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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Conservation catastrophes

22 02 2012

David Reed

The title of this post serves two functions: (1) to introduce the concept of ecological catastrophes in population viability modelling, and (2) to acknowledge the passing of the bloke who came up with a clever way of dealing with that uncertainty.

I’ll start with latter first. It came to my attention late last year that a fellow conservation biologist colleague, Dr. David Reed, died unexpectedly from congestive heart failure. I did not really mourn his passing, for I had never met him in person (I believe it is disingenuous, discourteous, and slightly egocentric to mourn someone who you do not really know personally – but that’s just my opinion), but I did think at the time that the conservation community had lost another clever progenitor of good conservation science. As many CB readers already know, we lost a great conservation thinker and doer last year, Professor Navjot Sodhi (and that, I did take personally). Coincidentally, both Navjot and David died at about the same age (49 and 48, respectively). I hope that the being in one’s late 40s isn’t particularly presaged for people in my line of business!

My friend, colleague and lab co-director, Professor Barry Brook, did, however, work a little with David, and together they published some pretty cool stuff (see References below). David was particularly good at looking for cross-taxa generalities in conservation phenomena, such as minimum viable population sizes, effects of inbreeding depression, applications of population viability analysis and extinction risk. But more on some of that below. Read the rest of this entry »





Classics: Effective population size ratio

27 04 2011

Here’s another concise Conservation Classic highlighted in our upcoming book chapter (see previous entries on this book). Today’s entry comes from a colleague of mine, Dick Frankham, who has literally written the book on conservation genetics. I’ve published with Dick a few times – absolutely lovely chap who really knows his field more than almost any other. It is a great pleasure to include one of his seminal works as a Conservation Classic.

This entry is highly related to our work on minimum viable population size, and the controversial SAFE index (more on that later).

Although it had long been recognized that inbreeding and loss of genetic diversity were accentuated in small, isolated populations (Charlesworth & Charlesworth, 1987), genetic hazards were generally considered to be of less consequence to extinction risk than demographic and environmental stochasticity. Frankham (1995) helped overturn this viewpoint, using a meta-analysis to draw together comprehensive evidence on the ratio of genetically effective to actual population size (Ne:N). Read the rest of this entry »





Inbreeding does matter

29 03 2010

I’ve been busy with Bill Laurance visiting the University of Adelaide over the last few days, and will be so over the next few as well (and Bill has promised us a guest post shortly), but I wanted to get a post in before the week got away on me.

I’ve come across what is probably the most succinct description of why inbreeding depression is an important aspect of extinctions in free-ranging species (see also previous posts here and here) by Mr. Conservation Genetics himself, Professor Richard Frankham.

Way back in the 1980s (oh, so long ago), Russ Lande produced a landmark paper in Science arguing that population demography was a far more important driver of extinctions than reduced genetic diversity per se. He stated:

“…demography may usually be of more immediate importance than population genetics in determining the minimum viable size of wild populations”

We now know, however, that genetics in fact DO matter, and no one could put it better than Dick Frankham in his latest commentary in Heredity.

I paraphrase some of his main points below:

  • Controversy broke out in the 1970 s when it was suggested that inbreeding was deleterious for captive wildlife, but Ralls and Ballou (1983) reported that 41/44 mammal populations had higher juvenile mortality among inbred than outbred individuals.
  • Crnokrak and Roff (1999) established that inbreeding depression occurred in 90 % of the datasets they examined, and was similarly deleterious across major plant and animal taxa.
  • They estimated that inbreeding depression in the wild has approximately seven times greater impact than in captivity.
  • It is unrealistic to omit inbreeding depression from population viability analysis models.
  • Lande’s contention was rejected when Spielman et al. (2004) found that genetic diversity in 170 threatened taxa was lower than in related non-threatened taxa

Lande might have been incorrect, but his contention spawned the entire modern discipline of conservation genetics. Dick sums up all this so much more eloquently than I’ve done here, so I encourage you to read his article.

CJA Bradshaw

ResearchBlogging.orgFrankham, R. (2009). Inbreeding in the wild really does matter Heredity, 104 (2), 124-124 DOI: 10.1038/hdy.2009.155

Lande, R. (1988). Genetics and demography in biological conservation Science, 241 (4872), 1455-1460 DOI: 10.1126/science.3420403

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