Maternal allocation of carotenoids increases tolerance to bacterial infection in brown trout

Abstract

Life-history theory predicts that iteroparous females allocate their resources differently among different breeding seasons depending on their residual reproductive value. In iteroparous salmonids there is typically much variation in egg size, egg number, and in the compounds that females allocate to their clutch. These compounds include various carotenoids whose functions are not sufficiently understood yet. We sampled 37 female and 35 male brown trout from natural streams, collected their gametes for in vitro fertilizations, experimentally produced 185 families in 7 full-factorial breeding blocks, raised the developing embryos singly (n = 2960), and either sham-treated or infected them with Pseudomonas fluorescens. We used female redness (as a measure of carotenoids stored in the skin) and their allocation of carotenoids to clutches to infer maternal strategies. Astaxanthin contents largely determined egg colour. Neither egg weight nor female size was correlated with the content of this carotenoid. However, astaxanthin content was positively correlated with larval growth and with tolerance against P. fluorescens. There was a negative correlation between female skin redness and the carotenoid content of their eggs. Although higher astaxanthin contents in the eggs were associated with an improvement of early fitness-related traits, some females appeared not to maximally support their current offspring as revealed by the negative correlation between female red skin colouration and egg carotenoid content. This correlation was not explained by female size and supports the prediction of a maternal trade-off between current and future reproduction.

No additive genetic variance for tolerance to ethynylestradiol exposure in natural populations of brown trout (Salmo trutta)

“…No water changes were performed throughout the experiment. This experimental protocol has been developed for salmonid embryos and has been repeatedly and successfully used in stress tolerance tests (e.g., Clark, Pompini, Marques da Cunha, & Wedekind, 2014;von Siebenthal et al, 2009;Wilkins, Marques da Cunha, Menin et al, 2017).…”

Consumption of carotenoids not increased by bacterial infection in brown trout embryos (Salmo trutta)

“…Importantly, egg carotenoid contents varied significantly among females (some females allocated several times more of certain carotenoids to the eggs than others). Wilkins et al [23] and Wilkins et al [24] investigated the potential significance of this variation in carotenoids for embryo performance. In their first study [23], embryos were stressed by an experimentally induced organic pollution.…”

“…P. fluorescens is an opportunistic pathogen that naturally occurs on brown trout eggs [25] and that can be used in experimental infections [11,15]. Wilkins et al [24] found astaxanthin egg contents to be positively correlated to larval growth in all treatment groups. Moreover, astaxanthin contents seemed to protect embryos from the virulence caused by the pathogen.…”

“…Here, we studied carotenoid consumption in brown trout embryos that had been experimentally exposed to P. fluorescens in order to test the aforementioned hypotheses. We used a new sample of offspring of the females that Wilkins et al [24] had studied. This allowed us to link carotenoid consumptions to the life-history traits that were described in Wilkins et al [24], and that are closely linked to two fitness-relevant traits of salmonids, namely the timing of emergence from the gravel bed and the size at emergence [30,31].…”

“…We used a new sample of offspring of the females that Wilkins et al [24] had studied. This allowed us to link carotenoid consumptions to the life-history traits that were described in Wilkins et al [24], and that are closely linked to two fitness-relevant traits of salmonids, namely the timing of emergence from the gravel bed and the size at emergence [30,31]. We investigated whether carotenoids simply prevent pathogenic stress or are used by the embryo defence against the bacterial pathogen.…”