Biopolym. Cell. 2019; 35(3):195-196.
Chronicle and Information
The cell nucleus as sensor of environmental pollution: Amyloid, neurodegeneration and aging
1Piechulek A., 1Berwanger L., 2Scharf A., 1von Mikecz A.
  1. IUF-Leibniz Research Institute of Environmental Medicine at Heinrich-Heine-University Duesseldorf
    Duesseldorf, Germany
  2. Washington University
    St. Louis, USA


Two major environmental challenges are predominant - climate change and the biodiversity crisis. Also, pollutants are distributed globally. We identified the cell nucleus as a sensitive sensor for bio-effects of pollutants such as mercury and nanoparticles. Our investigations focus on the role of pollutant-induced nuclear amyloid formation in neural signaling, neurotoxicity and accelerated aging in the nematode Caenorhabditis elegans. Methods: At present, the majority of investigations on the toxicology of pollutants address short-term effects. While this approach allows for the identification of uptake pathways, exposition and acute toxicity, xenobiotic-organism interactions that manifest later in an adult life are missed. To characterize effects of pollutants over the entire life span, all analyses are performed in the nematode C. elegans. Results: We show that mercury and nano silica effect widespread protein aggregation. Proteomic profiling revealed that both pollutants promote segregation of proteins belonging to the gene ontology (GO) group of ‘protein folding, proteolysis and stress response’ to an SDS-resistant aggregome network. Candidate proteins in this group include chaperones, heat shock proteins and subunits of the 26S proteasome which are all decisively involved in protein homeostasis. Another emerging GO group is translation. Crucial proteins such as the methyltransferase fibrillarin aggregate, segregate and thus reduce translational activity. The metabolic changes contribute to neurodegeneration and starvation which in turn manifests in petite worms showing motoric and olfactory deficits. Conclusions: A picture emerges that pollutants induce premature aging, thereby reducing the health span and longevity of C. elegans. The neural system of the worm represents a prominent target organ showing neuromuscular defects that among others manifest in neurodegeneration of single neurons in combination with altered locomotion, reduced fecundity and impaired olfaction. As C. elegans leads a dual life, e.g. in the lab and in ecosystems, our results explain how environmental pollutants reduce the fitness of wild worms. Concerning the survival of wild populations the flexibility of adaptive gene expression and proteomes likely determines biodiversity, namely resilience against pollutantand climate-stress.