A research team including members of the College of Science has discovered a previously unknown chemical mechanism that may explain why harmful algal blooms are so persistent in nutrient-polluted lakes and reservoirs.
In a study published in PLOS One, the team found that cyanobacteria in Oregon’s Upper Klamath Lake produce bacimethrin, a toxic mimic of vitamin B1 that disrupts the metabolism of competing microbes. By selectively poisoning bacteria that depend on vitamin B1 from their environment while leaving bloom-forming cyanobacteria unharmed, bacimethrin may allow harmful algal blooms (HABs) to maintain ecological dominance for long periods of time.
The research team combined chemical measurements with DNA- and RNA-based analyses of microbes collected from Upper Klamath Lake and connected rivers and reservoirs before and during major bloom events. They found that bacimethrin concentrations rose with bloom intensity and were closely linked to changes in microbial gene activity.
Bloom-forming cyanobacteria are genetically equipped to synthesize their own vitamin B1, making them resistant to bacimethrin. Many other bacteria are not. When bacimethrin levels rose, these vitamin-dependent microbes showed reduced metabolic activity, effectively clearing ecological space for harmful algae to expand.
The findings could open new avenues for resource managers to use to control HABs beyond traditional nutrient management strategies.
The study was led by Department of Microbiology researchers Christopher Suffridge and Kelly Shannon and included other College of Science contributors Frederick Colwell, Byron Crump, Elizabeth Brennan, Gillian St. John and Robin Gould.
The research was supported by the U.S. Fish and Wildlife Service, the California Department of Fish and Wildlife and the National Science Foundation.
