Though not of direct ecological importance, as their natural occurence is extremely rare (if it occurs at all), host-independant (H-I) mutants of Bdellovibrio are an extremely valuable tool to the studying and understanding of the naturally occuring obligatory-parasite counterpart. The benefit of these mutations is that the complete dimorphic life cycle can still be observed and manipulated, but without any host interference.
Usually facultatively prey-independant, mutants appear to arise spontaneously, when grown under high density in nutrient-rich medium (Gray and Ruby, 1989). As it occurs with a frequency of 10ex6-10ex7, it may very well be a single mutation event (Cotter et al, 1996). The resulting H-I mutants are saprophytic, but if the environment is nutrient poor the dimorphic life-cycle can be retained, though with slightly less efficiency than the wild-type (Cotter et al, 1996). The invasive capability is lost completely if the mutant is grown axenically for an extended period of time (Barel and Jurkevitch, 2001).
The exact mechanism for the change to the H-I state is unclear as of yet. It may involve changes in the cell structure, or possibly physiological activities (Pan et al, 1997). A specific genetic loci has been identified as a likely factor, though it role is not well understood (Pan et al, 1997). It has been called the hit (host interaction) locus, and many studies have shown there to be mutations at various positions of this genein H-I mutants (Cotter et al, 1992). Yet other studies have shown that the hit locus is not involved in all H-I mutants, but instead may be a secondary mutation that is unrelated (Barel and Jurkevitch, 2001).
An interesting observation of the H-I mutants is that they have pleiotrophic phenotypes, and accumulate additional mutations with passing time (Barel and Jurkevitch, 2001). A common feature of all mutants, however, appears to be the yellow colony colour, indicating the presence of a carotenoid pigment (Pan et al, 1997). Morphological variation seems to be much more pronounced in mutants too, with cell lengths of 2-30�m, varying shapes (short spirals to long rods), and various plaque sizes (Barel and Jurkevitch, 2001). Mutants also vary in growth rate and growth capacity (Barel and Jurkevitch, 2001). Presently the relation between these commonly occuring mutations is unknown, however. |
