January 12-16, 2008
Town & Country Convention Center
San Diego, CA
Summer mortality, described for decades in the Pacific oyster Crassostrea gigas, is responsible for important economic loss in this major aquaculture species. A complex combination of environmental and biological parameters has been suggested as the cause of this phenomenon (Samain et al., 2007). One way to overcome this problem would be to select oysters more tolerant to summer mortality, as this trait was shown to be highly heritable (Degrémont et al., 2007). Resistant and susceptible lines were selected for, allowing the identification of genes differentially expressed between them (Huvet et al, 2004) and the identification of QTLs, using the available SSR-based linkage mapped (Hubert and Hedgecock, 2004) and a recently developed SNPs (Sauvage et al., 2007). These markers were notably characterized in several genes involved in the immune response and energetic pathways, testing for the colocalization of QTLs and some of these genes.
Linkage maps were built for three F2 segregating oyster families showing a strong differential response during a summer mortality event in 2006. In addition to survival, the viral load in Ostreid Herpes Virus (OsHV1) was individually quantified by Q-PCR (Pépin et al., submitted) and these two traits have been analysed
Our first results show that two QTLs were detected for the viral load in one of the three families. Further analyses are in currently progress. We will present and discuss our most recent results, contributing to a better understanding of the genetic architecture of resistance to summer mortality in the Pacific oyster.