QTL for Stress and Disease Resistance in European Sea Bass, Dicentrarhus labrax L.

Abstract

There is a growing interest in selective breeding in European sea bass (Dicentrarchus labrax), especially regarding family selection based on growth performance. In particular, quantitative trait loci (QTL) identification in sea bass enhances the application of marker-assisted breeding for the genetic improvement of the production traits. The aims of the study were to identify potential QTL affecting stress and immunological indicators, body weight, and mortality after vibriosis injection in sea bass as well as to estimate heritability and genetic/phenotypic correlations for the aforementioned traits. To this end, stress test was performed on 960 offspring and a sub-group of them (420) was selected to explore the mortality after vibrio injection. Selective genotyping was performed in 620 offspring for 35 microsatellite markers and distributed into 6 linkage groups. The length of the genetic linkage map was 283.6 cM and the mean distance between the markers was 8.1 cM. QTL affecting body weight in three different growth periods detected on linkage groups LG1, LG4, LG6, and LG14. A QTL associated with weight in early growth stages (290–306 days post-hatching) was also identified on LG3. QTL analysis confirmed the existence of QTL affecting cortisol levels, on LG3 and LG14. Moreover, new QTL affecting only cortisol and glucose levels were detected on LG1 and LG23. No QTL affecting hormonal or biochemical marks was found on LG4 and LG6. Heritability of cortisol, lysozyme levels, and mortality were high (0.36, 0.55, and 0.38, respectively).

Genomic Selection and Genome-Wide Association Analysis for Stress Response, Disease Resistance and Body Weight in European Seabass

“…In the European seabass, using molecular tools, such as microsatellite markers, Massault et al [22] identified three suggestive Quantitative Trait Locus (QTL) for stress response of cortisol levels. Additionally, Chatziplis et al [17] confirmed the above QTL in other populations and further reported one more on LG23. In the previous study, apart from QTL affecting cortisol levels, QTL affecting glucose levels have also been reported.…”

“…Further research for post-stress cortisol levels showed that individuals of this species could be clustered into two distinctive categories showing low and high cortisol response to stress (LR and HR, respectively) [14,15]. Pinpointing on genetic parameters, studies reported a moderate heritability of cortisol levels such as 0.34 ± 0.09 to 0.37 ± 0.08 [16,17], however, earlier, Volckaert et al [18] have reported a low heritability estimate (0.08). Moreover, a consistently negative genetic correlation was reported between cortisol levels and body weight, ranging from −0.43 to −0.60 [16][17][18].…”

“…Pinpointing on genetic parameters, studies reported a moderate heritability of cortisol levels such as 0.34 ± 0.09 to 0.37 ± 0.08 [16,17], however, earlier, Volckaert et al [18] have reported a low heritability estimate (0.08). Moreover, a consistently negative genetic correlation was reported between cortisol levels and body weight, ranging from −0.43 to −0.60 [16][17][18]. Following the interpretation of these genetic correlations, it is evident that fish that are more easily affected by stress (HR) will have impaired growth.…”

“…Following the interpretation of these genetic correlations, it is evident that fish that are more easily affected by stress (HR) will have impaired growth. Furthermore, bodyweight has a range of heritability estimates from 0.38 to 0.63 [16][17][18][19][20][21]. More recently, the first approach of heritability estimation of glucose levels and lysozyme blood levels reported heritability estimates of 0.23 to 0.33 for glucose (depending on the model) and 0.56 for lysozyme levels [17].…”

“…In the previous study, apart from QTL affecting cortisol levels, QTL affecting glucose levels have also been reported. Many studies were also performed to identify QTL for traits of commercial interest such as body weight and disease resistance [17,[22][23][24][25].…”