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dc.contributor.authorZhou, Zhuo
dc.date.accessioned2011-04-19T23:20:51Z
dc.date.available2011-04-19T23:20:51Z
dc.date.issued2010
dc.identifier.urihttp://hdl.handle.net/10179/2287
dc.description.abstractDuring adaptation to the host environment, many microorganisms undergo rapid variation in cell surface phenotype through genetic alteration in hypermutable contingency genes. One of the main mechanisms underlying these changes is alteration in the number of DNA repeat units that results in a large and flexible repertoire of similar but non-identical surface proteins. SSR1, a gene in the opportunistic pathogen Candida albicans, encodes a repeat-containing cell wall protein which may play a role in maintaining cell wall strength. This gene contains 2 regions with multiple 6 bp tandem repeat units, encoding the amino acids serine and alanine, separated by a 200 bp non-repetitive DNA region. This study investigated whether SSR1 was a hypermutable contingency gene. Among a worldwide collection of 96 infection-causing C. albicans strains, 24 alleles and 40 allele combinations were identified by fluorescent-based genotyping of SSR1 PCR products. Sequencing results confirmed that the differences in allele size were caused by variation in number of tandem repeats. Two very similar allele combinations were overrepresented (30% and 28%) among a cluster of generalpurpose genotype (GPG) strains (which is the most widespread cluster) compared with non-GPG strains (Fisher’s exact test, P=0.0001 and P<0.0001). Among a worldwide collection of 36 commensal GPG C. albicans strains, 8 allele combinations were identified by genotyping. One of the two allele combinations that were overrepresented in GPG infection-causing strains was found significantly less in GPG commensal strains (Fisher’s exact test, P=0.0004). After culture of C. albicans cells in vitro for 300 generations, mutation of repeats in SSR1 occurred, giving a high mutation rate of 1.11×10-4 per cell division. The results indicate that SSR1 is a hypermutable gene and that it shows clade-specificity with the GPG cluster. Growth in a rat model did not seem to cause variation in SSR1 and human host body sites did not seem to be associated with specific SSR1 alleles, suggesting that SSR1 is not used for short-term adaptation in these environments. However, the different allele distribution in commensal and infection-causing GPG strains suggest that SSR1 may have a role in short-term adaptation in GPG strains, contributing to the change between commensalism and infection. In this case, SSR1 may act as a hypermutable contingency gene.en_US
dc.language.isoenen_US
dc.publisherMassey Universityen_US
dc.rightsThe Authoren_US
dc.subjectCandida albicansen_US
dc.subjectGeneticsen_US
dc.subjectSSR1en_US
dc.subjectHypermutable contingency geneen_US
dc.subjectMicrobiology
dc.titleEvidence that SSR1 can act as a hypermutable contingency gene in Candida albicans : a thesis presented in partial fulfillment of the requirement for the degree of Master of Science in Microbiology at Massey University, Palmerston North, New Zealanden_US
dc.typeThesisen_US
thesis.degree.grantorMassey University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.Sc.)


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