Characterization of PIR 32, a candida albicans cell wall protein. (c2009)

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dc.contributor.author Bahnan, Wael G.
dc.date.accessioned 2011-10-28T10:17:05Z
dc.date.available 2011-10-28T10:17:05Z
dc.date.copyright 2009 en_US
dc.date.issued 2011-10-28
dc.date.submitted 2009-08-17
dc.identifier.uri http://hdl.handle.net/10725/942
dc.description Includes bibliographical references (leaves 42-48). en_US
dc.description.abstract Candida albicans is a common opportunistic pathogen that causes a wide variety of diseases in a human immunocompromised host. C .albicans is the most common fungal pathogen retrieved from the blood as well as from superficial infection sites. In a pathogen, cell wall proteins are important for stability as well as for acting as antigenic determinants and virulence factors. This study has characterized Pir32, a C. albicans cell wall protein. Pir32 is a member of the Pir protein family previously shown to be upregulated in response to macrophage contact and whose other member, Pirl, was found to be necessary for cell wall rigidity. We have thus generated a pir32 homozygote null strain by the use of PCR generated cassettes that underwent homologous recombination at the native PIR32 ORF's. PIR32 is not an essential gene since a homozygous null was successfully generated. The homozygote null mutant was then subjected to a battery of tests to reveal the role that Pir32 plays. Our mutant was shown to be slightly hyperftlamentous, resistant to sodium dodecyl sulfate, hydrogen peroxide, sodium chloride, and more virulent in a mouse model when compared to the wild type. Also the mutant exhibited a slight yet significant deficiency in biofilm formation and showed a delay in adhesion to human epithelial cells. Pir32 however seems not to playa role in antifungal drug resistance, sensitivity to cell wall disrupting agents or involved in heat shock stress response. Our mutation seems to have strengthened the cell surface, rather than weakened it. This has rendered it more resistant to external stress factors. The question remains however as to what factors were upregulated in the mutant to compensate for the Pir32 deletion increasing the rigidity of the cell surface and thus opening the door to further experimentation. en_US
dc.language.iso en en_US
dc.subject Candida albicans en_US
dc.subject Bacterial cell walls en_US
dc.title Characterization of PIR 32, a candida albicans cell wall protein. (c2009) en_US
dc.type Thesis en_US
dc.term.submitted Summer II en_US
dc.author.degree MS in Molecular Biology en_US
dc.author.school Arts and Sciences en_US
dc.author.idnumber 200300587 en_US
dc.author.commembers Sima Tokajian
dc.author.commembers Brigitte Wex
dc.author.woa OA en_US
dc.description.physdesc 1 bound copy: xi, 48 leaves; ill., some col; 30 cm. Available at RNL. en_US
dc.author.division Biology en_US
dc.author.advisor Roy Khalaf
dc.identifier.doi https://doi.org/10.26756/th.2009.55 en_US
dc.publisher.institution Lebanese American University en_US

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