Alteration in gene expression levels underlies many of the phenotypic differences across species. Because of their highly mutable nature, proximity to the +1 transcription start site (TSS), and the emerging evidence of functional impact on gene expression, core promoter short tandem repeats (STRs) may be considered an ideal source of variation across species. In a genome-scale analysis of the entire Homo sapiens protein-coding genes, we have previously identified core promoters with at least one STR of ≥ 6-repeats, with possible selective advantage in this species. In the current study, we performed reverse analysis of the entire Homo sapiens orthologous genes in mouse in the Ensembl database, in order to identify conserved STRs that have shrunk as an evolutionary advantage to humans. Two protocols were used to minimize ascertainment bias. Firstly, two species sharing a more recent ancestor with Homo sapiens (i.e. Pan troglodytes and Gorilla gorilla gorilla) were also included in the study. Secondly, four non-primate species encompassing the major orders across Mammals, including Scandentia, Laurasiatheria, Afrotheria, and Xenarthra were analyzed as out-groups. We introduce STR evolutionary events specifically identical in primates (i.e. Homo sapiens, Pan troglodytes, and Gorilla gorilla gorilla) vs. non-primate out-groups. The average frequency of the identically shared STR motifs across those primates ranged between 0.00005 and 0.06. The identified genes are involved in important evolutionary and developmental processes, such as normal craniofacial development (TFAP2B), regulation of cell shape (PALMD), learning and long-term memory (RGS14), nervous system development (GFRA2), embryonic limb morphogenesis (PBX2), and forebrain development (APAF1). We provide evidence of core promoter STRs as evolutionary switch codes for primate speciation, and the first instance of identity-by-descent for those motifs at the interspecies level.
ObjectivesEscherichia coli is regarded as the most important etiological agent of urinary tract infections. Fluoroquinolones are routinely used in the treatment of these infections; however, in recent years, a growing rate of resistance to these drugs has been reported globally. The aims of this study were to detect plasmid-mediated qnrA, qnrB, and qnrS genes among the quinolone-nonsusceptible E. coli isolates and to investigate their clonal relatedness in Qazvin and Zanjan Provinces, Iran.MethodsA total of 200 clinical isolates of E. coli were collected from hospitalized patients. The bacterial isolates were identified through standard laboratory protocols and further confirmed using API 20E test strips. Antimicrobial susceptibility was determined by the standard disk diffusion method. Polymerase chain reaction (PCR) and sequencing were used for detecting qnrA, qnrB, and qnrS genes and the clonal relatedness of qnr-positive isolates was evaluated by enterobacterial repetitive intergenic consensus-PCR (ERIC-PCR) method.ResultsIn total, 136 (68%) isolates were nonsusceptible to quinolone compounds, among which 45 (33.1%) and 71 (52.2%) isolates showed high- and low-level quinolone resistance, respectively. Of the 136 isolates, four (2.9%) isolates were positive for the qnrS1 gene. The results from ERIC-PCR revealed that two (50%) cases of qnr-positive isolates were related genetically.ConclusionOur study results were indicative of the presence of low frequency of qnr genes among the clinical isolates of E. coli in Qazvin and Zanjan Provinces, which emphasizes the need for establishing tactful policies associated with infection-control measures in our hospital settings.
Multiple sclerosis (MS) is an autoimmune disorder of central nervous system with several genetic and environmental risk factors. Genes with regulatory roles on immune system have been implicated in its pathogenesis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to control some aspects of immune response. Among them is antisense non-coding RNA in the INK4 locus (ANRIL) whose involvement in NF-κB signaling pathway has been highlighted. In the current study, we evaluated the association between rs1333045, rs4977574, rs1333048, and rs10757278 variants of ANRIL and MS risk in a population of 410 Iranian MS patients and 410 healthy subjects. There was no significant difference in allele and genotype frequencies between MS patients and healthy subjects. However, haplotype analysis (rs1333045, rs1333048, rs4977574, and rs10757278 respectively) demonstrated protective effect of CCGG and TAAA haplotypes against MS (P values of 0.043 and 0.0026 respectively). In addition, TAGG and CCGA haplotypes were significantly associated with MS risk in the studied population (P values of 0.0065 and 0.024 respectively). The present study reveals a possible role for ANRIL in the pathogenesis of MS.
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