Disruption of nitrogen fixing symbiosis by pesticides and endocrine disrupting chemicals
Description
A subset of synthetic chemicals present in the environment, such as organochlorine pesticides and plastics by-products, are able to mimic endogenous estrogen-induced signaling in representatives of each vertebrate class; as such, they are termed endocrine disrupting chemicals (EDCs). Similarly, estrogen-like signaling has also been observed when vertebrates are exposed to plant products called phytoestrogens. Previous research has focused on what effects synthetic and plant estrogens may have on estrogen receptor (ER) function and estrogenic signaling in humans and wildlife, while the evolutionary signaling targets of phytoestrogens, namely soil bacteria capable of nitrogen-fixing symbiosis with leguminous plants, had not been studied to determine if EDCs may interfere with crucial phytoestrogen-bacterial signaling Here I show that, in much the same way estrogen signaling with ERs is disrupted by the presence of EDCs, phytoestrogen signaling with its natural target, soil bacterial nodulation D (NodD) transcriptional activator proteins, is also disrupted by a similar profile of endocrine disrupting pesticides and pollutants. The similarities between ERs and NodD proteins may be explained by convergent evolution in which both NodD and ER separately evolved to adapt to the presence of natural estrogenic ligands, both vertebrate estrogens and phytoestrogens, as well as synthetic chemicals found in the environment that are able to mimic the natural ligands of both ER and NodD. I hypothesize that synthetic environmental compounds with similar structural properties to phytoestrogens, such as EDCs, may disrupt phytoestrogen-NodD signaling My studies herein show that the presence of a subset of EDCs: (1) inhibit phytoestrogen-NodD signaling and reduce the activation of key nod genes as measured in vitro, (2) the same EDCs tested in an in vivo plant-bacterial ecosystem inhibit symbiosis, nitrogen fixation, and adversely affect crop yield in treated plants. I demonstrate that both estrogenic and NodD signaling systems are adversely affected by the presence of a similar profile of EDCs at environmentally relevant concentrations. Therefore, I conclude that signaling components used by plants and pathways present in bacteria may have previously unrecognized similarities to those present in animals, and both of these systems are vulnerable to endocrine disruptors present in the environment