Proteomic analyses of the cell walls of candida albicans PGA1 and PIR32 null mutants. (c2017)

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dc.contributor.author Khoury, Pamela Milad El
dc.date.accessioned 2018-07-09T08:52:57Z
dc.date.available 2018-07-09T08:52:57Z
dc.date.copyright 2017 en_US
dc.date.issued 2018-07-09
dc.date.submitted 2017-12-18
dc.identifier.uri http://hdl.handle.net/10725/8178
dc.description.abstract Though residing asymptomatically in mammalian tissues and mucosal surfaces, specific environmental cues can induce the opportunistic fungus Candida albicans to become pathogenic resulting in severe systemic and disseminated infection. The cell wall of this fungus is dynamic and its architecture is constantly modified and adapted as many virulence attributes are localized to the cell surface. Pga1 and Pir32 are two cell wall proteins that have been characterized by our lab following the generation of pga1 and pir32 null strains and comparing their respective phenotypes to the parental wild type strain. The pga1 null strain was less adherent and virulent than the wild type strain and exhibited reductions in chitin deposition, biofilm formation, filamentation, and resistance to stress. The pir32 null strain on the other hand showed more pronounced phenotypes such as hyperfilamentation ability, and increased resistance to oxidative stress in part due to a two fold increase in chitin deposition. In this study, cell wall proteomic profiles for both mutant strains were established and compared with the parental strain in order to explain the previously observed phenotypes. Major virulence proteins like Hsp70 and Mp65 were not detected in the pga1 null strain. Lipases (Lip6, 8, and 10), Sap1 and Exg2 functioning in host degradation and nutrient collection, were also undetected. Additionally, the mutant appears to lack Sod5, Erg1, Cdc11 and other proteins that have roles in cell wall integrity and resistance to environmental stress and antifungal treatment. On the other hand, key virulence factors required for proper dissemination were detected exclusively in the pir32 null strain. Such factors include the adhesin Als3, in addition to lipases, superoxide dismutases and secreted aspartyl protease family members. The mutant also appeared to be differentially expressing proteins involved in filamentous growth such as Cdc42 and Ssu81, explaining the observed hyperfilamentous phenotype. As such, cell wall proteomic analysis is a powerful tool that allowed us to identify key virulence traits responsible for the observed phenotypes of the mutant strains. en_US
dc.language.iso en en_US
dc.subject Lebanese American University -- Dissertations en_US
dc.subject Dissertations, Academic en_US
dc.subject Candida albicans en_US
dc.subject Fungal cell walls en_US
dc.subject Bacterial proteins en_US
dc.title Proteomic analyses of the cell walls of candida albicans PGA1 and PIR32 null mutants. (c2017) en_US
dc.type Thesis en_US
dc.term.submitted Fall en_US
dc.author.degree MS in Molecular Biology en_US
dc.author.school SAS en_US
dc.author.idnumber 201003007 en_US
dc.author.commembers Wex, Brigitte
dc.author.commembers Khazen, Georges
dc.author.commembers Khnayzer, Rony
dc.author.department Natural Sciences en_US
dc.description.embargo N/A en_US
dc.description.physdesc 1 hard copy: xi, 65 leaves; 30 cm. available at RNL. en_US
dc.author.advisor Khalaf, Roy
dc.keywords Candida albicans en_US
dc.keywords Proteomics en_US
dc.keywords CWPs en_US
dc.keywords Pga1 en_US
dc.keywords Pir32 en_US
dc.keywords MALDI MS/MS en_US
dc.description.bibliographiccitations Bibliography : leaves 52-65. en_US
dc.identifier.doi https://doi.org/10.26756/th.2018.57 en_US
dc.author.email pamela.elkhoury@lau.edu.lb en_US
dc.identifier.tou http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php en_US
dc.publisher.institution Lebanese American University en_US
dc.author.affiliation Lebanese American University en_US

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