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Fusobacterium nucleatum apoptosis-inducing outer membrane protein
1Molecular Biology Institute, Section of Periodontics, UCLA School of Dentistry, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA.
Journal of Dental Research
|July 26, 2005
Summary
Fusobacterium nucleatum causes lymphocyte apoptosis. A specific protein, aim1, contributes to this process by reducing apoptosis by 41% in a genetically modified strain.
Area of Science:
- Microbiology
- Immunology
Background:
- Fusobacterium nucleatum is a periodontal pathogen.
- F. nucleatum induces apoptosis in lymphocytes.
- The autotransporter protein Fap2 from F. nucleatum strain PK1594 induces lymphocyte apoptosis when expressed in Escherichia coli.
Purpose of the Study:
- To identify Fap2 homologs in F. nucleatum strain ATCC 23726.
- To determine the role of these homologs in inducing lymphocyte apoptosis.
- To characterize the function of the aim1 gene in F. nucleatum-induced apoptosis.
Main Methods:
- Gene inactivation using a novel thiamphenicol resistance vector (pHS31).
- Construction of an aim1-deficient mutant.
- Transcriptional analysis to confirm gene disruption.
- Phenotypic analysis using Jurkat cells to assess apoptosis induction.
Main Results:
- Identified Fap2 homologs in F. nucleatum ATCC 23726.
- Generated an aim1 mutant with confirmed disruption of aim1 expression.
- The aim1 mutant showed a 41% decrease in apoptosis induction in Jurkat cells compared to the wild-type strain.
Conclusions:
- The aim1 gene contributes to F. nucleatum-induced apoptosis in its native host cell background.
- This study reports the first genetically defined and phenotypically characterized mutation in F. nucleatum.
- Understanding aim1's role provides insights into F. nucleatum pathogenesis.