuclease (MNase) accessibility to the core promoter of test genes was observed between rbt mutants and the wild-type strain, indicating that the higher-order chromatin structure of the core promoter region is not significantly altered in these mutants. The rbt1 to rbt4 mutations are suppressed by the Dgal11 mutation as in the case of the sin4 mutation, but give rise to a different profile from the sin4 mutation with regard to the activity of some of the promoters. From these observations, we suggest that RBT gene product(s) could be novel mediators that act with or in close association with Sin4 but have a function distinct from that of Sin4. Moreover, the fact that rbt mutations nullify Tup1-Ssn6 general repressor-mediated repression is consistent with the idea that the mechanisms of Rbt (mediator)- and Tup1-Ssn6 (general repressor)-mediated repression are interconnected but substantially different.
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PMID:Genetic characterization of rbt mutants that enhance basal transcription from core promoters in Saccharomyces cerevisiae. 1101 Nov 39

Estradiol has been shown to act in the central nervous system to promote neuronal growth, differentiation, and synaptic plasticity. Recent evidence indicates that estrogens exert these effects by enhancing the expression of genes that encode key proteins of the neuronal cytoskeleton and synaptic membranes. In a previous report, we demonstrated a sex-related difference in the developmental expression of Class II beta-tubulin (RBT(1)) mRNA, which encodes a neural-specific tubulin isotype. This difference, not shared by Class IV beta-tubulin mRNA or the mRNAs encoding neurofilament proteins, was restricted to the hypothalamus. RBT(1) mRNA levels were found to decrease in both sexes during postnatal development, but significantly earlier in females than in males, suggesting that the difference is steroid-dependent. The present experiments demonstrate that 17beta-estradiol increases, in a stereospecific manner, RBT(1) mRNA levels in the hypothalamus of developing female rats. The effect was also region-specific, us it was not detected in either the cerebral cortex or the cerebellum. The increase in RBT(1) mRNA levels was observed after either in vivo administration of 17beta-estradiol or in vitro exposure of the hypothalamus to the steroid, and it was evident during both neonatal-infantile development (4 to 12 days of age) and near the time of puberty (29 days of age). The effect was detected by RNA blot hybridization and verified by a sensitive, sequence-specific ribonuclease (RNase) protection assay. In vitro exposure of hypothalamic fragments containing the arcuate/ventromedial nucleus-median eminence region of 28-day-old animals to 17beta-estradiol prevented the decline in RBT(1) mRNA levels that follows selective blockade of mRNA synthesis via pharmacological inhibition of RNA polymerase II. The results suggest that the neurotrophic effects exerted by 17beta-estradiol during early postnatal development of the hypothalamus and in the arcuate/ventromedial nuclei at the time of puberty are, at least in part, mediated by an increase in RBT(1) mRNA levels, the consequence of an estradiol-dependent increase in RBT(1) mRNA stability.
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PMID:Estradiol Increases Neural-Specific Class II-beta-Tubulin mRNA Levels in the Developing Female Hypothalamus by Regulating mRNA Stability. 1991 49