Genetic correlations and little genetic variance for reaction norms may limit potential for adaptation to pollution by ionic and nanoparticulate silver in a whitefish (Salmonidae)

Abstract

For natural populations to adapt to anthropogenic threats, heritable variation must persist in tolerance traits. Silver nanoparticles, the most widely used engineered nanoparticles, are expected to increase in concentrations in freshwaters. Little is known about how these particles affect wild populations, and whether genetic variation persists in tolerance to permit rapid evolutionary responses. We sampled wild adult whitefish and crossed them in vitro full factorially. In total, 2896 singly raised embryos of 48 families were exposed to two concentrations (0.5 μg/L; 100 μg/L) of differently sized silver nanoparticles or ions (silver nitrate). These doses were not lethal; yet higher concentrations prompted embryos to hatch earlier and at a smaller size. The induced hatching did not vary with nanoparticle size and was stronger in the silver nitrate group. Additive genetic variation for hatching time was significant across all treatments, with no apparent environmental dependencies. No genetic variation was found for hatching plasticity. We found some treatment‐dependent heritable variation for larval length and yolk volume, and one instance of additive genetic variation for the reaction norm on length at hatching. Our assessment suggests that the effects of silver exposure on additive genetic variation vary according to trait and silver source. While the long‐term fitness consequences of low‐level silver exposure on whitefish embryos must be further investigated to determine whether it is, in fact, detrimental, our results suggest that the evolutionary potential for adaptation to these types of pollutants may be low.

Environmental stress linked to consumption of maternally derived carotenoids in brown trout embryos (Salmo trutta)

“…Such genetic effects can be interpreted as the overall genetic quality of the embryo; for example, its immune competence or its genetic load (Neff & Pitcher, ). The fitness‐associated traits include, for example, tolerance to uncontrolled epidemics or nonspecified stressors (e.g., Evans, Neff, & Heath, ; Pitcher & Neff, ; Wedekind, Müller, & Spicher, ), specific bacterial infections (Clark et al., ; von Siebenthal, Jacob, & Wedekind, ), chemical pollution (Brazzola, Chèvre, & Wedekind, ), or pollution by nanoparticles (Clark, Pompini, Uppal, & Wedekind, ). The present study adds organic pollution to this list.…”

Effects of host genetics and environment on egg‐associated microbiotas in brown trout (Salmo trutta)

“…, ), size at hatching (Clark et al . , ) and immune gene expression (Clark et al . ; Wilkins et al .…”

“…At later developmental stages, the importance of zygotic gene expression becomes crucial for the interaction with associated bacteria (Finn 2007;Clark et al 2013aClark et al , 2014. Host genetic effects could be revealed for important embryo life-history traits such as mortality in Oncorhynchus tshawytscha (Aykanat et al 2012), Salmo trutta (Jacob et al 2010;Clark et al 2013b) or Coregonus palaea (von Siebenthal et al 2009;Clark & Wedekind 2011;Clark et al 2014) and time until hatching (Clark et al 2013a(Clark et al , 2014, size at hatching (Clark et al 2014(Clark et al , 2016 and immune gene expression (Clark et al 2013a;Wilkins et al 2015c) in C. palaea. The interplay of fish embryos with their associated bacteria also depends on environmental factors, which, for example, can turn opportunistic bacteria into virulent fish pathogens (Jacob et al 2010;Wedekind et al 2010).…”

Low adaptive potential for tolerance to ethynylestradiol, but also low toxicity, in a grayling population (Thymallus thymallus)

“…However, such an error is unlikely here because (i) our analysis is based on a large sample size (1,555 singly-reared embryos) and 40 sib groups, (ii) our sample revealed overall additive genetic variance [58,59], pathogens [60] or even waterborne cues linked to infection [61].…”