IPN gene and resistance mechanism identified19 June, 2014 –
THROUGH a collaborative project with national and international research institutions, AquaGen has identified the exact positions of the gene that codes for IPN resistance in salmon.
The identification of the gene responsible for IPN resistance in salmon enables a great accuracy in the selection of broodstock, ensuring the offspring to be resistant to IPN.
This gene is found to have two mutations that prevent the IPN virus from infecting salmon cells.
On 10-12 June 2014 the second international conference on integrated salmon biology was held in Vancouver, Canada.
This conference marked the completion of the salmon genome project. This work started in 2010 as a collaborative project between academia, industry and government funding agencies in Chile, Canada and Norway.
It is expected that the reference genome for salmon will provide important information of great benefit to the salmon farming in the future.
One example of the use of genetic information that has already brought significant improvements for farmed fish are genetic markers for resistance to infectious pancreatic necrosis (IPN) in salmon.
At the conference, senior scientist Thomas Moen from AquaGen presented the work done to discover the actual gene and reveal the mechanism behind IPN resistance in salmon.
IPN is a very common viral disease, and is one that has been responsible for significant losses in salmon farming.
The disease has proven to be very difficult to control by vaccination or other preventive or loss-reduction measures adopted over the years.
By the late 90s it had been documented that there was a significant genetic variation in salmon susceptibility to IPN.
In 2005 AquaGen started a project, in collaboration with Nofima and CIGENE by NMBU, to attempt to identify the gene regions of the salmon that are linked to IPN resistance.
In 2007, it became clear that the trait is mostly controlled by a single area on the genome and a test was developed that used gene markers to identify IPN resistant and IPN susceptible fish.
These markers were put to use in the production of eggs that were delivered to salmon farmers from 2009 onwards.
It quickly became clear that these fish were very resistant to IPN and disease problems disappeared on the sites that used these IPN-QTL eggs.
More and more farmers then began using resistant eggs, which eventually affected the Norwegian statistics for IPN.
After remaining stable at around 200 outbreaks annually for decades, it was as low as 50 outbreaks in 2013.
In parallel with these developments, substantial research work was carried out to uncover the actual mechanism behind IPN resistance in salmon.
An important component of this work consisted of the creation of a continuous DNA sequence that covered the area where it was assumed that the IPN gene was located.
This has been a challenging task, since salmon have been shown to have a very complex genome. Despite this the task was achieved, aided by the international sequencing project to create a continuous sequence covering large parts of chromosome 26, where the IPN gene is located.
Early results of the project were novel DNA markers, which made AquaGen able to select for increased IPN resistance with even greater accuracy.
The mechanism behind IPN resistance shows that salmon do not have a single, but two mutations that are both able to make salmon resistant to IPN.
These two mutations are located in the same gene, and there is now evidence that this gene is actually a necessary component of the mechanism the virus uses to get into salmon cells.
In other words, it is the two mutations that prevent the virus from infecting fish.
This knowledge may also have implications for further research on viral infections in humans, mammals and fish, as we have identified an entirely new mechanism for uptake of virus into the host cell.
The discovery of the IPN gene has been possible due to the good cooperation between AquaGen and Norwegian and international research institutions, in particular CIGENE, Nofima and Simon Fraser University of Canada.
Financial support from the Norwegian Research Council has also been crucial in achieving the goals of this project.