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  • Makati City: Philippine Institute for Development Studies (PIDS)
  • Molecular Diversity Preservation International (MDPI)
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  • 1
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    Molecular Diversity Preservation International (MDPI)
    In: Genes
    Publication Date: 2012-10-13
    Description: Although bacterial genomes have been traditionally viewed as being very compact, with relatively low amounts of repetitive and non-coding DNA, this view has dramatically changed in recent years. The increase of available complete bacterial genomes has revealed that many species present abundant repetitive DNA (i.e., insertion sequences, prophages or paralogous genes) and that many of these sequences are not functional but can have evolutionary consequences as concerns the adaptation to specialized host-related ecological niches. Comparative genomics analyses with close relatives that live in non-specialized environments reveal the nature and fate of this bacterial junk DNA. In addition, the number of insertion sequences and pseudogenes, as well as the size of the intergenic regions, can be used as markers of the evolutionary stage of a genome.
    Electronic ISSN: 2073-4425
    Topics: Biology
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  • 2
    Publication Date: 2017-09-30
    Description: Genes, Vol. 8, Pages 247: Et tu, Brute? Not Even Intracellular Mutualistic Symbionts Escape Horizontal Gene Transfer Genes doi: 10.3390/genes8100247 Authors: Sergio López-Madrigal Rosario Gil Many insect species maintain mutualistic relationships with endosymbiotic bacteria. In contrast to their free-living relatives, horizontal gene transfer (HGT) has traditionally been considered rare in long-term endosymbionts. Nevertheless, meta-omics exploration of certain symbiotic models has unveiled an increasing number of bacteria-bacteria and bacteria-host genetic transfers. The abundance and function of transferred loci suggest that HGT might play a major role in the evolution of the corresponding consortia, enhancing their adaptive value or buffering detrimental effects derived from the reductive evolution of endosymbionts’ genomes. Here, we comprehensively review the HGT cases recorded to date in insect-bacteria mutualistic consortia, and discuss their impact on the evolutionary success of these associations.
    Electronic ISSN: 2073-4425
    Topics: Biology
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  • 3
    Publication Date: 2017-10-04
    Description: Genes, Vol. 8, Pages 253: Exonization of an Intronic LINE-1 Element Causing Becker Muscular Dystrophy as a Novel Mutational Mechanism in Dystrophin Gene Genes doi: 10.3390/genes8100253 Authors: Ana Gonçalves Jorge Oliveira Teresa Coelho Ricardo Taipa Manuel Melo-Pires Mário Sousa Rosário Santos A broad mutational spectrum in the dystrophin (DMD) gene, from large deletions/duplications to point mutations, causes Duchenne/Becker muscular dystrophy (D/BMD). Comprehensive genotyping is particularly relevant considering the mutation-centered therapies for dystrophinopathies. We report the genetic characterization of a patient with disease onset at age 13 years, elevated creatine kinase levels and reduced dystrophin labeling, where multiplex-ligation probe amplification (MLPA) and genomic sequencing failed to detect pathogenic variants. Bioinformatic, transcriptomic (real time PCR, RT-PCR), and genomic approaches (Southern blot, long-range PCR, and single molecule real-time sequencing) were used to characterize the mutation. An aberrant transcript was identified, containing a 103-nucleotide insertion between exons 51 and 52, with no similarity with the DMD gene. This corresponded to the partial exonization of a long interspersed nuclear element (LINE-1), disrupting the open reading frame. Further characterization identified a complete LINE-1 (~6 kb with typical hallmarks) deeply inserted in intron 51. Haplotyping and segregation analysis demonstrated that the mutation had a de novo origin. Besides underscoring the importance of mRNA studies in genetically unsolved cases, this is the first report of a disease-causing fully intronic LINE-1 element in DMD, adding to the diversity of mutational events that give rise to D/BMD.
    Electronic ISSN: 2073-4425
    Topics: Biology
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  • 4
    Publication Date: 2018-04-06
    Description: Genes, Vol. 9, Pages 195: TRAP1 Regulation of Cancer Metabolism: Dual Role as Oncogene or Tumor Suppressor Genes doi: 10.3390/genes9040195 Authors: Danilo Swann Matassa Ilenia Agliarulo Rosario Avolio Matteo Landriscina Franca Esposito Metabolic reprogramming is an important issue in tumor biology. An unexpected inter- and intra-tumor metabolic heterogeneity has been strictly correlated to tumor outcome. Tumor Necrosis Factor Receptor-Associated Protein 1 (TRAP1) is a molecular chaperone involved in the regulation of energetic metabolism in cancer cells. This protein is highly expressed in several cancers, such as glioblastoma, colon, breast, prostate and lung cancers and is often associated with drug resistance. However, TRAP1 is also downregulated in specific tumors, such as ovarian, bladder and renal cancers, where its lower expression is correlated with the worst prognoses and chemoresistance. TRAP1 is the only mitochondrial member of the Heat Shock Protein 90 (HSP90) family that directly interacts with respiratory complexes, contributing to their stability and activity but it is still unclear if such interactions lead to reduced or increased respiratory capacity. The role of TRAP1 is to enhance or suppress oxidative phosphorylation; the effects of such regulation on tumor development and progression are controversial. These observations encourage the study of the mechanisms responsible for the dualist role of TRAP1 as an oncogene or oncosuppressor in specific tumor types. In this review, TRAP1 puzzling functions were recapitulated with a special focus on the correlation between metabolic reprogramming and tumor outcome. We wanted to investigate whether metabolism-targeting drugs can efficiently interfere with tumor progression and whether they might be combined with chemotherapeutics or molecular-targeted agents to counteract drug resistance and reduce therapeutic failure.
    Electronic ISSN: 2073-4425
    Topics: Biology
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