Linked Life Data

9748287

Source:http://linkedlifedata.com/resource/pubmed/id/9748287

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
40
pubmed:dateCreated
1998-11-12
pubmed:databankReference
pubmed:abstractText
The Candida albicans PLB1 gene was cloned using a polymerase chain reaction-based approach relying on degenerate oligonucleotide primers designed according to the amino acid sequences of two peptide fragments obtained from a purified candidal enzyme displaying phospholipase activity (Mirbod, F., Banno, Y., Ghannoum, M. A., Ibrahim, A. S., Nakashima, S., Yasuo, K., Cole, G. T., and Nozawa, Y. (1995) Biochim. Biophys. Acta 1257, 181-188). Sequence analysis of a 6.7-kilobase pair EcoRI-ClaI genomic clone revealed a single open reading frame of 1818 base pairs that predicts for a pre-protein of 605 residues. Comparison of the putative candidal phospholipase with those of other proteins in data base revealed significant homology to known fungal phospholipase Bs from Saccharomyces cerevisiae (45%), Penicillium notatum (42%), Torulaspora delbrueckii (48%), and Schizosaccharomyces pombe (38%). Thus, we have cloned the gene encoding a C. albicans phospholipase B homolog. This gene, designated caPLB1, was mapped to chromosome 6. Disruption experiments revealed that the caplb1 null mutant is viable and displays no obvious phenotype. However, the virulence of strains deleted for caPLB1, as assessed in a murine model for hematogenously disseminated candidiasis, was significantly attenuated compared with the isogenic wild-type parental strain. Although deletion of caPLB1 did not produce any detectable effects on candidal adherence to human endothelial or epithelial cells, the ability of the caplb1 null mutant to penetrate host cells was dramatically reduced. Thus, phospholipase B may well contribute to the pathogenicity of C. albicans by abetting the fungus in damaging and traversing host cell membranes, processes which likely increase the rapidity of disseminated infection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
273
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
26078-86
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9748287-Amino Acid Sequence, pubmed-meshheading:9748287-Animals, pubmed-meshheading:9748287-Base Sequence, pubmed-meshheading:9748287-Candida albicans, pubmed-meshheading:9748287-Candidiasis, pubmed-meshheading:9748287-Cell Adhesion, pubmed-meshheading:9748287-Chromosome Mapping, pubmed-meshheading:9748287-Cloning, Molecular, pubmed-meshheading:9748287-Disease Models, Animal, pubmed-meshheading:9748287-Fungal Proteins, pubmed-meshheading:9748287-Gene Targeting, pubmed-meshheading:9748287-Kidney, pubmed-meshheading:9748287-Lysophospholipase, pubmed-meshheading:9748287-Membrane Proteins, pubmed-meshheading:9748287-Mice, pubmed-meshheading:9748287-Mice, Inbred BALB C, pubmed-meshheading:9748287-Microscopy, Immunoelectron, pubmed-meshheading:9748287-Molecular Sequence Data, pubmed-meshheading:9748287-Saccharomyces cerevisiae Proteins, pubmed-meshheading:9748287-Sequence Alignment, pubmed-meshheading:9748287-Sequence Analysis, DNA, pubmed-meshheading:9748287-Virulence
pubmed:year
1998
pubmed:articleTitle
Cloning and disruption of caPLB1, a phospholipase B gene involved in the pathogenicity of Candida albicans.
pubmed:affiliation
Center for Medical Mycology, University Hospitals of Cleveland, and Case Western Reserve University, Cleveland, Ohio 44106-5028, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't