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Identification of a pathogenicity factor generally involves making a mutant fungal strain with a non-functioning version of the gene by targeted gene deletion and assaying the ability of the mutant to cause disease.
Our observations therefore suggest that it would be of interest to compare the ability of the oppD mutant to cause disease and maintain bacterial burden during both the chronic and the persistent phases of infection.
On the other hand, after two days of acute lung infection, the bacterial lung counts and the ability of the glpT mutant to cause death did not differ from the parental strain.
The ability of the map/espF/eae/tir quadruple mutant to cause detachment-linked TER decreases ruled out roles for Map, EspF and Intimin in the process.
The fact that the deletion of pppA-ppkA genes influenced stress tolerance and substantially decreased intracellular survival in the murine macrophages raised the possibility that it could also have significant implications in the ability of this mutant to cause disease.
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The ability of these mutants to cause sepsis was evaluated.
In parallel to the above binding studies, we also analysed the ability of the STIL mutants to cause centriole amplification.
The exact mechanisms of reduced effectiveness of Sar/Agr mutants to cause SA or osteomyelitis are not known.
In addition, we compared the ability of these wild-type and mutant strains to cause abscesses and sepsis in mouse models of infection.
Application of our instrument to larvae homozygous for a Tropomyosin mutant known to cause DCM in the adult fly reveals for the first time, to our knowledge, that an arrhythmia is associated with this mutation in this organism.
Consistent with the reduced binding of UBXN7 ΔUIM to CUL2, over-expression of this mutant failed to cause an up-shift of CUL2 to the neddylated form.
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