Short communication
Non-additive genetic effects contribute to larval spinal deformity in two populations
of Chinook salmon (Oncorhynchus tshawytscha)
Melissa L. Evans, Bryan D. Neff
⁎
Department of Biology, University of Western Ontario, 1151 Richmond St. N, London, Ontario, Canada N6A 5B7
abstractarticle info
Article history:
Received 7 April 2009
Received in revised form 25 June 2009
Accepted 15 August 2009
Keywords:
Spinal deformity
Oncorhynchus tshawytscha
Quantitative genetics
Relatedness
Offspring sex
LSK
Losses due to larval spinal deformities are widespread in hatchery production. However, the aetiology of this
disease remains unclear in most fishes, despite overwhelming evidence for a genetic role in other vertebrate
taxa. We examined the contribution of additive and non-additive genetic effects and maternal effects to the
incidence of spinal deformity in 50,800 larval Chinook salmon (Oncorhynchus tshawytscha) derived from a
full factorial quantitative genetic breeding experiment conducted on two populations from British Columbia,
Canada. The overall incidence of spinal deformity was low at only 0.69% and 0.05% of offspring in the Big
Qualicum and Quinsam populations, respectively. However, spinal deformities affected 34% and 13% of
families within the two respective populations, and up to 21% of offspring were affected within susceptible
families. Non-additive genetic effects, but not additive or maternal effects, were significantly associated with
spinal deformity in larvae. In the Big Qualicum population, non-additive genetic effects explained 100% of the
total phenotypic variance in spinal deformity, whereas 80% of the phenotypic variance was explained by
non-additive genetic effects in the Quinsam population. Relatedness between parents and offspring sex was
not associated with spinal deformity. These results contrast to other studies of salmonids that have shown
the effects of additive genetic variance on spinal deformity in later life-history stages and relatedness
between parents on larval spinal deformity. Our results instead indicate that the interaction between
parental genomes outside of inbreeding plays an important role in the occurrence of spinal deformity in
Chinook salmon larvae.
© 2009 Elsevier B.V. All rights reserved.
1. Introduction
Deformity of the spine is a commonly observed disease across
vertebrate taxa. In fishes, spinal deformities can take the form of lordosis
(swayback), scoliosis (curvature from side to side), and kyphosis
(hunchback). These deformities are generally referred to as LSK. The
occurrence of spinal deformity in fishes has been reported for many
species including the economically important Atlantic salmon (Salmo
salar), rainbow trout (Oncorhynchus mykiss), gilthead sea bream (Sparus
aurata)andseabass(Dicentrarchus labrax; McKay and Gjerde, 1986;
Andrades et al., 1996; Divanach et al., 1997). These species are
commonly reared in an aquaculture setting and the occurrence of
spinal deformity has been cause for significant economic and animal
welfare concern (Sullivan et al., 2007a). Spinal deformity may lower
levels of production due to decreased survival (Andrades et al., 1996)
and deformed individuals are often unacceptable to consumers (Gjerde
et al., 2005). Moreover, spinal deformities are relatively widespread in
aquaculture and hatchery settings relative to what has been observed in
the wild, so there is significant interest in addressing the potential
causes of these deformities (Boglione et al., 2001). Nevertheless, the
aetiology of spinal deformity remains poorly understood.
It has been suggested that spinal deformities result from both
environmental and genetic factors (Valentine, 1975). However, studies
examining the development of spinal deformities in fish species have
largely focused on assessing the role of only the environmental factors.
For example, a study on goldfish (Carrassius auratus)hasshownthat
water temperature is associated with spinal abnormalities (Wiegand
et al., 1989). Kyphosis of the spine is associated with infection by a
Myxozoan parasite in Japanese mackerel (Scomber japonicus; Yokoyama
et al., 2005). Insufficient dietary components (see Cahu et al., 2003 for
review) or exposure to pollutants such as organophosphates or
organochlorines (Mount and Stephen, 1967; Couch et al., 1977)has
alsobeen implicated in the development of spinal abnormalities, as have
high water current settings during development in hatcheries (Chatain,
1994; Divanach et al., 1997).
Relatively few studies in nonmodel fishes have examined the
potential role of genetics in spinal deformities despite overwhelming
evidence for a genetic basis in humans and in model systems (Pourquié
and Kusumi, 2001; Gorman and Breden, 2007; Heary and Madhaven,
2008). Research in humans has suggested that spinal deformities are
X-chromosome linked, as females exhibit a two-fold higher incidence of
the disease than do males (Justice et al., 2003). Yet, other research
Aquaculture 296 (2009) 169–173
⁎ Corresponding author. Tel.: +1 519 850 2532; fax: +1 519 661 3935.
E-mail address: bneff@uwo.ca (B.D. Neff).
0044-8486/$ – see front matter © 2009 Elsevier B.V. All rights reserved.
doi:10.1016/j.aquaculture.2009.08.018
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