The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
Josep Casadesús - One of the best experts on this subject based on the ideXlab platform.
-
Regulation of traJ transcription in the Salmonella virulence plasmid by Strand‐specific DNA adenine hemimethylation
Molecular microbiology, 2005Co-Authors: Eva María Camacho, Josep CasadesúsAbstract:The traJ gene of the virulence plasmid of Salmonella enterica serovar Typhimurium (pSLT) encodes a transcriptional activator of the transfer operon. The leucine-responsive regulatory protein (Lrp) is an activator of traJ transcription. The upstream-activating-sequence of the pSLT traJ promoter contains two Lrp binding sites (LRP-1 and LRP-2), both necessary for transcriptional activation. The promoter-proximal site (LRP-2) contains a GATC site (GATC-II) whose methylation state affects Lrp binding: GATC-II methylation in both DNA Strands decreases the affinity of Lrp for the LRP-2 site, while efficient Lrp binding occurs to a non-methylated GATC-II site. The effect of GATC-II hemimethylation on Lrp binding is Strand-specific: methylation of the traJ non-Coding Strand permits formation of the major Lrp-DNA retardation complex, but methylation of the Coding Strand does not. This asymmetry supports a model in which passage of the replication fork may permit Lrp-mediated activation of conjugal transfer in one daughter plasmid molecule but not in the other. A remarkable trait of this regulatory design is that hemimethylation of a single GATC site can generate distinct epigenetic signals in otherwise identical plasmid DNA molecules.
Luis E. Figuera - One of the best experts on this subject based on the ideXlab platform.
-
snp 668c 44 alters a nf κb1 putative binding site in non Coding Strand of human β defensin 1 defb1 and is associated with lepromatous leprosy
Infection Genetics and Evolution, 2009Co-Authors: Ernesto Prado-montes De Oca, Jesus Salvador Velardefelix, Juan Jose Riostostado, Veronica Judith Picoscardenas, Luis E. FigueraAbstract:Abstract Leprosy is an infectious disease caused by Mycobacterium leprae. The peptide human β-defensin 1 is an antimicrobial effector of innate epithelial immunity. A study was done on the association of three single nucleotide polymorphisms (SNPs) in the β-defensin 1 gene (DEFB1) – 668 C/G (−44 C/G or rs1800972; in 5′ UTR), 692 A/G (−20 A/G or rs11362; in 5′ UTR) and A1836G (rs1800971; in 3′ UTR) – with leprosy susceptibility per se and clinical leprosy variants. The SNPs were genotyped by real-time polymerase chain reaction (rt-PCR) and PCR-restriction fragment length polymorphisms. Subjects were of Mexican mestizo ethnicity from Sinaloa state, Mexico. Analysis was done on borderline leprosy, lepromatous leprosy (L-lep) and indeterminate leprosy subgroups compared with healthy controls. Results: The genotypes associated with L-lep and no other leprosy subgroup after Bonferroni correction were those that contain 668C in a dominant model (OR = 3.06, 95% CI 1.47–6.4, p = 0.024). Estimated haplotype CGA is over-represented in L-lep (p = 0.009; OR = 2.25, 1.23–4.03). Five NF-κB1 putative binding sites (NPBSs) were identified with JASPAR software in non-Coding Strand spanning the 5′ UTR and intron 1 of DEFB1, including one which is altered when SNP 668C is present. SNP 668C probably abrogates NF-κB-dependent DEFB1 upregulation leading to L-lep variant.
-
SNP 668C (−44) alters a NF-κB1 putative binding site in non-Coding Strand of human β-defensin 1 (DEFB1) and is associated with lepromatous leprosy
Infection genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 2009Co-Authors: Ernesto Prado-montes De Oca, Jesús Salvador Velarde-félix, Juan José Ríos-tostado, Verónica Judith Picos-cárdenas, Luis E. FigueraAbstract:Abstract Leprosy is an infectious disease caused by Mycobacterium leprae. The peptide human β-defensin 1 is an antimicrobial effector of innate epithelial immunity. A study was done on the association of three single nucleotide polymorphisms (SNPs) in the β-defensin 1 gene (DEFB1) – 668 C/G (−44 C/G or rs1800972; in 5′ UTR), 692 A/G (−20 A/G or rs11362; in 5′ UTR) and A1836G (rs1800971; in 3′ UTR) – with leprosy susceptibility per se and clinical leprosy variants. The SNPs were genotyped by real-time polymerase chain reaction (rt-PCR) and PCR-restriction fragment length polymorphisms. Subjects were of Mexican mestizo ethnicity from Sinaloa state, Mexico. Analysis was done on borderline leprosy, lepromatous leprosy (L-lep) and indeterminate leprosy subgroups compared with healthy controls. Results: The genotypes associated with L-lep and no other leprosy subgroup after Bonferroni correction were those that contain 668C in a dominant model (OR = 3.06, 95% CI 1.47–6.4, p = 0.024). Estimated haplotype CGA is over-represented in L-lep (p = 0.009; OR = 2.25, 1.23–4.03). Five NF-κB1 putative binding sites (NPBSs) were identified with JASPAR software in non-Coding Strand spanning the 5′ UTR and intron 1 of DEFB1, including one which is altered when SNP 668C is present. SNP 668C probably abrogates NF-κB-dependent DEFB1 upregulation leading to L-lep variant.
Eva María Camacho - One of the best experts on this subject based on the ideXlab platform.
-
Regulation of traJ transcription in the Salmonella virulence plasmid by Strand‐specific DNA adenine hemimethylation
Molecular microbiology, 2005Co-Authors: Eva María Camacho, Josep CasadesúsAbstract:The traJ gene of the virulence plasmid of Salmonella enterica serovar Typhimurium (pSLT) encodes a transcriptional activator of the transfer operon. The leucine-responsive regulatory protein (Lrp) is an activator of traJ transcription. The upstream-activating-sequence of the pSLT traJ promoter contains two Lrp binding sites (LRP-1 and LRP-2), both necessary for transcriptional activation. The promoter-proximal site (LRP-2) contains a GATC site (GATC-II) whose methylation state affects Lrp binding: GATC-II methylation in both DNA Strands decreases the affinity of Lrp for the LRP-2 site, while efficient Lrp binding occurs to a non-methylated GATC-II site. The effect of GATC-II hemimethylation on Lrp binding is Strand-specific: methylation of the traJ non-Coding Strand permits formation of the major Lrp-DNA retardation complex, but methylation of the Coding Strand does not. This asymmetry supports a model in which passage of the replication fork may permit Lrp-mediated activation of conjugal transfer in one daughter plasmid molecule but not in the other. A remarkable trait of this regulatory design is that hemimethylation of a single GATC site can generate distinct epigenetic signals in otherwise identical plasmid DNA molecules.
Gerardo C. Glikin - One of the best experts on this subject based on the ideXlab platform.
-
Single Strand binding protein specific for the polyoma early-Coding Strand of PEA1 (AP1) regulatory sequence
Nucleic acids research, 1991Co-Authors: Liliana M.e. Finocchiaro, Paolo Amati, Gerardo C. GlikinAbstract:We have shown that nuclear and cytosolic proteins from embryonal carcinoma F9 cells are able to bind to the early-Coding Strand of polyoma enhancer A domain. As demonstrated by mobility shift specific competition experiments, DNase I footprinting, depurination and depyrimidation interference, and proteolytic clipping performed with single Stranded oligonucleotides, some of these proteins bind specifically to the early-Coding PEA1 (AP1) motif. In addition, 'Southwestern' analysis has made possible the identification of a 46 KD nuclear protein that binds to this sequence. These cellular proteins did not bind to the complementary single Strand as demonstrated by mobility shift analysis, nor did they bind to RNA synthesized in vitro by using the complementary Strand as template. They were also shown to be different from their corresponding double Strand binding factors. This new dimension in the functional flexibility and complexity of the polyoma enhancer suggests new properties of the classic regulating sequences that could provide additional modulation of regulating activities.
Joan Pons - One of the best experts on this subject based on the ideXlab platform.
-
Mitochondrial genomes of twelve species of hyperdiverse Trigonopterus weevils.
PeerJ, 2020Co-Authors: Raden Pramesa Narakusumo, Alexander Riedel, Joan PonsAbstract:Mitochondrial genomes of twelve species of Trigonopterus weevils are presented, ten of them complete. We describe their gene order and molecular features and test their potential for reconstructing the phylogeny of this hyperdiverse genus comprising > 1,000 species. The complete mitochondrial genomes examined herein ranged from 16,501 bp to 21,007 bp in length, with an average AT content of 64.2% to 69.7%. Composition frequencies and skews were generally lower across species for atp6, cox1-3, and cob genes, while atp8 and genes coded on the minus Strand showed much higher divergence at both nucleotide and amino acid levels. Most variation within genes was found at the codon level with high variation at third codon sites across species, and with lesser degree at the Coding Strand level. Two large non-Coding regions were found, CR1 (between rrnS and trnI genes) and CR2 (between trnI and trnQ), but both with large variability in length; this peculiar structure of the non-Coding region may be a derived character of Curculionoidea. The nad1 and cob genes exhibited an unusually high interspecific length variation of up to 24 bp near the 3' end. This pattern was probably caused by a single evolutionary event since both genes are only separated by trnS2 and length variation is extremely rare in mitochondrial protein Coding genes. We inferred phylogenetic trees using protein Coding gene sequences implementing both maximum likelihood and Bayesian approaches, each for both nucleotide and amino acid sequences. While some clades could be retrieved from all reconstructions with high confidence, there were also a number of differences and relatively low support for some basal nodes. The best partition scheme of the 13 protein Coding sequences obtained by IQTREE suggested that phylogenetic signal is more accurate by splitting sequence variation at the codon site level as well as Coding Strand, rather than at the gene level. This result corroborated the different patterns found in Trigonopterus regarding to A+T frequencies and AT and GC skews that also greatly diverge at the codon site and Coding Strand levels.