Early male maturation is one of the major problems in farming of Atlantic salmon (Salmo salar), as premature puberty in males is associated with increased disease susceptibility and osmoregulatory problems, leading to higher mortalities, production losses and reduced animal welfare. Previous studies have identified a major effect locus for age at maturation in the vgll3 gene on chromosome 25, with alleles responsible for early and late maturation. However, it is not clear how vgll3a controls the onset of puberty in salmon. We therefore decided to generate a vgll3a loss-of-function mutant using CRISPR/Cas9 to study the role of vgll3 in onset of male maturation in salmon in vivo.
We have followed the F1 generation of vgll3 mutants until the fish were 2 years old. Males were subjected to two different environmental conditions known to stimulate the onset of puberty in salmon: i) 16 degrees, constant light, freshwater, for 6 weeks about one year post hatching, or ii) 13 degrees and constant light in freshwater from start feeding until 2 years post hatching. Individual growth was recorded every second month after start feeding and the maturation status was determined by ultrasound, steroid hormone concentrations and dissection.
Our results showed that wild type and heterozygous males matured as expected (61-100% maturation), while the knockout males showed significantly lower maturation rates (below 30%).
Atlantic salmon males lacking vgll3a show a delayed entry into maturation. Further studies will reveal if the use of fish lacking vgll3a could be a potential solution to reducing the problem with early male maturation in Atlantic salmon farming.