The unifying thread linking my work is an interest in how sublethal exposure to these stressors shapes biodiversity and ecosystem functions. My overarching goal is to generate science that will influence evidence-based policies and practices, thus creating resilient ecosystems whose services meet the needs of both nature and humans. My approach combines field and laboratory experiments, quantitative methods, and interdisciplinary collaborations to advance the application of toxicological data to inform ecosystem-based management.
Harmful algal blooms (HABs) are a prime example of one such threat to aquatic ecosystems in the Anthropocene. They are expanding due, in part, to changes in the global environment and increases in human activities, both of which are rendering agricultural and aquatic landscapes less resilient. Before my work, longstanding concerns remained that microcystins, the most potent toxin produced by HABs, could accumulate up the aquatic food chain at sublethal concentrations and threaten fisheries. These concerns stemmed from limited mechanistic understanding of microcystins accumulation by, and levels in, aquatic organisms. Consequently, the risk(s) to human consumers of these organisms were poorly understood, threatening fisheries and populations who consume a high proportion of fish.
Harmful algal blooms (HABs) are a prime example of one such threat to aquatic ecosystems in the Anthropocene. They are expanding due, in part, to changes in the global environment and increases in human activities, both of which are rendering agricultural and aquatic landscapes less resilient. Before my work, longstanding concerns remained that microcystins, the most potent toxin produced by HABs, could accumulate up the aquatic food chain at sublethal concentrations and threaten fisheries. These concerns stemmed from limited mechanistic understanding of microcystins accumulation by, and levels in, aquatic organisms. Consequently, the risk(s) to human consumers of these organisms were poorly understood, threatening fisheries and populations who consume a high proportion of fish.
Previous research
My previous and ongoing work resolved these concerns by answering a series of sequential questions starting from the bottom of the aquatic food chain:
- What conditions drive HABs to produce and maintain microcystins?
- To what extent do microcystins at sublethal concentrations cause adverse outcomes in key functional traits of aquatic organisms?
- Do fish at varying life stages and species accumulate and retain microcystins at similar levels?
- What are the human health risks of consuming fish that encounter and accumulate microcystins from HABs?
Using a toxigenic strain of the bloom-forming cyanobacterium Microcystis aeruginosa, my doctoral work showed that microcystins at sublethal concentrations have drastic and negative impacts on the functional traits of plankton and fish species. For instance, using a model organism, Daphnia magna, I showed that chronic dietary exposure to M. aeruginosa decreases Daphnia somatic growth rates and reproductive success. Employing proteomics, I also found that D. magna adults invest more energy towards growth and survival, whereas juveniles have decreased immunity and capacity to metabolize cyanobacteria. The implications of these findings are substantial for plankton populations who regularly encounter HABs. Using another model organism, Rainbow Trout, I showed that aqueous exposure to microcystins within and outside of M. aeruginosa differ in accumulation potential in fish tissues, yet demonstrate near-equal potential to dysregulate proteins linked to oxidative stress and carcinogenesis, and also form necrosis and apoptosis in tissues. Intrigued by these findings, I additionally showed intraspecific and interspecific variation in the accumulation and retention of microcystins in Rainbow Trout and Lake Trout. While both species activated cellular responses related to oxidative stress, DNA repair, and carcinogenicity, I demonstrated that fish respond differently to toxicity within and among species. These findings corroborate outcomes from my extensive field work in Lake St. Clair and Lake Erie, where thousands of game fish across seven species demonstrated that microcystins accumulate at varying levels depending on the species and HAB intensity. As a whole, my doctoral work demonstrates the set of conditions under which toxins from HABs constitute an ecological concern and when they are likely to directly impact animal and human health.
KEY PAPERS
Shahmohamadloo, R.S., et al. (2022). Fish tissue accumulation and proteomic response to microcystins is species-dependent. Chemosphere, 132028. (PhD work). https://doi.org/10.1016/j.chemosphere.2021.132028 | PDF
Shahmohamadloo, R.S., et al. (2021). Cyanotoxins within and outside of Microcystis aeruginosa cause adverse effects in Rainbow Trout (Oncorhynchus mykiss). Environ. Sci. Technol., 55(15), 10422-10431. (PhD work). https://doi.org/10.1021/acs.est.1c01501 | PDF
Shahmohamadloo, R.S., et al. (2020). Shotgun proteomics analysis reveals sub-lethal effects in Daphnia magna exposed to cell-bound microcystins produced by Microcystis aeruginosa. Comp. Biochem. Phys. D., 33, 100656. (PhD work). http://doi.org/10.1016/j.cbd.2020.100656 | PDF
Shahmohamadloo, R.S., et al. (2020). Assessing the toxicity of cell-bound microcystins on freshwater pelagic and benthic invertebrates. Ecotox. Environ. Safe., 188, 109945. (PhD work). http://doi.org/10.1016/j.ecoenv.2019.109945 | PDF
Shahmohamadloo, R.S., et al. (2022). Fish tissue accumulation and proteomic response to microcystins is species-dependent. Chemosphere, 132028. (PhD work). https://doi.org/10.1016/j.chemosphere.2021.132028 | PDF
Shahmohamadloo, R.S., et al. (2021). Cyanotoxins within and outside of Microcystis aeruginosa cause adverse effects in Rainbow Trout (Oncorhynchus mykiss). Environ. Sci. Technol., 55(15), 10422-10431. (PhD work). https://doi.org/10.1021/acs.est.1c01501 | PDF
Shahmohamadloo, R.S., et al. (2020). Shotgun proteomics analysis reveals sub-lethal effects in Daphnia magna exposed to cell-bound microcystins produced by Microcystis aeruginosa. Comp. Biochem. Phys. D., 33, 100656. (PhD work). http://doi.org/10.1016/j.cbd.2020.100656 | PDF
Shahmohamadloo, R.S., et al. (2020). Assessing the toxicity of cell-bound microcystins on freshwater pelagic and benthic invertebrates. Ecotox. Environ. Safe., 188, 109945. (PhD work). http://doi.org/10.1016/j.ecoenv.2019.109945 | PDF
Postdoctoral research
My postdoctoral research, funded by NSERC and Liber Ero, incorporates eco-evolutionary dynamics to understand:
- The role of intraspecific genetic variation within cyanobacterial species driving the frequency, severity, and toxicity of HABs.
- The role of intraspecific genetic variation within zooplankton enabling rapid adaptation and population persistence in response to HABs.
Despite decades of research many aspects of the ecology of Microcystis blooms are unresolved, owing, in large part, to substantial intraspecific genetic variation. In addition to this genetic variation, there are strong genotype-by-environment interactions that shape clonal response to temperature, light, nutrients, herbivory, and parasitism that enable Microcystis to dominate plankton communities across a wide range of physicochemical conditions over time and seasonal changes. The scale of intraspecific genetic diversity within Microcystis strains in genotype and phenotype is immense and accounting for this variation could be key to understanding the dynamics of HABs. Daphnia also shows substantial intraspecific diversity and rapid adaptation, including the ability to effectively feed on and reduce the abundance of toxic Microcystis.
To understand the dynamics of HABs and uncover new management actions for aquatic ecosystems, I am testing the predictability and determining the ecological consequences of rapid evolution in both Microcystis and Daphnia. I combining growth trials, mathematical modeling, and large-scale mesocosm experiments to determine the rate, genomic basis, and phenotypic consequences of D. magna evolution in response to toxic Microcystis. By studying key functional traits, including growth, reproductive output, gut-microbiome composition, and the feeding rate of 20 genetically distinct clones of D. magna on toxic Microcystis, my research investigates the mechanisms that allow for top-down control of HABs. A major focus of this research is using genetic variation to study rapid clonal evolution between zooplankton and HABs, achieved using highly parallelized amplicon sequencing protocols. Shotgun proteomics is employed as a complimentary tool for explaining the molecular initiating events involved in the early stages of adverse outcome pathways. Demography is utilized to capture changes in population structure over the lifespans of organisms. Using these approaches, my collaborators and I are testing for quantitative links spanning the genetics of a single organism to aspects of the ecosystem that directly influence human health and well-being.
To understand the dynamics of HABs and uncover new management actions for aquatic ecosystems, I am testing the predictability and determining the ecological consequences of rapid evolution in both Microcystis and Daphnia. I combining growth trials, mathematical modeling, and large-scale mesocosm experiments to determine the rate, genomic basis, and phenotypic consequences of D. magna evolution in response to toxic Microcystis. By studying key functional traits, including growth, reproductive output, gut-microbiome composition, and the feeding rate of 20 genetically distinct clones of D. magna on toxic Microcystis, my research investigates the mechanisms that allow for top-down control of HABs. A major focus of this research is using genetic variation to study rapid clonal evolution between zooplankton and HABs, achieved using highly parallelized amplicon sequencing protocols. Shotgun proteomics is employed as a complimentary tool for explaining the molecular initiating events involved in the early stages of adverse outcome pathways. Demography is utilized to capture changes in population structure over the lifespans of organisms. Using these approaches, my collaborators and I are testing for quantitative links spanning the genetics of a single organism to aspects of the ecosystem that directly influence human health and well-being.
