scholarly journals Hyperinvasiveness ofListeria monocytogenessequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins

2019 ◽  
Vol 8 (7) ◽  
Author(s):  
Bulent Gözel ◽  
Camille Monney ◽  
Lisandra Aguilar‐Bultet ◽  
Sebastian Rupp ◽  
Joachim Frey ◽  
...  
Keyword(s):  
Genes Encoding

scholarly journals Intra- and Interspecies Signaling betweenStreptococcus salivarius and Streptococcus pyogenes Mediated by SalA and SalA1 Lantibiotic Peptides

2001 ◽  
Vol 183 (13) ◽  
pp. 3931-3938 ◽  
Author(s):  
M. Upton ◽  
J. R. Tagg ◽  
P. Wescombe ◽  
H. F. Jenkinson
Keyword(s):  
Streptococcus Pyogenes ◽  
Response Regulator ◽  
Genetic Locus ◽  
Two Component System ◽  
Peptide Modification ◽  
Insertional Inactivation ◽  
Two Component ◽  
Genes Encoding ◽  
Dose Dependent

ABSTRACT Streptococcus salivarius 20P3 produces a 22-amino-acid residue lantibiotic, designated salivaricin A (SalA), that inhibits the growth of a range of streptococci, including all strains ofStreptococcus pyogenes. Lantibiotic production is associated with the sal genetic locus comprisingsalA, the lantibiotic structural gene; salBCTXgenes encoding peptide modification and export machinery proteins; andsalYKR genes encoding a putative immunity protein and two-component sensor-regulator system. Insertional inactivation ofsalB in S. salivarius 20P3 resulted in abrogation of SalA peptide production, of immunity to SalA, and ofsalA transcription. Addition of exogenous SalA peptide tosalB mutant cultures induced dose-dependent expression ofsalA mRNA (0.2 kb), demonstrating that SalA production was normally autoregulated. Inactivation of salR encoding the response regulator of the SalKR two-component system led to reduced production of, and immunity to, SalA. The sal genetic locus was also present in S. pyogenes SF370 (M type 1), but because of a deletion across the salBCT genes, the corresponding lantibiotic peptide, designated SalA1, was not produced. However, in S. pyogenes T11 (M type 4) the sallocus gene complement was apparently complete, and active SalA1 peptide was synthesized. Exogenously added SalA1 peptide from S. pyogenes T11 induced salA1 transcription in S. pyogenes SF370 and in an isogenic S. pyogenes T11salB mutant and salA transcription in S. salivarius 20P3 salB. Thus, SalA and SalA1 are examples of streptococcal lantibiotics whose production is autoregulated. These peptides act as intra- and interspecies signaling molecules, modulating lantibiotic production and possibly influencing streptococcal population ecology in the oral cavity.

Polymorphisms in the Genes Encoding TGF-β1, TNF-α, and IL-6 Show Association with Type 1 Diabetes Mellitus in the Slovak Population

2010 ◽  
Vol 58 (5) ◽  
pp. 385-393 ◽  
Author(s):  
Juraj Javor ◽  
Stanislav Ferencik ◽  
Maria Bucova ◽  
Martina Stuchlikova ◽  
Emil Martinka ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Slovak Population ◽  
Tnf Α ◽  
Genes Encoding ◽  
Tgf Β1

scholarly journals Decreased Expression of Type 1 Fimbriae by apstMutant of Uropathogenic Escherichia coli Reduces Urinary Tract Infection

2012 ◽  
Vol 80 (8) ◽  
pp. 2802-2815 ◽  
Author(s):  
Sébastien Crépin ◽  
Sébastien Houle ◽  
Marie-Ève Charbonneau ◽  
Michaël Mourez ◽  
Josée Harel ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Bacterial Virulence ◽  
Pho Regulon ◽  
Upec Strain ◽  
Content Type ◽  
Type 1 Fimbriae ◽  
Genes Encoding ◽  
Tract Infections

ABSTRACTThepstSCAB-phoUoperon encodes the phosphate-specific transport system (Pst). Loss of Pst constitutively activates the Pho regulon and decreases bacterial virulence. However, specific mechanisms underlying decreased bacterial virulence through inactivation of Pst are poorly understood. In uropathogenicEscherichia coli(UPEC) strain CFT073, inactivation ofpstdecreased urinary tract colonization in CBA/J mice. Thepstmutant was deficient in production of type 1 fimbriae and showed decreased expression of thefimAstructural gene which correlated with differential expression of thefimB,fimE,ipuA, andipbAgenes, encoding recombinases, mediating inversion of thefimpromoter. The role offimdownregulation in attenuation of thepstmutant was confirmed using afimphase-locked-on derivative, which demonstrated a significant gain in virulence. In addition, thepstmutant was less able to invade human bladder epithelial cells. Since type 1 fimbriae contribute to UPEC virulence by promoting colonization and invasion of bladder cells, the reduced bladder colonization by thepstmutant is predominantly attributed to downregulation of these fimbriae. Elucidation of mechanisms mediating the control of type 1 fimbriae through activation of the Pho regulon in UPEC may open new avenues for therapeutics or prophylactics against urinary tract infections.

scholarly journals Organization of the genes encoding complement receptors type 1 and 2, decay-accelerating factor, and C4-binding protein in the RCA locus on human chromosome 1.

1988 ◽  
Vol 167 (4) ◽  
pp. 1271-1280 ◽  
Author(s):  
M C Carroll ◽  
E M Alicot ◽  
P J Katzman ◽  
L B Klickstein ◽  
J A Smith ◽  
...  
Keyword(s):  
Gel Electrophoresis ◽  
Southern Blotting ◽  
Chromosome 1 ◽  
Complement Receptors ◽  
Coding Sequences ◽  
Physical Linkage ◽  
Genes Encoding ◽  
Gradient Gel Electrophoresis ◽  
Human Chromosome 1

The organization and physical linkage of four members of a major complement locus, the RCA locus, have been determined using the technique of pulsed field gradient gel electrophoresis in conjunction with Southern blotting. The genes encoding CR1, CR2, DAF, and C4bp were aligned in that order within a region of 750 kb. In addition, the 5' to 3' orientation of the CR1 gene (5' proximal to CR2) was determined using 5'- and 3'-specific DNA probes. The proximity of these genes may be related to structural and functional homologies of the protein products. Overall, a restriction map including 1,500 kb of DNA was prepared, and this map will be important for positioning of additional coding sequences within this region on the long arm of chromosome 1.

scholarly journals Five novel mutations in the SCNN1A gene causing autosomal recessive pseudohypoaldosteronism type 1

2013 ◽  
Vol 168 (5) ◽  
pp. 707-715 ◽  
Author(s):  
Maik Welzel ◽  
Leyla Akin ◽  
Anja Büscher ◽  
Tülay Güran ◽  
Berthold P Hauffa ◽  
...  
Keyword(s):  
Autosomal Recessive ◽  
Current Knowledge ◽  
Monogenic Disease ◽  
Α Subunit ◽  
Recessive Mutations ◽  
Neonatal Onset ◽  
Genes Encoding ◽  
Heterozygous Carriers ◽  
Pseudohypoaldosteronism Type

BackgroundPseudohypoaldosteronism type 1 (PHA1) is a monogenic disease caused by mutations in the genes encoding the human mineralocorticoid receptor (MR) or the α (SCNN1A), β (SCNN1B) or γ (SCNN1G) subunit of the epithelial Na+ channel (ENaC). While autosomal dominant mutation of the MR cause renal PHA1, autosomal recessive mutations of the ENaC lead to systemic PHA1. In the latter, affected children suffer from neonatal onset of multi-organ salt loss and often exhibit cystic fibrosis-like pulmonary symptoms.ObjectiveWe searched for underlying mutations in seven unrelated children with systemic PHA1, all offsprings of healthy consanguineous parents.Methods and resultsAmplification of the SCNN1A gene and sequencing of all 13 coding exons unraveled mutations in all of our patients. We found five novel homozygous mutations (c.587_588insC in two patients, c.1342_1343insTACA, c.742delG, c.189C>A, c.1361-2A>G) and one known mutation (c.1474C>T) leading to truncation of the αENaC protein. All parents were asymptomatic heterozygous carriers of the respective mutations, confirming the autosomal recessive mode of inheritance. Five out of seven patients exhibited pulmonary symptoms in the neonatal period.ConclusionThe α subunit is essential for ENaC function and mutations truncating the pore-forming part of the protein leading to systemic PHA1. Based on current knowledge, the pulmonary phenotype cannot be satisfactorily predicted.

scholarly journals Thymus Dysfunction in the Development of Type 1 Diabetes and Endocrine Autoimmune Diseases

2009 ◽  
Vol 05 (0) ◽  
pp. 24
Author(s):  
Vincent Geenen ◽  
Olivier Dardenne ◽  
◽  
Keyword(s):  
Type 1 Diabetes ◽  
Autoimmune Diseases ◽  
Autoimmune Response ◽  
Thymic Epithelial Cells ◽  
Self Tolerance ◽  
Genes Encoding ◽  
Organ Specific ◽  
Dominant Member ◽  
Large Repertoire

The discovery that thymic epithelium from many species expresses a large repertoire of genes encoding neuroendocrine and other tissuerestricted antigens has radically changed our knowledge of the pathogenic mechanisms underlying the development of organ-specific autoimmune diseases such as type 1 diabetes and autoimmune endocrine diseases. Rather than a breakdown of immunological selftolerance in periphery, there is mounting evidence that the diabetogenic autoimmune response may first arise from a thymus dysfunction in the central programming of β-cell self-tolerance. Insulin-like growth factor 2 (IGF-2) is the dominant member of the insulin gene/protein family expressed in thymic epithelial cells (TECs) from different species, and Igf2-/- mice fail to programme complete tolerance to insulin. Based on the homology between insulin, the primary and immunogenic auto-antigen of type 1 diabetes, and IGF-2, the tolerogenic selfantigen of the insulin family, the design of a regulatory/negative self-vaccination for prevention against type 1 diabetes has been proposed and is under development.

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