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Creators/Authors contains: "John‐Alder, Henry"

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  1. Free, publicly-accessible full text available November 1, 2025
  2. Allen Moore, University of (Ed.)
    Abstract Parasitism is nearly ubiquitous in animals and is frequently associated with fitness costs in host organisms, including reduced growth, foraging, and reproduction. In many species, males tend to be more heavily parasitized than females and thus may bear greater costs of parasitism.Sceloporus undulatusis a female‐larger, sexually size dimorphic lizard species that is heavily parasitized by chigger mites (Eutrombicula alfreddugesi). In particular, the intensity of mite parasitism is higher in male than in female juveniles during the period of time when sex differences in growth rate lead to the development of sexual size dimorphism (SSD). Sex‐biased differences in fitness costs of parasitism have been documented in other species. We investigated whether there are growth costs of mite ectoparasitism, at a time coinciding with sex differences in growth rate and the onset of SSD. If there are sex‐biased growth costs of parasitism, then this could suggest a contribution to the development of SSD inS. undulatus. We measured growth and mite loads in two cohorts of unmanipulated, field‐active yearlings by conducting descriptive mark‐recapture studies during the activity seasons of 2016 and 2019. Yearling males had consistently higher mid‐summer mite loads and consistently lower growth rates than females. However, we found that growth rate and body condition were independent of mite load in both sexes. Furthermore, growth ratesandmite loads were higher in 2019 than in 2016. Our findings suggest that juveniles ofS. undulatusare highly tolerant of chigger mites and that any costs imposed by mites may be at the expense of functions other than growth. We conclude that sex‐biased mite ectoparasitism does not contribute to sex differences in growth rate and, therefore, does not contribute to the development of SSD. 
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  3. null (Ed.)
    Synopsis Previous research has demonstrated that testosterone (T) can inhibit growth in female-larger species and stimulate growth in male-larger species, but the underlying mechanisms of this regulatory bipotentiality have not been investigated. In this study, we investigated the effects of T on the expression of hepatic insulin-like growth factor-1 (IGF-1) mRNA and circulating IGF-1 hormone in Sceloporus undulatus, a species of lizard in which females grow faster to become larger than males and in which T inhibits growth. Experiments were performed in captivity on mature female and male adults in the asymptotic phase of their growth curve and on actively growing, pre-reproductive juveniles. In adult males, the expression of hepatic IGF-1 mRNA increased following surgical castration and returned to control levels with T replacement; in intact adult females, exogenous T had no effect on IGF-1 mRNA expression. In juveniles, T significantly reduced both growth and the expression of hepatic IGF-1 mRNA to similar extents in intact females and in castrated males. The relative inhibitory effects of T on mRNA expression were greater in juveniles than in adults. Plasma IGF-1 hormone was about four times higher in juveniles than in adults, but T had no significant effect on IGF-1 hormone in either sex or in either age group. Our finding of inhibition of the expression of hepatic IGF-1 mRNA stands in contrast to the stimulatory effects of T in the published body of literature. We attribute our novel finding to our use of a species in which T inhibits rather than stimulates growth. Our findings begin to explain how T has the regulatory bipotentiality to be stimulatory in some species and inhibitory in others, requiring only an evolutionary reversal in the molecular regulation of growth-regulatory genes including IGF-1. Further comparative transcriptomic studies will be required to fully resolve the molecular mechanism of growth inhibition. 
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