scholarly journals The core genome m5C methyltransferase JHP1050 (M.Hpy99III) plays an important role in orchestrating gene expression in Helicobacter pylori

2018 ◽  
Author(s):  
Iratxe Estibariz ◽  
Annemarie Overmann ◽  
Florent Ailloud ◽  
Juliane Krebes ◽  
Josenhans Josenhans ◽  
...  

ABSTRACTHelicobacter pylori encodes a large number of Restriction-Modification (R-M) systems despite its small genome.R-M systems have been described as “primitive immune systems” in bacteria, but the role of methylation in bacterial gene regulation and other processes is increasingly accepted. Every H.pylori strain harbours a unique set of R-M systems resulting in a highly diverse methylome. We identified a highly conserved GCGC-specific m5C MTase (JHP1050) that was predicted to be active in all of 459 H.pylori genome sequences analyzed. Transcriptome analysis of two H.pylori strains and their respective MTase mutants showed that inactivation of the MTase led to changes in the expression of 225 genes in strain J99, and 29 genes in strain BCM-300.10 genes were differentially expressed in both mutated strains. Combining bioinformatic analysis and site-directed mutagenesis, we demonstrated that motifs overlapping the promoter influence the expression of genes directly, while methylation of other motifs might cause secondary effects.Thus, m5C methylation modifies the transcription of multiple genes, affecting important phenotypic traits that include adherence to host cells, natural competence for DNA uptake, bacterial cell shape, and susceptibility to copper.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alessia Oppezzo ◽  
Filippo Rosselli

AbstractHaematopoiesis, the process by which a restrained population of stem cells terminally differentiates into specific types of blood cells, depends on the tightly regulated temporospatial activity of several transcription factors (TFs). The deregulation of their activity or expression is a main cause of pathological haematopoiesis, leading to bone marrow failure (BMF), anaemia and leukaemia. TFs can be induced and/or activated by different stimuli, to which they respond by regulating the expression of genes and gene networks. Most TFs are highly pleiotropic; i.e., they are capable of influencing two or more apparently unrelated phenotypic traits, and the action of a single TF in a specific setting often depends on its interaction with other TFs and signalling pathway components. The microphthalmia-associated TF (MiTF) is a prototype TF in multiple situations. MiTF has been described extensively as a key regulator of melanocyte and melanoma development because it acts mainly as an oncogene. Mitf-mutated mice show a plethora of pleiotropic phenotypes, such as microphthalmia, deafness, abnormal pigmentation, retinal degeneration, reduced mast cell numbers and osteopetrosis, revealing a greater requirement for MiTF activity in cells and tissue. A growing amount of evidence has led to the delineation of key roles for MiTF in haematopoiesis and/or in cells of haematopoietic origin, including haematopoietic stem cells, mast cells, NK cells, basophiles, B cells and osteoclasts. This review summarizes several roles of MiTF in cells of the haematopoietic system and how MiTFs can impact BM development.


2014 ◽  
Vol 21 (10) ◽  
pp. 1057-1064 ◽  
Author(s):  
Ramamourthy Gopal ◽  
Eunsil Jeong ◽  
Chang Seo ◽  
Yoonkyung Park

2018 ◽  
Vol 17 (6) ◽  
Author(s):  
J. Kountouras ◽  
M. Boziki ◽  
S.A. Polyzos ◽  
P. Katsinelos ◽  
E. Gavalas ◽  
...  

2020 ◽  
Vol 28 ◽  
Author(s):  
Seyed Mohammad Nabavi ◽  
Kasi Pandima Devi ◽  
Sethuraman Sathya ◽  
Ana Sanches-Silva ◽  
Listos Joanna ◽  
...  

: Obesity is a major health concern for a growing fraction of the population, with the prevalence of obesity and its related metabolic disorders not being fully understood. Over the last decade, many attempts have been undertaken to understand the mechanisms at the basis of this condition, in which the accumulation of fat occurring in adipose tissue, leads to the pathogenesis of obesity related disorders. Among the most recent studies, those on Peroxisome Proliferator Activated Receptors (PPARs) revealed that these nuclear receptor proteins acting as transcription factors, among others, regulate the expression of genes involved in energy, lipid, and glucose metabolisms, and chronic inflammation. The three different isotypes of PPARs, with different tissue expression and ligand binding specificity, exert similar or overlapping functions directly or indirectly linked to obesity. In this study, we reviewed the available scientific reports concerning the PPARs structure and functions, especially in obesity, considering both natural and synthetic ligands and their role in the therapy of obesity and obesity-associated disorders. In the whole, the collected data show that there are both natural and synthetic compounds that show beneficial promising activity as PPAR agonists in chronic diseases related to obesity.


Author(s):  
Maren N. Vitousek ◽  
Laura A. Schoenle

Hormones mediate the expression of life history traits—phenotypic traits that contribute to lifetime fitness (i.e., reproductive timing, growth rate, number and size of offspring). The endocrine system shapes phenotype by organizing tissues during developmental periods and by activating changes in behavior, physiology, and morphology in response to varying physical and social environments. Because hormones can simultaneously regulate many traits (hormonal pleiotropy), they are important mediators of life history trade-offs among growth, reproduction, and survival. This chapter reviews the role of hormones in shaping life histories with an emphasis on developmental plasticity and reversible flexibility in endocrine and life history traits. It also discusses the advantages of studying hormone–behavior interactions from an evolutionary perspective. Recent research in evolutionary endocrinology has provided insight into the heritability of endocrine traits, how selection on hormone systems may influence the evolution of life histories, and the role of hormonal pleiotropy in driving or constraining evolution.


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