This week I took a trip up the Marine Institute (MI) in Newport, Mayo with my PhD supervisor for a day packed full of meeting and discussions about the project and plans for the next few weeks, months and years. It was a great trip don’t get me wrong, but my mind is going a mile a minute and my ‘noodle is well and truly fried’ (Reed 2017) because of the meetings. However, I do now know which direction I should be pushing my work in, and I have even more to think about in regards to the whole anadromy vs residency question regarding the trout.
Right, so what did we actually talk about up in ‘sunny’ Mayo?
Well first,I met the members of the MI that I hadn’t met yet, like the research assistants who are vital to the salmonid projects, the lecturers, PhD students and researchers based up in Newport who are working on similar research involving trout or salmon. The first meeting was between my supervisors and the staff of the MI, the aim of this meeting was to try to sculpt and structure the PhD and assess its overall aims.
The first meeting lead into a second in which I was brought up to speed on the background of the area, the population statistic before and after the fish farm induced collapse in 1989.
Back in 1975 there was a sea-trout run in the Burshoole river system was around 3,400 fish. However from 1989 to around the 2000’s approximately 160 fish were counted with a low points of sea-trout run of <100 individuals during this time. Additionally a 50% sea mortality was documented, which has repetitively been attributed to salmon farms. As they increase parasite loads, particularly with sea lice, which increases morbidity within the population which, in turn results in increased mortality. (see below for image of sea lice infection)
After I was brought up to speed, there was a third meeting, for which many more researchers, PhDs and staff members joined us. The main point was to discuss the logistics and timing of the common garden and reciprocal transplant experiments that I have mentioned in an earlier blog.
Just to recap, the plan is to conduct a reciprocal transplant experiment to gain greater insight and understanding of the roles that genes and environment play when shaping facultative anadromy in good old brown trout. Through this experiment we plan to assess whether phenotypic differences among trout populations with alternate life history traits reflect genetic divergence. The experiment will involve crossing two populations of brown trout, one which shows naturally high rates of anadromy (Erriff river population) and the other which shows naturally low rates(Rough river population). The offspring, of pure and hybrids will be categorized into 6 groups:
- Erriff female x Erriff male (pure)
- Erriff female x Rough Below Falls male (hybrid)
- Erriff female x Rough Above Falls male (hybrid)
- Rough Below Falls female x Erriff male (hybrid)
- Rough Below Falls female x Rough Below Falls male (pure)
- Rough Below Falls female x Rough Above Falls male (pure)
The offspring will be reared under completely wild conditions in both ‘home’ and ‘away’ river environments, each equipped with downstream traps to catch migrants.
Okay, so what’s new? Whats changed?
Well Originally the plan was to have ~20,000 eggs from the 6 groups (~3,300 per group) which would be split; 10,000 deposited into the Rough and 10,000 in the Glendavock tributary of the Erriff. But, as often is the case in academia, there were a few problems during stripping (process of obtaining eggs and sperm of fish) as many of the fish returning from sea were finnock and not fully mature sea-trout. This coupled with higher mortality than we anticipated after mixing of the eggs and sperm, substantially reduced the counts of our eggs. Current estimate stand between 15,000 and 12,000 eggs. I know this sounds like lots of eggs, but when you factor the 2 rivers which divides the figure by two and then the additional divide between the 6 groups per river. We start to see that these number are not huge, and this is before factoring in an estimated 1% survival rate. So after weeks of debate and back and forth between my supervisors and experts in the field, a new plan was developed, which allowed us to keep the reciprocal transplant, with a back up of a common garden experiment. Now the plan is to deposit 10,ooo-12,000 unfed fry into the Rough, and 2,000 into the Glendavock. However, there is still degrees of dissonance about the correct course of action that we should take, so again this is still subject to change and I will update the blogs as decisions are made.
As the third meeting progressed we started to focus on interesting points for potential chapters for my PhD and further discussed the phenotype candidates and physiological markers for migration/anadromy including:
- Growth rate*
- Standard metabolic rate*
- Maximum metabolic rate*
- Aerobic scopes
- Adipose measures
- Fatty acid status/compositions
- Otholith growth and analysis
- Isotope comp
- Feeding behaviour
- Quantitative trait locus (QTLs) i.e MEP-2
So this got me thinking about the genes that are involved in regulating these physiological markers, and whether there is clear differential expression of these genes between anadromous and resident trout.
Many studies have looked into the role of differential gene expression resulting in plasticity in phenotype and even evolution of alternate life history tactics within sympatric populations. So the next step, would be to look into the different gene expression levels between sea-trout (anadromous brown trout) and residents. However, all of this got us thinking, wouldn’t it be cool to try to see when these changes happen? When are these genes being up or down regulated? is this something that is predetermined when growing in the egg? is it something that is switched on when a certain threshold is met? is there possibly a non-genetic component due to differential methylation patterns passed on through epigenetic inheritance? All these points came up and were discussed during the meeting which was brilliant, however, it still left me thinking what should I do next?
Prior to going up to Mayo, ‘team trout UCC’ had a day in the lab. We sacrificed 20 fish which have shared origin to the fish in my experiment. Certain organs were harvested and stored in RNAlater, with the aim of looking at the gene expression of Na-K ATPase in the gills and other organs. We did this in order check for signs of smoltification in the fish housed at UCC for another PhD project which aims to gain insight into the extent of phenotypic plasticity in ALH tactics with respect to food and temperature and to see if there is there an interactive effect of food and temperature on life histories. As these fish are early life stage, we could repeat this over time to try to get an idea of the changes that occur between the ALH tactics and also to see if the levels of gene expression is different between not only anadromous and resident fish in general but also between the anadromous and resident fish from different populations (Erriff and Rough).