Host–Symbiont Interaction Model Explains Non-monotonic Response of Soybean Growth and Seed Production to Nano-CeO2 Exposure

Klanjšček, Tin; Muller, Erik B.; Holden, Patricia A.; Nisbet, Roger M. (2017) Host–Symbiont Interaction Model Explains Non-monotonic Response of Soybean Growth and Seed Production to Nano-CeO2 Exposure. Environmental Science and Technology, 51 (9). pp. 4944-4950. ISSN 0013-936X

| Request a personal copy from author

Official URL: https://pubs.acs.org/doi/abs/10.1021/acs.est.6b066...

Abstract

Recent nanotoxicity studies have demonstrated non-monotonic dose–response mechanisms for planted soybean that have a symbiotic relationship with bacteroids in their root nodules: reduction of growth and seed production was greater for low, as compared to high, exposures. To investigate mechanistic underpinnings of the observed patterns, we formulated an energy budget model coupled to a toxicokinetic module describing bioaccumulation, and two toxicodynamic modules describing toxic effects on host plant and symbionts. By fitting data on plants exposed to engineered CeO2 nanoparticles to the newly formulated model, we show that the non-monotonic patterns can be explained as the interaction of two, individually monotonic, dose–response processes: one for the plant and the other for the symbiont. We further validate the newly formulated model by showing that, without the need for additional parameters, the model successfully predicts changes in dinitrogen fixation potential as a function of exposure (dinitrogen fixation potential data not used in model fitting). The symbiont buffers overall toxicity only when, in the absence of exposure to a toxicant, it has a parasitic interaction with the host plant. If the interaction is mutualistic or commensal, there is no buffering and only monotonic toxic responses are possible. Because the model is based on general biological principles, we expect it to be applicable to other similar symbiotic systems, especially other nodule-forming legumes.

Item Type:

Article

Additional Information:

The authors thank J. H. Priester for providing data in digital form and helping with useful information and insights, Y. Wang and J. Rohr for valuable discussions and advice, and T. Jager for sharing statistical programs. This research was primarily funded by the National Science Foundation (NSF) and the United States Environmental Protection Agency (U.S. EPA) under Cooperative Agreements DBI-0830117 and 1266377 (to Patricia A. Holden and Roger M. Nisbet) and the U.S. EPA under STAR Grant 835797 to Roger M. Nisbet and Erik B. Muller. Additional funding was provided by the Croatian National Science Foundation (HRZZ) under the Project 2202-ACCTA. Any opinions, findings, and conclusions expressed in this material are those of the author(s) and do not necessarily reflect those of the NSF, U.S. EPA, or HRZZ. This work has not been subjected to U.S. EPA review, and no official endorsement should be inferred.

Uncontrolled Keywords:

reactive oxygen species (ROS), cellular damage, organismal response to stress, modeling damage repair, stability, runaway ROS and damage

Subjects:

NATURAL SCIENCES > Biology

Divisions:

Division for Marine and Enviromental Research

Projects: