the causative agent of Lyme disease. By applying PCR to archival 

 museum specimens of the vector of Lyme disease (ticks) , it was 

 possible to retrieve and analyze preserved DNA from preserved 

 samples. This led to the discovery that the historical entry of 

 Lyme disease into the United States occurred before the disease was 

 clinically recognized (Persing et al., 1990). Such techniques 

 applied to older samples may allow molecular characterization of 

 ancient species, and a better understanding of the processes 

 influencing their evolution. In a similar fashion, can we 

 correlate genetic changes documented in the geological record? 

 Does rapid environmental change correlate with rapid evolutionary 

 change at the genetic level? Such information would provide 

 insight into the genetic responses of individuals and species to 

 environmental fluctuations. 



Is environmental stress a significant factor eliciting genetic 

 change, and if so, how? Just as chronic stress may influence 

 population dynamics and species composition, it may also influence 

 the rate (and possibly direction) of genetic change (mutation) in 

 individuals. For example, the classic paradigm of Neodarwinian 

 evolution presumes that the probability of any individual mutation 

 occurring is essentially random, and relatively independent of 

 environmental influences. However, recent evidence indicates that 

 mutations at some genetic loci may, in fact, arise at a greater 

 frequency under specific environmental conditions. Missense 

 mutations (from tryptophan auxotrophy [trp-] to tryptophan 

 prototrophy [trp+]) in tryptophan-requiring strains of E. coli 

 occur at much greater frequency under (nonselective) conditions 

 which are advantageous for resulting mutants, than under neutral 

 conditions (Hall, 1990) . Yet mutation rates at other genetic loci 

 do not increase during tryptophan starvation, and starvation for 

 other amino acids does not increase the rate of tryptophan 

 mutations. It appears, then, that at least for the tryptophan 

 operon in E. coli , mutation rates can be specifically increased 

 under certain specific environmental conditions. This is a clear 

 example of how incompletely we understand the environmental 

 factors, and genetic responses, which may influence the rate and 

 direction of mutational change. How prevalent is this phenomenon 

 for other organisms, and at other genetic loci? Do environmental 

 stresses increase mutation rates, and if so, are they great enough 

 to perturb community structure and function? Do anthropogenic 

 environmental changes significantly increase the rate of mutation 

 in natural populations? 



III-6 



