scholarly journals Horizontally Acquired Homologs of Xenogeneic Silencers: Modulators of Gene Expression Encoded by Plasmids, Phages and Genomic Islands

Genes ◽  
2020 ◽  
Vol 11 (2) ◽  
pp. 142 ◽  
Author(s):  
Alejandro Piña-Iturbe ◽  
Isidora D. Suazo ◽  
Guillermo Hoppe-Elsholz ◽  
Diego Ulloa-Allendes ◽  
Pablo A. González ◽  
...  
Keyword(s):  
Regulatory Networks ◽  
Core Genome ◽  
Current Knowledge ◽  
Genomic Islands ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Related Group ◽  
Bacterial Fitness ◽  
Foreign Dna ◽  
Horizontal Acquisition

Acquisition of mobile elements by horizontal gene transfer can play a major role in bacterial adaptation and genome evolution by providing traits that contribute to bacterial fitness. However, gaining foreign DNA can also impose significant fitness costs to the host bacteria and can even produce detrimental effects. The efficiency of horizontal acquisition of DNA is thought to be improved by the activity of xenogeneic silencers. These molecules are a functionally related group of proteins that possess affinity for the acquired DNA. Binding of xenogeneic silencers suppresses the otherwise uncontrolled expression of genes from the newly acquired nucleic acid, facilitating their integration to the bacterial regulatory networks. Even when the genes encoding for xenogeneic silencers are part of the core genome, homologs encoded by horizontally acquired elements have also been identified and studied. In this article, we discuss the current knowledge about horizontally acquired xenogeneic silencer homologs, focusing on those encoded by genomic islands, highlighting their distribution and the major traits that allow these proteins to become part of the host regulatory networks.

Regulation of the ANF and BNP promoters by GATA factors: Lessons learned for cardiac transcription

2001 ◽  
Vol 79 (8) ◽  
pp. 673-681 ◽  
Author(s):  
Kevin McBride ◽  
Mona Nemer
Keyword(s):  
Transcription Factors ◽  
Natriuretic Peptide ◽  
Regulatory Networks ◽  
Current Knowledge ◽  
Lessons Learned ◽  
Clinical Markers ◽  
Gata Factors ◽  
Major Mechanism ◽  
Genes Encoding ◽  
Cardiac Gene

The identification and molecular cloning of the cardiac transcription factors GATA-4, -5, and -6 has greatly contributed to our understanding of how tissue-specific transcription is achieved during cardiac growth and development. Through analysis of their interacting partners, it has also become apparent that a major mechanism underlying spatial and temporal specificity within the heart as well as in the response to cardiogenic regulators is the combinatorial interaction between cardiac-restricted and inducible transcription factors. The cardiac GATA factors appear to be fundamental contributors to these regulatory networks. Two of the first targets identified for the cardiac GATA factors were the natriuretic peptide genes encoding atrial natriuretic factor (ANF) and B-type natriuretic peptide (BNP), the major heart secretory products that are also accepted clinical markers of the diseased heart. Studies using the ANF and BNP promoters as models of cardiac-specific transcription have unraveled the pivotal role that GATA proteins play in cardiac gene expression. We review the current knowledge on the modulation of the natriuretic peptide promoters by GATA factors, including examples of combinatorial interactions between GATA proteins and diverse transcription factors.Key words: ANF, BNP, GATA factors, cardiac transcription.

scholarly journals Evaluation of the effects of sdiA, a luxR homologue, on adherence and motility of Escherichia coli O157 : H7

Microbiology ◽  
2010 ◽  
Vol 156 (5) ◽  
pp. 1303-1312 ◽  
Author(s):  
Vijay K. Sharma ◽  
Shawn M. D. Bearson ◽  
Bradley L. Bearson
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Mutant Strain ◽  
Regulatory Networks ◽  
Double Mutant ◽  
Negative Regulator ◽  
Wild Type ◽  
Reverse Transcription Pcr ◽  
Expression Of Genes ◽  
Genes Encoding

Quorum-sensing (QS) signalling pathways are important regulatory networks for controlling the expression of genes promoting adherence of enterohaemorrhagic Escherichia coli (EHEC) O157 : H7 to epithelial cells. A recent study has shown that EHEC O157 : H7 encodes a luxR homologue, called sdiA, which upon overexpression reduces the expression of genes encoding flagellar and locus of enterocyte effacement (LEE) proteins, thus negatively impacting on the motility and intimate adherence phenotypes, respectively. Here, we show that the deletion of sdiA from EHEC O157 : H7 strain 86-24, and from a hha (a negative regulator of ler) mutant of this strain, enhanced bacterial adherence to HEp-2 epithelial cells of the sdiA mutant strains relative to the strains containing a wild-type copy of sdiA. Quantitative reverse transcription PCR showed that the expression of LEE-encoded genes ler, espA and eae in strains with the sdiA deletions was not significantly different from that of the strains wild-type for sdiA. Similarly, no additional increases in the expression of LEE genes were observed in a sdiA hha double mutant strain relative to that observed in the hha deletion mutant. While the expression of fliC, which encodes flagellin, was enhanced in the sdiA mutant strain, the expression of fliC was reduced by several fold in the hha mutant strain, irrespective of the presence or absence of sdiA, indicating that the genes sdiA and hha exert opposing effects on the expression of fliC. The strains with deletions in sdiA or hha showed enhanced expression of csgA, encoding curlin of the curli fimbriae, with the expression of csgA highest in the sdiA hha double mutant, suggesting an additive effect of these two gene deletions on the expression of csgA. No significant differences were observed in the expression of the genes lpfA and fimA of the operons encoding long polar and type 1 fimbriae in the sdiA mutant strain. These data indicate that SdiA has no significant effect on the expression of LEE genes, but that it appears to act as a strong repressor of genes encoding flagella and curli fimbriae, and the alleviation of the SdiA-mediated repression of these genes in an EHEC O157 : H7 sdiA mutant strain contributes to enhanced bacterial motility and increased adherence to HEp-2 epithelial cells.

scholarly journals ClpP of Streptococcus mutans Differentially Regulates Expression of Genomic Islands, Mutacin Production, and Antibiotic Tolerance

2009 ◽  
Vol 192 (5) ◽  
pp. 1312-1323 ◽  
Author(s):  
Partho Chattoraj ◽  
Anirban Banerjee ◽  
Saswati Biswas ◽  
Indranil Biswas
Keyword(s):  
Streptococcus Mutans ◽  
Mutant Strain ◽  
Protein Profile ◽  
Vital Role ◽  
Genomic Islands ◽  
Wild Type ◽  
Proteomic Data ◽  
Altered Protein ◽  
Expression Of Genes ◽  
Genes Encoding

ABSTRACT Streptococcus mutans is the primary etiological agent of human dental caries and, at times, of infective endocarditis. Within the oral cavity, the pathogen is subjected to conditions of stress. A well-conserved protein complex named ClpP (caseinolytic protease) plays a vital role in adaptation under stress conditions. To gain a better understanding of the global role of the ClpP protease in cellular homeostasis, a transcriptome analysis was performed using a ΔclpP mutant strain. The expression levels of more than 100 genes were up- or downregulated in the ΔclpP mutant compared to the wild type. Notably, the expression of genes in several genomic islands, such as TnSmu1 and TnSmu2, was differentially modulated in the ΔclpP mutant strain. ClpP deficiency also increased the expression of genes associated with a putative CRISPR locus. Furthermore, several stress-related genes and genes encoding bacteriocin-related peptides and many transcription factors were also found to be altered in the ΔclpP mutant strain. A comparative analysis of the two-dimensional protein profile of the wild type and the ΔclpP mutant strains showed altered protein profiles. Comparison of the transcriptome data with the proteomic data identified four common gene products, suggesting that the observed altered protein expression of these genes could be due to altered transcription. The results presented here indicate that ClpP-mediated proteolysis plays an important global role in the regulation of several important traits in this pathogen.

Intracrinology and gastric cancer

2017 ◽  
Vol 86 (1) ◽  
pp. 76
Author(s):  
Bartosz Adam Frycz ◽  
Paweł Piotr Jagodziński
Keyword(s):  
Gastric Cancer ◽  
Steroid Hormones ◽  
Malignant Tumors ◽  
Current Knowledge ◽  
Short Review ◽  
Therapeutic Approaches ◽  
Peripheral Tissues ◽  
Expression Of Genes ◽  
Genes Encoding

Overall incidence of gastric cancer (GC) in most populations is approximately two times higher in men than women. Therefore, steroid hormones are suspect to play a role in gastric carcinogenesis. Large amounts of steroid hormones in postmenopausal women and older men are synthesized in peripheral tissues through enzymatic conversion of blood derived precursors into active estrogens and androgens in so called, intracrine mechanism. Moreover, abnormal expression of genes encoding steroidogenic enzymes was shown in numerous malignant tumors including GC. These abnormalities can be associated with deregulated production of steroid hormones in gastric tissue and thus affect the risk of GC. For that reason this short review aims to summarize the current knowledge about the expression of genes involved in metabolism of steroid hormones in normal and malignant gastric mucosa and thus, estimate the potential of these tissues to intracrine synthesis of steroid hormones. This findings could be useful in understanding the role of above mechanism in GC and could help to find therapeutic approaches in future.

Regulation of differentiation of vascular smooth muscle cells

1995 ◽  
Vol 75 (3) ◽  
pp. 487-517 ◽  
Author(s):  
G. K. Owens
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Molecular Mechanisms ◽  
Contractile Function ◽  
Current Knowledge ◽  
Vascular Diseases ◽  
Principal Function ◽  
Environmental Signals ◽  
Expression Of Genes ◽  
Genes Encoding

The vascular smooth muscle cell (SMC) in mature animals is a highly specialized cell whose principal function is contraction. The fully differentiated or mature SMC proliferates at an extremely low rate and is a cell almost completely geared for contraction. It expresses a unique repertoire of contractile proteins, ion channels, and signaling molecules that are required for its contractile function and that when taken in aggregate clearly distinguish it from any other cell type. During vasculogenesis, however, the SMC's principal function is proliferation and production of matrix components of the blood vessel wall. Moreover, even in mature animals, the SMC retains remarkable plasticity, such that it can undergo relatively rapid and reversible changes in its phenotype in response to changes in local environmental cues normally required for maintenance of its differentiated state. A key to understanding SMC differentiation is to identify the key environmental signals and factors that induce or maintain the differentiated state of the SMC and to determine the molecular mechanisms that control the coordinate expression of genes encoding for proteins that are necessary for the contractile function of the SMC. The purpose of this review is to summarize our current knowledge of the regulation of SMC differentiation, with a particular emphasis on consideration of how this process is controlled during normal vascular development and how these control processes might be altered in vascular diseases such as atherosclerosis, which are characterized by marked alterations in the differentiated state of the SMC.

Plant Compounds for the Treatment of Diabetes, a Metabolic Disorder: NF-κB as a Therapeutic Target

2020 ◽  
Vol 26 (39) ◽  
pp. 4955-4969
Author(s):  
Ravi Sahukari ◽  
Jyothi Punabaka ◽  
Shanmugam Bhasha ◽  
Venkata S. Ganjikunta ◽  
Shanmugam K. Ramudu ◽  
...  
Keyword(s):  
Diabetic Complications ◽  
Current Knowledge ◽  
World Population ◽  
Future Studies ◽  
Expression Of Genes ◽  
Treatment Of Diabetes ◽  
Online Library ◽  
And Oxidative Stress ◽  
Stress Activation ◽  
Plant Compounds

Background: The prevalence of diabetes in the world population hás reached 8.8 % and is expected to rise to 10.4% by 2040. Hence, there is an urgent need for the discovery of drugs against therapeutic targets to sojourn its prevalence. Previous studies proved that NF-κB serves as a central agent in the development of diabetic complications. Objectives: This review intended to list the natural plant compounds that would act as inhibitors of NF-κB signalling in different organs under the diabetic condition with their possible mechanism of action. Methods: Information on NF-κB, diabetes, natural products, and relation in between them, was gathered from scientific literature databases such as Pubmed, Medline, Google scholar, Science Direct, Springer, Wiley online library. Results and Conclusion: NF-κB plays a crucial role in the development of diabetic complications because of its link in the expression of genes that are responsible for organs damage such as kidney, brain, eye, liver, heart, muscle, endothelium, adipose tissue and pancreas by inflammation, apoptosis and oxidative stress. Activation of PPAR-α, SIRT3/1, and FXR through many cascades by plant compounds such as terpenoids, iridoids, flavonoids, alkaloids, phenols, tannins, carbohydrates, and phytocannabinoids recovers diabetic complications. These compounds also exhibit the prevention of NF-κB translocation into the nucleus by inhibiting NF-κB activators, such as VEGFR, RAGE and TLR4 receptors, which in turn, prevent the activation of many genes involved in tissue damage. Current knowledge on the treatment of diabetes by targeting NF-κB is limited, so future studies would enlighten accordingly.

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