Upstream activating sequence

About: Upstream activating sequence is a research topic. Over the lifetime, 1633 publications have been published within this topic receiving 100112 citations.

Interaction between Transactivation Domain of p53 and Middle Part of TBP-Like Protein (TLP) Is Involved in TLP-Stimulated and p53-Activated Transcription from the p21 Upstream Promoter

Abstract: TBP-like protein (TLP) is involved in transcriptional activation of an upstream promoter of the human p21 gene. TLP binds to p53 and facilitates p53-activated transcription from the upstream promoter. In this study, we clarified that in vitro affinity between TLP and p53 is about one-third of that between TBP and p53. Extensive mutation analyses revealed that the TLP-stimulated function resides in transcription activating domain 1 (TAD1) in the N-terminus of p53. Among the mutants, #22.23, which has two amino acid substitutions in TAD1, exhibited a typical mutant phenotype. Moreover, #22.23 exhibited the strongest mutant phenotype for TLP-binding ability. It is thus thought that TLP-stimulated and p53-dependent transcriptional activation is involved in TAD1 binding of TLP. #22.23 had a decreased transcriptional activation function, especially for the upstream promoter of the endogenous p21 gene, compared with wild-type p53. This mutant did not facilitate p53-dependent growth repression and etoposide-mediated cell-death as wild-type p53 does. Moreover, mutation analysis revealed that middle part of TLP, which is requited for p53 binding, is involved in TLP-stimulated and p53-dependent promoter activation and cell growth repression. These results suggest that activation of the p21 upstream promoter is mediated by interaction between specific regions of TLP and p53.

Complex Regulatory Network for nif and fix Gene Expression in Bradyrhizobium Japonicum

Abstract: In the nitrogen-fixing soybean symbiont, Bradyrhizobium japonicum, the expression of nif and fix genes is regulated predominantly, if not exclusively, in response to the cellular oxygen status. Activation of these genes occurs during symbiosis in root nodules or in free-living cells grown at low oxygen concentrations. We have identified three regulatory elements that are involved in oxygen control at different levels. First, with regard to nif and fix gene expression, the positive regulatory protein NifA plays a crucial role. It was demonstrated that the binding of NifA to its target site in the upstream region of the B japonicum nifD promoter was regulated by oxygen and required metal ions. Second, fixLJ-like genes that had been shown to activate the Rhizobium meliloti nifA gene under low oxygen conditions (1, 2), were identified also in B.japonicum. However, they were probably not involved in the expression of nifA, but in the regulation of other oxygen-controlled genes. Third, we found two functional genes (rpoNl, rpoN2) encoding specific σ factors (σ54) and demonstrated that rpoNl expression was oxygen regulated via a mechanism involving fixLJ whereas rpoN2 was subject to negative autoregulation.

Sequences downstream from the transcriptional start site are essential for microaerobic, but not symbiotic, expression of the Rhizobium meliloti nifHDK promoter.

Abstract: Deletion analysis studies have been carried out on the nifHDK promoter (P1) of R. meliloti in an attempt to determine sequences involved in the expression of this promoter under both free-living microaerobic and symbiotic conditions. Deletion of a region downstream (+17 to +61) from the promoter element resulted in low levels of expression under free-living microaerobic conditions. However, wild-type levels of expression were obtained during symbiosis with Alfalfa plants. The sequences in this region were designated the "downstream sequences'. The pattern of expression observed when the downstream sequences were deleted was similar to that observed when a previously identified upstream activator sequence (UAS) was deleted. Only when both the downstream sequences and the UAS were deleted, did activity from the P1 promoter become significantly decreased during symbiosis. Expression studies of the P1 promoter in a nifA mutant background indicate that nifA is required for symbiotic expression of P1 which is enhanced by the presence of the downstream sequences.