times of 10.2 and 12.6 h. At similar 1,2- PD concentrations, strain BE1 82 grew with generation times of 14.5 and 20.3 h followed by a period of "interrupted" growth and then much shorter generation times of 8 and 10.2 h. In strain BE1 82 (lJpduA), the duration of "interrupted" growth was shorter at a PD concentration of 0.200 (10 h) than at

0.4%o (20 h). Thus, "interrupted" growth was observed at higher concentrations, but not at lower concentrations of PD. This suggested that "interrupted" growth resulted from the accumulation of a toxic compound derived from PD. Propionaldehyde was a likely candidate since this compound is an intermediate of PD degradation, and aldehydes are well known to have toxic effects on cells. Amino acid supplementation was not used in this experiment as very slight growth occurred on the amino acids alone. Consequently, the generation times observed are longer than those shown in Figure 3-10. BE182 (*lduA) grew at a faster rate than the wild type at concentrations of CN-B312 from

0.003125 [tg/ml to 0.05 [tg/ml; the largest difference was seen at a concentration of

0.00625 [tg/ml where the generation times were 47.5 h for the wild type strain and 14.9 h for BE182 (*lduA). At CN-B312 concentrations of 0.1 and 0.2 [tg/ml, BE182 (lJpduA) reached a maximal growth rate similar to that of the wild type strain, but exhibited the aforementioned "interrupted" growth (see above). These findings are consistent with a model in which an intermediate of PD degradation has a toxic effect that "interrupts" growth. At higher CN-B312 concentrations, PD would be catabolized at a faster rate and the toxic compound would accumulate to higher levels. This would result in a more pronounced interruption of growth. Subsequently, genes that lessen the effects of the toxic compound would be induced and the growth rate would increase. In addition, the above results indicate that the polyhedral organelles act as a barrier to B12. The possible