Person:
Martin, Melissa Janet

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Martin

First Name

Melissa Janet

Name

Martin, Melissa Janet

Filters

2013 - 20163

Settings

Author's Publications: search.filters.isAuthorOfPublication.9c10cc63-4db1-480a-aa01-f8948d276334

Search Results

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    Structure, Function, and Biology of the Enterococcus faecalis Cytolysin
    (MDPI, 2013) Van tyne, Daria; Martin, Melissa Janet; Gilmore, Michael
    Enterococcus faecalis is a Gram-positive commensal member of the gut microbiota of a wide range of organisms. With the advent of antibiotic therapy, it has emerged as a multidrug resistant, hospital-acquired pathogen. Highly virulent strains of E. faecalis express a pore-forming exotoxin, called cytolysin, which lyses both bacterial and eukaryotic cells in response to quorum signals. Originally described in the 1930s, the cytolysin is a member of a large class of lanthionine-containing bacteriocins produced by Gram-positive bacteria. While the cytolysin shares some core features with other lantibiotics, it possesses unique characteristics as well. The current understanding of cytolysin biosynthesis, structure/function relationships, and contribution to the biology of E. faecalis are reviewed, and opportunities for using emerging technologies to advance this understanding are discussed.
  • Thumbnail Image
    Publication
    Complete Genome Sequence of Linezolid-Susceptible Staphylococcus haemolyticus Sh29/312/L2, a Clonal Derivative of a Linezolid-Resistant Clinical Strain
    (American Society for Microbiology, 2015) de Almeida, Lara M.; Pires, Carlos; Cerdeira, Louise T.; de Oliveira, Théo G. M.; McCulloch, John Anthony; Perez-Chaparro, Paula Juliana; Sacramento, Andrey G.; Brito, Artemir C.; da Silva, Joás L.; de Araújo, Maria Rita E.; Lincopan, Nilton; Martin, Melissa Janet; Gilmore, Michael; Mamizuka, Elsa M.
    We report the whole-genome sequence (WGS) of an in vitro susceptible derivative revertant mutant from a bloodstream isolate involved in a nosocomial outbreak in Brazil. The WGS comprises 2.5 Mb with 2,500 protein-coding sequences, 16rRNA genes, and 60 tRNA genes.
  • Thumbnail Image
    Publication
    Multidrug Intrinsic Resistance Factors inStaphylococcus aureusIdentified by Profiling Fitness within High-Diversity Transposon Libraries
    (American Society for Microbiology, 2016) Rajagopal, Mithila; Martin, Melissa Janet; Santiago, Marina; Lee, Wonsik; Kos, Veronica N.; Meredith, Timothy; Gilmore, Michael; Kahne, Suzanne
    Staphylococcus aureus is a leading cause of life-threatening infections worldwide. The MIC of an antibiotic against S. aureus, as well as other microbes, is determined by the affinity of the antibiotic for its target in addition to a complex interplay of many other cellular factors. Identifying nontarget factors impacting resistance to multiple antibiotics could inform the design of new compounds and lead to more-effective antimicrobial strategies. We examined large collections of transposon insertion mutants in S. aureus using transposon sequencing (Tn-Seq) to detect transposon mutants with reduced fitness in the presence of six clinically important antibiotics-ciprofloxacin, daptomycin, gentamicin, linezolid, oxacillin, and vancomycin. This approach allowed us to assess the relative fitness of many mutants simultaneously within these libraries. We identified pathways/genes previously known to be involved in resistance to individual antibiotics, including graRS and vraFG (graRS/vraFG), mprF, and fmtA, validating the approach, and found several to be important across multiple classes of antibiotics. We also identified two new, previously uncharacterized genes, SAOUHSC_01025 and SAOUHSC_01050, encoding polytopic membrane proteins, as important in limiting the effectiveness of multiple antibiotics. Machine learning identified similarities in the fitness profiles of graXRS/vraFG, SAOUHSC_01025, and SAOUHSC_01050 mutants upon antibiotic treatment, connecting these genes of unknown function to modulation of crucial cell envelope properties. Therapeutic strategies that combine a known antibiotic with a compound that targets these or other intrinsic resistance factors may be of value for enhancing the activity of existing antibiotics for treating otherwise-resistant S. aureus strains.