Translocations: the genetic rescue paradox

14 01 2013

helphindranceHarvesting and habitat alteration reduce many populations to just a few individuals, and then often extinction. A widely recommended conservation action is to supplement those populations with new individuals translocated from other regions. However, crossing local and foreign genes can worsen the prospects of recovery.

We are all hybrids or combinations of other people, experiences and things. Let’s think of teams (e.g., engineers, athletes, mushroom collectors). In team work, isolation from other team members might limit the appearance of innovative ideas, but the arrival of new (conflictive) individuals might in fact destroy group dynamics altogether. Chromosomes work much like this – too little or too much genetic variability among parents can break down the fitness of their descendants. These pernicious effects are known as ‘inbreeding depression‘ when they result from reproduction among related individuals, and ‘outbreeding depression‘ when parents are too genetically distant.

CB_OutbreedingDepression Photo
Location of the two USA sites providing spawners of largemouth bass for the experiments by Goldberg et al. (3): the Kaskaskia River (Mississipi Basin, Illinois) and the Big Cedar Lake (Great Lakes Basin, Wisconsin). Next to the map is shown an array of three of the 72-litre aquaria in an indoor environment under constant ambient temperature (25 ◦C), humidity (60%), and photoperiod (alternate 12 hours of light and darkness). Photo courtesy of T. Goldberg.

Recent studies have revised outbreeding depression in a variety of plants, invertebrates and vertebrates (1, 2). An example is Tony Goldberg’s experiments on largemouth bass (Micropterus salmoides), a freshwater fish native to North America. Since the 1990s, the USA populations have been hit by disease from a Ranavirus. Goldberg et al. (3) sampled healthy individuals from two freshwater bodies: the Mississipi River and the Great Lakes, and created two genetic lineages by having both populations isolated and reproducing in experimental ponds. Then, they inoculated the Ranavirus in a group of parents from each freshwater basin (generation P), and in the first (G1) and second (G2) generations of hybrids crossed from both basins. After 3 weeks in experimental aquaria, the proportion of survivors declined to nearly 30% in G2, and exceeded 80% in G1 and P. Clearly, crossing of different genetic lineages increased the susceptibility of this species to a pathogen, and the impact was most deleterious in G2. This investigation indicates that translocation of foreign individuals into a self-reproducing population can not only import diseases, but also weaken its descendants’ resistance to future epidemics.

A mechanism causing outbreeding depression occurs when hybridisation alters a gene that is only functional in combination with other genes. Immune systems are often regulated by these complexes of co-adapted genes (‘supergenes’) and their disruption is a potential candidate for the outbreeding depression reported by Goldberg et al. (3). Along with accentuating susceptibility to disease, outbreeding depression in animals and plants can cause a variety of deleterious effects such as dwarfism, low fertility, or shortened life span. Dick Frankham (one of our collaborators) has quantified that the probability of outbreeding depression increases when mixing takes place between (i) different species, (ii) conspecifics adapted to different habitats, (iii) conspecifics with fixed chromosomal differences, and (iv) populations free of genetic flow with other populations for more than 500 years (2).

A striking example supporting (some of) those criteria is the pink salmon (Oncorhynchus gorbuscha) from Auke Creek near Juneau (Alaska). The adults migrate from the Pacific to their native river where they spawn two years after birth, with the particularity that there are two strict broodlines that spawn in either even or odd year – that is, the same species in the same river, but with a lack of genetic flow between populations. In vitro mixture of the two broodlines and later release of hybrids in the wild have shown that the second generation of hybrids had nearly 50% higher mortality rates (i.e., failure to return to spawn following release) when born from crossings of parents from different broodlines than when broodlines were not mixed (4).

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Blog Action Day 2010 – Water neutrality and its biodiversity benefits

16 10 2010

In my little bid to participate in Change.org’s Blog Action Day 2010 – Water, I’ve re-hashed a post from 2008 on ‘water neutrality’. This will also benefit my recently joined readers, and re-invigorate a concept I don’t think has received nearly enough attention globally (or even in parched Australia where I live). So here we go:

The world’s freshwater ecosystems are in trouble. We’ve extracted, poisoned, polluted, damned and diverted a large proportion of the finite (and rather small!) amount of freshwater on the planet. Now, most people might immediately see the problem here from a selfish perspective – no clean, abundant water source = human disease, suffering and death. Definitely something to avoid, and a problem that all Australians are facing (i.e., it’s not just restricted to developing nations). Just look at the Murray-Darling problem.

In addition to affecting our own personal well-being, freshwater ecosystems are thought to support over 10000 fish species worldwide (see also a recent post on Africa’s freshwater biodiversity’s susceptibility to climate change), and the majority of amphibians and aquatic reptiles. Current estimates suggest that about 1/3 of all vertebrate biodiversity (in this case, number of species) is confined to freshwater. As an example, the Mekong River system alone is thought to support up to 1700 different species of fish.

So, what are some of the ways forward? The concept of ‘water neutrality’ is essentially the wet version of carbon neutrality. It basically means that water usage can be offset by interventions to improve freshwater habitats and supply. Read the rest of this entry »





Salamander Longshanks – breed them out

3 02 2010

© M. Dawson

Patrick McGoohan in his role as the less-than-sentimental King Edward ‘Longshanks’ in the 1995 production of ‘Braveheart’ said it best in his references to the invocation of ius primæ noctis:

If we can’t get them out, we’ll breed them out

What a charmer.

Dabbling in molecular ecology myself over the past few years with some gel-jockey types (e.g., Dick Frankham [author of Introduction to Conservation Genetics], Melanie Lancaster, Paul Sunnucks, Yuji Isagi inter alios), I’m quite fascinated by the application of good molecular techniques in conservation biology. So when I came across the paper by Fitzpatrick and colleagues entitled Rapid spread of invasive genes into a threatened native species in PNAS, I was quite pleased.

When people usually think about invasive species, they tend to think ‘predator eating naïve native prey’ or ‘weed outcompeting native plant’. These are all big problems (e.g., think feral cats in Australia or knapweed in the USA), but what people probably don’t think about is the insidious concept of ‘genomic extinction’. This is essentially a congener invasive species breeding with a native one, thus ‘diluting’ the native’s genome until it no longer resembles its former self. A veritable case of ‘breeding them out’.

Who cares if at least some of the original genome remains? Some would argue that ‘biodiversity’ should be measured in terms of genetic diversity, not just species richness (I tend to agree), so any loss of genes is a loss of biodiversity. Perhaps more practically, hybridisation can lead to reduced fitness, like we observed in hybridised fur seals on Macquarie Island.

Fitzpatrick and colleagues measured the introgression of alleles from the deliberately introduced barred tiger salamander (Ambystoma tigrinum mavortium) into threatened California tiger salamanders (A. californiense) out from the initial introduction site. While most invasive alleles neatly stopped appearing in sampled salamanders not far from the introduction site, three invasive alleles persisted up to 100 km from the introduction site. Not only was the distance remarkable for such a small, non-dispersing beastie, the rate of introgression was much faster than would be expected by chance (60 years), suggesting selection rather than passive genetic drift. Almost none of the native alleles persisted in the face of the three super-aggressive invasive alleles.

The authors claim that the effects on native salamander fitness are complex and it would probably be premature to claim that the introgression is contributing to their threatened status, but they do raise an important management conundrum. If species identification rests on the characterisation of a specific genome, then none of the native salamanders would qualify for protection under the USA’s Endangered Species Act. They believe then that so-called ‘genetic purity’ is an impractical conservation goal, but it can be used to shield remaining ‘mostly native’ populations from further introgression.

Nice study.

CJA Bradshaw

ResearchBlogging.orgFitzpatrick, B., Johnson, J., Kump, D., Smith, J., Voss, S., & Shaffer, H. (2010). Rapid spread of invasive genes into a threatened native species Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0911802107

Lancaster, M., Bradshaw, C.J.A., Goldsworthy, S.D., & Sunnucks, P. (2007). Lower reproductive success in hybrid fur seal males indicates fitness costs to hybridization Molecular Ecology, 16 (15), 3187-3197 DOI: 10.1111/j.1365-294X.2007.03339.x

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