scholarly journals Characterization of the mammalian DEAD-box protein DDX5 reveals functional conservation withS. cerevisiaeortholog Dbp2 in transcriptional control and glucose metabolism

RNA ◽  
2017 ◽  
Vol 23 (7) ◽  
pp. 1125-1138 ◽  
Author(s):  
Zheng Xing ◽  
Siwen Wang ◽  
Elizabeth J. Tran
1986 ◽  
Vol 6 (2) ◽  
pp. 688-702 ◽  
Author(s):  
J M Ivy ◽  
A J Klar ◽  
J B Hicks

Mating type in the yeast Saccharomyces cerevisiae is determined by the MAT (a or alpha) locus. HML and HMR, which usually contain copies of alpha and a mating type information, respectively, serve as donors in mating type interconversion and are under negative transcriptional control. Four trans-acting SIR (silent information regulator) loci are required for repression of transcription. A defect in any SIR gene results in expression of both HML and HMR. The four SIR genes were isolated from a genomic library by complementation of sir mutations in vivo. DNA blot analysis suggests that the four SIR genes share no sequence homology. RNA blots indicate that SIR2, SIR3, and SIR4 each encode one transcript and that SIR1 encodes two transcripts. Null mutations, made by replacement of the normal genomic allele with deletion-insertion mutations created in the cloned SIR genes, have a Sir- phenotype and are viable. Using the cloned genes, we showed that SIR3 at a high copy number is able to suppress mutations of SIR4. RNA blot analysis suggests that this suppression is not due to transcriptional regulation of SIR3 by SIR4; nor does any SIR4 gene transcriptionally regulate another SIR gene. Interestingly, a truncated SIR4 gene disrupts regulation of the silent mating type loci. We propose that interaction of at least the SIR3 and SIR4 gene products is involved in regulation of the silent mating type genes.


2008 ◽  
Vol 49 (10) ◽  
pp. 1563-1571 ◽  
Author(s):  
Jin Sun Kim ◽  
Kyung Ae Kim ◽  
Tae Rin Oh ◽  
Chul Min Park ◽  
Hunseung Kang

2015 ◽  
Vol 69 (3) ◽  
pp. 417-434
Author(s):  
Tetsuo Takahashi ◽  
Takashi Nedachi ◽  
Takuya Etoh ◽  
Hiroyuki Tachikawa ◽  
Xiao-Dong Gao

2021 ◽  
Author(s):  
Fatemeh Khakdan ◽  
Zahra Shirazi ◽  
Mojtaba Ranjbar

Abstract Methyl chavicol and methyl eugenol are important phenylpropanoid compounds previously purified from basil. These compounds are significantly enhanced by the water deficit stress-dependent mechanism. Here, for the first time, pObCVOMT and pObEOMT promoters were extracted by the genome walking method. They were then cloned into the upstream of the β-glucuronidase (GUS) reporter gene to identify the pattern of GUS water deficit stress-specific expression. Histochemical GUS assays showed in transgenic tobacco lines bearing the GUS gene driven by pObCVOMT and pObEOMT promoters, GUS was strongly expressed under water deficit stress. qRT-PCR analysis of pObCVOMT and pObEOMT transgenic plants confirmed the histochemical assays, indicating that the GUS expression is also significantly induced and up-regulated by increasing density of water deficit stress. This indicates these promoters are able to drive inducible expression. The cis-acting elements analysis showed that the pObCVOMT and pObEOMT promoters contained dehydration or water deficit-related transcriptional control elements.


2020 ◽  
Author(s):  
Manish Bhattacharjee ◽  
Navin Adhikari ◽  
Renu Sudhakar ◽  
Zeba Rizvi ◽  
Divya Das ◽  
...  

ABSTRACTA variety of post-translational modifications of Plasmodium falciparum proteins, including phosphorylation and ubiquitination, are shown to have key regulatory roles. The neural precursor cell expressed developmentally downregulated protein 8 (NEDD8) is a ubiquitin-like modifier of cullin-RING E3 ubiquitin ligases, which regulate diverse cellular processes, including the cell-cycle. Although neddylation pathway is conserved in eukaryotes, it is yet to be characterized in Plasmodium and related apicomplexan parasites. Towards studying the neddylation pathway in malaria parasites, we characterized P. falciparum NEDD8 (PfNEDD8) and identified cullins as its physiological substrates. PfNEDD8 is a 76 amino acid residue protein without the C-terminal tail, indicating that it can be readily conjugated. The wild type and mutant (Gly75Gly76 mutated to Ala75Ala76) PfNEDD8 were expressed in P. falciparum. Western blot of wild type PfNEDD8-expressing parasites indicated multiple high molecular weight conjugates, which were absent in the parasites expressing the mutant, indicating conjugation of NEDD8 to proteins through Gly76. Immunoprecipitation followed by mass spectrometry of wild type PfNEDD8-expressing parasites identified several proteins, including two putative cullins. Furthermore, we expressed PfNEDD8 in mutant S. cerevisiae strains that lacked endogenous NEDD8 (Δrub1) or NEDD8 conjugating E2 enzyme (ΔUbc12). The western blot of complemented strains and mass spectrometry of PfNEDD8 immunoprecipitate showed conjugation of PfNEDD8 to S. cerevisiae cullin cdc53, demonstrating functional conservation and cullins as the physiological substrates of PfNEDD8. The characterization of PfNEDD8 and identification of cullins as its substrates make ground for investigation of specific roles and drug target potential of neddylation pathway in malaria parasites.


1991 ◽  
Vol 11 (5) ◽  
pp. 2467-2480 ◽  
Author(s):  
K Gottesdiener ◽  
H M Chung ◽  
S D Brown ◽  
M G Lee ◽  
L H Van der Ploeg

The expressed variant cell surface glycoprotein (VSG) gene of Trypanosoma brucei is located at the 3' end of a large, telomeric, polycistronic transcription unit or expression site. We show that the region 45 kb upstream of the VSG gene, in the expression site on a 1.5-Mb chromosome, contains at least two promoters that are arranged in tandem, directing the transcription of the expression site. DNA rearrangement events occur specifically, at inactivation of the expression site, and these events delete the most upstream transcribed region and replace it with a large array of simple-sequence DNA, leaving the downstream promoter intact. Because of the placement of simple-sequence DNA, the remaining downstream promoter now becomes structurally identical to previously described VSG promoters. The downstream promoter is repetitive in the genome, since it is present at several different expression sites. Restriction fragment length polymorphism mapping allows grouping of the expression sites into two families, those with and those without an upstream transcription unit, and the DNA rearrangement events convert the expression sites from one type to the other. Deletion of the upstream transcription unit also leads to the loss of several steady-state RNAs. The findings may indicate a role for promoter-associated DNA rearrangement events, and/or interactions between tandemly arranged promoters, in expression site transcriptional control.


2020 ◽  
Vol 16 ◽  
pp. 117693432091325
Author(s):  
Mehtap Bayır ◽  
Gökhan Arslan ◽  
Abdulkadir Bayır

Four cpt 1 genes ( cpt 1α1a, cpt 1α2a, cpt 1α2b, and cpt 1β) were identified in the Nile tilapia genome. Two transmembrane helix domains (TMH) were identified for Cpt 1α1a, Cpt 1α2a, and Cpt 1β, while Cpt 1α2b had only one TMH domain. Evidence was found of conserved gene synteny between cpt 1 genes from Nile tilapia and the cpt 1/CPT 1 genes of zebrafish and human. Phylogenetic analysis showed that Nile tilapia Cpt 1 sequences clustered in distinct clades with their orthologous Cpt 1/CPT 1 from other vertebrates. Nile tilapia cpt 1α1a, cpt 1α2a, cpt 1α2b, and cpt 1β contain 18 coding exons encoding polypeptides of 771, 784, 788, and 786 amino acids in length, respectively. The cpt 1 genes were determined in all the tested tissues with varying tissue distribution patterns. These findings suggest that (1) cpt 1α1a, cpt 1α2a, and cpt 1α2b arose in the Nile tilapia genome as a result of the teleost-specific whole-genome duplication; (2) nonfunctionalization is the most likely cause of the loss of cpt 1α1b in the Nile tilapia genome; (3) the different tissue-specific transcription of cpt 1α2a and cpt 1α2b may be either due to the sub- or the neo-functionalization of transcriptional control side.


2001 ◽  
Vol 276 (34) ◽  
pp. 32056-32063 ◽  
Author(s):  
Rut Valgardsdottir ◽  
Gaute Brede ◽  
Liv G. Eide ◽  
Eirik Frengen ◽  
Hans Prydz

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