| To determine whether metazoan mitochondria retain the capacity to evolve on their own in response to selection pressure, I conducted an eight-month selection experiment on six populations of the monogonont rotifer Brachionus plicatilis. Rotifers were cultivated in brine shrimp hatchers under constant light, and were periodically exposed to the protein synthesis inhibitors chloramphenicol or cycloheximide. I uncoupled mitochondrial from recombinant chromosomal heredity in the test populations, either by destroying resting eggs to isolate mtDNA within all-clone lineages, or by restricting chemical exposure to males to halt mtDNA transmission to offspring. Rotifers' tolerance for toxins was tested after 10, 23, and 30 exposures; partial mitochondrial 16S rRNA gene sequences were also obtained from rotifer populations after 30 treatments. A novel genetic polymorphism that correlated with an increase in chloramphenicol resistance in the CAP-treated asexual B. plicatilis population was noted. Other toxin-treated rotifer populations' gene sequences exhibited no such increase in frequency for mitochondrial variants, even in cases where a population's resistance to toxins did improve. This is consistent with my hypothesis that asexual rotifers' mitochondria would adapt to the CAP antibiotic most easily, whereas the males-only treatment groups' chromosomes would adapt more easily to the cytoplasmic toxin cycloheximide. |
