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Posts Tagged conservation

New Zealand forests still threatened, but not THAT threatened Hilary Miller Feb 08

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Last week Conservation International published its list of the world’s ten most threatened forest hotspots, where biodiversity and endemism is high and less than 10% of the original habitat is remaining.  New Zealand was, somewhat shockingly, number 2 on their list.  I must admit I thought this was a little odd – especially as their list claims we have only 5% of our forest (which is listed as tropical and subtropical broadleaf forest) remaining – and well, it turns out the folks at Conservation International were a little confused.

Apparently New Zealand was confused with New Caledonia, and is actually ranked number 22 on the list, with 22% of its original forest cover remaining.  Easy mistake to make, I guess (although the folks over at Kiwiblog of course think its all a big conspiracy of the part of the Greens).

So its not quite as alarming as we thought, but this is no reason to be complacent about the state of our forests.  A timely bit of research published online in the journal Science last week shows how even small changes in the makeup of our forests, like extinction of one or two key species, can have a cascading effect on biodiversity.  I’m not sure that it matters whether we are number 2 or 22 on Conservation International’s list, when we still have one of the worst records of biodiversity loss in the world.

Cheetah genetic diversity revisited Hilary Miller Feb 04

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ResearchBlogging.org

Another chapter has been added to the story of genetic variation in the cheetah, with a paper out in next month’s Molecular Biology and Evolution journal giving a detailed description of variation at key immune genes in the species.  I first became familiar with the cheetah story as a PhD student when I was studying genetic diversity in the black robin.  At the time the cheetah was something of a poster child for the perils of low genetic variation, but this most recent paper suggests that their immune system is not as genetically invariant as first thought, and they may not be so vulnerable to disease after all.

Back in 1985, Stephen O’Brien and colleagues at the National Cancer Institute in Maryland reported extremely low levels of genetic variation in cheetahs - so low in fact, that skin grafts from one animal were not rejected by another, a sign that their immune systems are genetically identical.  This lack of genetic variation was attributed to a decline in population numbers at end of last ice age, plus more recent declines that have led to inbreeding.  The species appeared to be highly susceptible to feline infectious peritonitis (FIP), a disease which had decimated some captive populations, and attempts to breed cheetahs in captivity were hampered by poor reproductive success and apparently high levels of sperm defects.  O’Brien and colleagues attributed these problems to their extremely low levels of genetic variation, and the species quickly became a classic example of the perils of inbreeding. 

The cheetah (Acinonyx jubatus) is found mainly in southern and eastern Africa

However, in the early 1990′s, field studies questioned whether the cheetah’s survival in the wild was being compromised by their lack of genetic variation.  In a commentary in Science in 1994, Caro and Laurenson pointed out that disease susceptibility and breeding problems only appeared to be an issue for captive cheetahs, and that predation of cubs, habitat destruction and persecution by humans were greater threats to the species.

Still, a lack of variation at immune genes is still an important potential threat to any species, as shown by the case of the Tasmanian devil, where low variation at Major Histocompatibility Complex, or MHC genes, has allowed Devil Facial Tumour Disease to spread unchecked throughout the population.  MHC genes are key part of the immune system in vertebrates as they code for the molecules that distinguish self from non-self, and instruct the immune system to respond when foreign proteins (i.e. from a pathogen) are detected.  High diversity at MHC genes plays an important role in protecting populations from disease epidemics as it allows wide array of foreign pathogens to be resisted, and means that some individuals are likely to be more resistant to new diseases than others (instead of all individuals being equally susceptible).  

The skin graft experiments of the mid-1980s indicated that cheetahs have virtually no MHC variation, because of the absence of an immune response when skin from one cheetah was grafted onto another.  However the disease susceptibility seen in captive cheetahs doesn’t seem to extend to cheetahs in the wild – a recent study on wild cheetahs in Namibia  found that the population was generally in good health, and that many individuals carried antibodies to a range of diseases (suggesting they had been exposed to those diseases) but no clinical symptoms of acute disease.  These results suggest that wild cheetahs may have more MHC diversity than the captive population, and that their immune systems work just fine. 

Somewhat surprisingly, only a couple of studies in the 26 years since the skin-graft study was published have actually attempted to quantify cheetah MHC diversity.  These studies found low diversity and seemed to corroborate the skin-graft results, but either used low resolution methods to measure MHC diversity or had small sample sizes, so weren’t particularly conclusive.

This latest study, by Aines Castro-Prieto, Simone Sommer and colleagues at the Leibniz Institute for Zoo and Wildlife Research in Berlin, takes a much more comprehensive approach to measuring genetic variation.  Castro-Prieto and colleagues determined how many different alleles are present at two types of MHC genes in 149 Namibian cheetahs.  They found more variation than was previously described for the first type (Class I MHC), but not for the second type of gene (Class II MHC).  The number of different MHC alleles counted in the Namibian cheetahs is still quite low compared with what is seen in other big cat populations, so it appears that cheetahs have lost a fair amount of variation as their numbers have declined.  However, the amount of DNA sequence variation among the alleles is fairly high - that is the different alleles code for proteins that are quite different from one another in their sequence, so overall they can probably recognise a wide array of foreign proteins. 

Castro-Prieto and colleagues also found hallmarks of selection on the MHC sequences, and speculate that selection, driven by exposure to a range of pathogens over thousands of generations, has led to highly divergent alleles being retained.  However, they point out that although wild cheetahs appear to have enough MHC variation to respond to common infectious diseases, they may still be at risk from new emerging diseases, as the few remaining alleles might not be sufficient to be able to recognise and ward off an entirely new pathogen.   

This study provides some much-needed data on immune variation in cheetahs, and it seems that the idea of the cheetah being a classic case of disease vulnerability associated with low genetic diversity is looking a little shaky.  As Castro-Prieto et al point out, “the long term survival of free-ranging cheetahs in Namibia seems more likely to depend on human-induced rather than genetic factors”.

Reference: Castro-Prieto A, Wachter B, & Sommer S (2010). Cheetah paradigm revisited: MHC diversity in the world’s largest free-ranging population. Molecular biology and evolution PMID: 21183613

Further reading:

For an excellent write-up on why genetic diversity is important (and more stuff about cheetahs), see this (fairly old) post on Mauka to Makai .

O’Brien SJ, Roelke ME, Marker L, Newman A, Winkler CA, Meltzer D, Colly L, Evermann JF, Bush M, Wildt DE (1985) Genetic basis for species vulnerability in the cheetah. Science 227: 1428-1434

Caro TM, Laurenson MK (1994) Ecological and genetic factors in conservation: a cautionary tale. Science 263: 485-486.

Thalwitzer S, Wachter B, Robert N, Wibbelt G, Muller T, Lonzer J, Meli ML, Bay G, Hofer H, Lutz H (2010) Seroprevalences to Viral Pathogens in Free-Ranging and Captive Cheetahs (Acinonyx jubatus) on Namibian Farmland. Clin. Vaccine Immunol. 17: 232-238.

RIP Richard Henry Hilary Miller Jan 14

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From Codfish Island this morning comes the sad news of the death of Richard Henry, the last remaining Fiordland kakapo.  Richard Henry was captured in Fiordland in 1975, at a time when kakapo were thought to be virtually extinct.  All other kakapo currently living are descended from birds discovered on Stewart Island in 1977.  A 2003 study* showed that kakapo have low genetic variation, with the exception of Richard Henry who was genetically distinct from all the Stewart Island birds.  Richard Henry had thus become an important player in the kakapo recovery program as the recovery team attempted to boost the genetic diversity of the species. 

This DNA fingerprint of kakapo clearly shows how distinct Richard Henry was. His fingerprint is marked with an asterisk – all the others are from Stewart Is. birds

More from Stuff.co.nz:

One of the key players in the Kakapo Recovery Programme was found dead on Codfish Island yesterday, marking the end of an era.

Kakapo Richard Henry was discovered by one of the recovery team members after what was believed to be an 80-year life.

Richard Henry, who was named after a Victorian conservationist who pioneered kakapo recovery, was originally found as an adult in Fiordland in 1975 when his species was believed to be extinct.

Since that time he has contributed to the genetic diversity of kakapo in the recovery programme and is well known for his efforts.

Department of Conservation programme scientist Ron Moorhouse said Richard Henry would be sorely missed by everyone who knew him.

“Richard Henry was a living link to the early days of kakapo recovery and perhaps even to a time before stoats when kakapo could boom unmolested in Fiordland,” he said.

Richard Henry was showing signs of ageing for some time before he was found, including blindness in one eye, slow movement and wrinkles, he said.

Meanwhile, the kakapo breeding season is under way on Codfish and Anchor islands and the first eggs are expected to appear next month.

*Disclaimer: I was part of that study, and the fingerprint gel is one of my more arty pieces of molecular biology, so I thought I’d post it in tribute.

The reference is: Miller HC, Lambert DM, Millar CD, Robertson BC, Minot EO (2003) Minisatellite DNA profiling detects lineages and parentage in the endangered kakapo (Strigops habroptilus) despite low microsatellite DNA variation. Conservation Genetics, 4: 265-274.

 

Presence of observers prevents fur seal attacks Hilary Miller Dec 08

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Further to the recent attacks on fur seals in Kaikoura, comes a timely study just published in Conservation Biology.  Alejandro Acedevo-Gutierrez and Lisa Acedevo of Western Washington University, and Laura Boren, DoC’s national marine mammal coordinator, found that the presence of an official-looking volunteer stationed at a popular seal viewing areas was enough to deter tourists from harassing seals. 

The researchers carried out their study at Ohau stream waterfall, Kaikoura, near the location of the recent attacks that saw 23 animals bludgeoned to death.  Over a period of 9 months they recorded the behaviour of tourists in the presence or absence of a volunteer observer who was wearing a neon vest and made to look “official”.  Tourists were deemed to be harassing the seals when they approached the animals to within a few metres or threw an object at them.  They found that harassment dropped by two-thirds when the observer was present – from 38.4% down to 13% of groups with at least one person who harassed the seals  - even if the observer said nothing to the tourists. 

Viewing of fur seals is regulated by the Marine Mammals Protection Act 1992, but the researchers had previously found that simply having a sign up stating these regulations does nothing to ensure that tourists actually comply.  Having an actual person wearing a neon vest is far more effective at preventing harassment, even if this person is a volunteer with no authority to actually enforce compliance with the regulations. 

The researchers point out that using volunteers in this way is a cheap and effective way of managing tourist-wildlife interactions at popular wildlife viewing areas, and has the added bonus of observers being able to educate tourists about the animals. They found that approximately half the tourist groups approached the observer and asked questions about the behaviour of the seals, and all of them had misconceptions about how to behave around young seals.

Other posts on sciblogs about the fur seal attacks are here and here

Reference:

Acedevo-Gutierrez et al.  Effects of the Presence of Official-Looking Volunteers on Harassment of New Zealand Fur Seals.  Conservation Biology. Article first published online: 3 DEC 2010 | DOI: 10.1111/j.1523-1739.2010.01611.x

   

Tuatara tuesday — how cold is too cold for a tuatara? Hilary Miller Oct 05

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ResearchBlogging.org Tuatara like it cold.  Unusually so, for a reptile.  While reptiles in most other countries are happiest with temperatures over 25 degrees celcius, here in New Zealand our reptiles prefer much lower temperatures.  Alison Cree’s group at the University of Otago has been investigating exactly which temperatures tuatara prefer, with a view to determining whether new populations of tuatara could be established in the southern South Island.

Research just published in Animal Conservation by PhD student Anne Besson examined the effects of cool temperature on juvenile tuatara sourced from Stephens Island, the southern-most natural population.  Sub-fossil remains tell us that tuatara were once present in Otago and Southland, but they have been extinct in this region for possibly hundreds of years.  Temperatures on Stephens Island are on average 3-4 degrees warmer than those at proposed translocation sites in Otago, and it is possible that tuatara originally living in the deep south had special adaptations to enable them to withstand the cold that are absent in animals from more northerly present-day populations.  To test whether Stephens Island tuatara are likely to be able to survive in the deep south, Besson compared tuatara behaviour at low temperatures with that of three lizard species found in the wild in Otago (common geckos, jewelled geckos and McCann’s skinks), hypothesizing that if tuatara have the same responses as these lizard species, then its likely they will be able to survive similar temperatures.

Besson investigated feeding behaviour at 20, 12 and 5 degrees, measuring the time it took an animal to catch, handle and digest prey at the three different temperatures.  She found few differences between tuatara and the lizards.  For all species, feeding performance dropped off significantly at 5 degrees as animals became very sluggish at catching and handling their food, and neither skinks or tuatara could digest food at this temperature.  However, one important difference between tuatara and lizards was seen at 12 degrees.  At this temperature lizards were able to digest food, albiet more slowly than at warmer temperatures, but tuatara were not.  Besson also measured preferred body temperature and critical thermal minimum (i.e. the temperature at which animals can effectively no longer function) across the four species and again found little difference between tuatara and the lizard species.

Besson’s results suggest that Stephens Island tuatara would survive a move south, but their inability to digest food at temperatures of 12 degrees or lower has important implications for choosing translocation sites in Otago, given that ambient temperatures rarely rise above 12 degrees in winter in this region.  As tuatara do not hibernate and still feed throughout the winter, Besson and Cree recommend that proposed translocation sites for tuatara should provide plenty of opportunities for animals to bask in the sun in order to digest their food.

Testing physiological and behavioural responses to investigate whether animals are likely to be survive in new environments is something that is rarely done in conservation studies, but is likely to become increasingly important in the face of climate change.  Tuatara are particularly vulnerable to warming temperatures, as sex determination in tuatara is temperature-dependent and warming temperatures are likely to produce an excess of males.  Establishing new populations further south may be one way of countering future temperature rises.  Besson’s research shows that this is likely to be a viable strategy for conservation management of tuatara, but whether they can produce self-sustaining populations at cooler temperatures still needs to be tested.

Besson, A., & Cree, A. (2010). Integrating physiology into conservation: an approach to help guide translocations of a rare reptile in a warming environment Animal Conservation DOI: 10.1111/j.1469-1795.2010.00386.x

New Zealand Conservation Week Hilary Miller Sep 12

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This week (September 12-19th) is New Zealand Conservation Week. There are a huge number of events planned around the country, including weed swaps, planting days, beach clean ups, and talks.  The chickenoreggblog family will be doing its bit by taking to the Darwin’s Barberry seedlings that are threatening to take over the garden here on our windy Karori hillside.

Details are on the Department of Conservation website, so get out there and participate!

Cloning extinct species #2: Should we bother? Hilary Miller May 10

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Two weeks ago I posted about how, theoretically at least, one could go about bringing an extinct species back to life by cloning.  Its clear that for long-extinct species like the mammoth, where only degraded remains are available, cloning is still a very long way off and in fact may not ever be possible.  But for species that have only recently gone extinct, or are on the verge of extinction, correct preservation of tissues could see clones created (in fact this has already happened in the case of the pyrenean ibex).  But should we bother going down this path?

Some people would say that we have a moral imperative to bring back extinct species, once we have the technology to do so, in situations where humans caused the extinction.  However in many cases the original extinction was caused by hunting, habitat loss and/or the introduction of predators, and these underlying issues are still present.  For instance, mammoth habitat of cold tundra grasslands, which during the ice ages ranged across northern Europe and the Americas, is now restricted to the Arctic, and is increasingly at risk from climate change.  Loss of this habitat at the end of the last ice age is thought to be one of the main reasons mammoths went extinct in the first place, and the situation hasn’t improved.  Should we really be contemplating bringing back populations of extinct species when we have trouble even saving the species we still have, and we are destroying habitat at an ever-increasing rate?  Introductions of long-extinct species could also significantly alter already fragile ecosystems and have disastrous consequences for the organisms already present.

Aside from suitable habitat, for a species to be viable and self-sustaining there needs to be sufficient genetic diversity in the population to guard against the detrimental effects of inbreeding depression, and for the species to be able to adapt to new environmental challenges.  Simply producing several clones from one specimen would not create a viable breeding population – for one thing you would at least need one male and one female.  Clones of several genetically different individuals would be required to ensure the population’s survival.  This may not be too difficult for critically endangered or recently extinct species where several well-preserved tissue specimens are available.  However, for the majority of extinct species the genome would have to be artificially “rebuilt” before cloning could take place, so you would need to have genome sequences of several different individuals in order to produce genetically different clones.  For many extinct species we simply don’t have enough different well-preserved specimens to achieve this.

There is a danger that cloning will be persued for the sake of it, because wouldn’t it be cool to see a live mammoth/tasmanian tiger/huia once again?  However, with this attitude the cloned animal is likely to end up being little more than a curiosity in an amusement park.  There may be some merit in bring back an extinct species for what it could tell us about evolution and physiology, but I don’t think this is enough to justify the enormous cost.  The millions of dollars it would take to bring back a few specimens of an extinct species would be better spent on preserving large chunks of habitat, eradicting introduced predators, and educating the public about for our critically endangered species, to ensure that in future we don’t have to rely on cloning to save the species we still have.

Footnote: The Neanderthal genome was published in Science last week, and along with it is an interesting news focus article about cloning Neanderthals. Its an interesting read (unfortunately its behind a pay-wall, so for those without full-text access to Science, the brief synopsis is that the ethical and technical issues around cloning Neanderthals are so great is unlikely they’ll ever be overcome).

Cloning extinct species #1: A how-to guide Hilary Miller Apr 30

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 Fancy seeing herds of mammoths running across the tundra, moa crashing through the undergrowth, or perhaps a tasmanian tiger lurking in the Aussie bush? Well in the near future these images might not just be the stuff of far-fetched Hollywood movie plots.  Advances in molecular biology and genomics mean that the ability to clone extinct species is getting closer. In theory, at least.  In this post I’m going to look at how one would go about bringing back to life their favourite extinct species, and in a later post I’ll discuss whether we should bother.

The technology required to clone extinct species is largely already here.  In fact, in November 2008 Japanese researchers reported cloning mice that had been frozen 16 years, and last year researchers in Spain reported cloning the bucardo (Pyrenean ibex), a subspecies of the Spanish ibex which went extinct in 2000, from a piece of frozen skin (although the animal died soon after birth).  Whole genome sequencing for extinct species is also becoming a reality – a partial genome sequence for the mammoth was published in Nature in 2008.   

The Woolly Mammoth may have had its genome sequenced, but cloning is still a long way off

While a genome sequence is a good start for resurrecting an extinct species, that alone is not enough.  In order to turn the DNA sequence of the genome into a living organism, the DNA has to be packaged into chromosomes and the information in the DNA expressed in living cells.  Conventional reproductive cloning (like that used to create Dolly the sheep) is performed using Somatic Cell Nuclear Transfer (SCNT), where the genetic material (ie the nucleus of a cell) from one organism is transferred into an egg from which the nucleus has been removed.  Because the nucleus that is transferred comes from a somatic cell, it already has a full diploid genome (ie 2 copies of each chromosome), and with a bit of kick-starting behaves like a freshly fertilized egg, developing into an organism identical to the one from which the nucleus came from.   

So to clone an extinct species using this method, you would need a closely related living species to provide an egg, and an intact nucleus containing a full set of chromosomes in good condition.  This is where things get tricky, as the DNA extracted from remains of extinct organisms is normally extremely degraded.  Even obtaining genome sequences from this material is only possible due to the advent of high throughput “next generation” sequencers, which can sequence billions of short fragments of DNA.  Heavy duty computer power is then required to stitch those sequences back together to decipher the genome sequence – a bit like a giant jigsaw puzzle.  Having a genome sequence for a closely related species for comparison helps enormously with this assembly, as it can be used as a sort of template on which to assemble the genome of the extinct species.   

Once you have the genome there are two ways in which (theoretically) you could rebuild the chromosomes of the extinct organism. Firstly, you could modify the DNA of a closely related species at each base that it differs from the extinct species.  For instance in the case of mammoths you could use African elephant DNA, which differs at about 400,000 sites.  Or alternatively, you could synthesize the whole genome from scratch.   However, so far only small bacterial genomes have been successfully synthesized, and then there is the problem of how to package the synthesized DNA into chromosomes and enclose the whole lot in a nuclear membrane.  These are not a trivial problems, as for many extinct species we don’t even know how many chromosomes there were, let alone which bits of DNA go where*.    

Of course these problems of rebuilding a genome can be circumvented if well-preserved tissue from the organism is available. If this is the case, an intact nucleus could be transferred directly a la Dolly the sheep.  This was the method used to clone the bucardo.  In 1999, researchers in Spain had the foresight to take skin samples from the last living bucardo, and froze them in liquid nitrogen.  The bucardo genetic material was then transferred into the eggs of a domestic goat, and the resulting embryo implanted into other species of spanish ibex or goat-ibex hybrids.  Researchers at the Audubon Centre for Research of Endangered Species (part of Audubon Nature Institute) are also using this method to clone critically endangered species such as the african wildcat.    

Using an intact nucleus from frozen tissue is obviously a much easier approach than rebuilding a whole genome from scratch, but for the majority of extinct species we don’t have a good enough tissue source.  Even exceptionally well preserved remains, such as those frozen in permafrost, show significant amounts of degradation, and the chances of finding an intact nucleus with undegraded DNA in a specimen that is several thousand years old are virtually nil.  Organisations around the world are now beginning to realise the importance of frozen tissue resources, and are creating frozen zoos, where archives of tissue from endangered species are cryopreserved for future use.  These resources won’t help resurrect the mammoth, but might facilitate future cloning endeavours on critically endangered species.  

Its also unlikely we’ll be seeing cloned moa, huia or giant eagles any time soon, as somatic cell nuclear transfer currently only works in mammals.  No one has yet successfully cloned a bird, reptile, amphibian or fish using these methods, because differences in the structure of the eggs in these species provide added complications.  Oh and you can forget about cloning dinosaurs too.  Although researchers at North Carolina State University have claimed to have extracted protein from dinosaur bones, no DNA has been found and it seems extremely unlikely that DNA could survive intact for more than a few hundred thousand years.  Virtually all reports of DNA extracted from samples that are many millions of years old have failed closer inspection, so it seems that the idea of extracting DNA from dinosaur blood found in mosquitos fossilized in amber belongs firmly in the realm of fantasy.  

* This news feature in Nature provides more detail and a really nice explanation of the methodological difficulties that have yet to be overcome with this type of cloning

Rare giant gecko turns up (dead) in mainland sanctuary Hilary Miller Apr 22

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Here’s one from the good news but bad news file:  The good news is that a Duvaucel’s gecko (Hoplodactylus duvaucelii) has been found on the New Zealand mainland for the first time in nearly 100 years.  The bad news is that it was found dead in a mouse trap.

Duvaucels geckos are the largest of our native geckos, and one of the biggest geckos in the world, growing to up to 30cm in total length.  They are found on a number of offshore islands off the north-east of the North Island and in Cook Strait, and were thought to be extinct on mainland New Zealand.  The last recorded sighting of this species on the mainland was near Thames in the 1920s, but subfossil remains have been found on both the North and South Islands, suggesting it was once widespread across the country. 

The dead gecko was found at Maungatautari, in the Waikato.  Maungatautari is a 3400 ha nature reserve ringed with a predator-proof fence, making it the largest pest-free area on the mainland.  Many rare species have been released into the sanctuary, including kiwi, kaka, takahe and hihi, and reintroductions of many more species are planned.  The Duvaucel’s gecko find suggests that there is a remnant nautral population of the species in the sanctuary, which somehow survived the years when the area was overrun with introduced predators. The hunt is now underway for more of the geckos (which will hopefully be found alive).

This discovery shows that you never know what you might find when you protect an area instead of mining it.

More on the discovery on Stuff.

Tasmanian devil facial tumour disease: too good a match for the immune system Hilary Miller Apr 13

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ResearchBlogging.org
A central premise in conservation genetics is that high genetic diversity is good for a species’ continued survival, and low genetic diversity is bad. This seems intuitively obvious (after all, we all know that you shouldn’t marry your cousin) but actually finding examples in nature where we can say for sure that low genetic diversity has contributed to a population’s demise is difficult.   

However, the recent decline of tasmanian devil populations due to disease provides an excellent example of the perils of low genetic diversity.  Wild devil populations in eastern Tasmania have been decimated in recent years by devil facial tumour disease (DFTD).  This nasty disease is a transmissible cancer spread by biting, and causes large tumours to form around the mouth, interferring with feeding and eventually causing death.  Kathy Belov’s group at the University of Sydney has been studying the genetic basis of DFTD susceptibility in devils and has found that a lack of variation in immune system genes is responsible for the spread of the cancer in some populations.    

Tasmanian devil with facial tumour disease (photo: Menna Jones)

Belov’s group has been studying the genes of the Major Histocompatibility Complex, or MHC.  MHC molecules are a crucial part of the immune system in vertebrates, as they are responsible for recognising foreign invaders and mounting an immune response.  MHC molecules are also an important part of the process of self/non-self recognition that prevents the immune system attacking the body’s own cells.  MHC genes are normally highly variable in populations, with a large number of different alleles (or variants) for each gene.  This variability allows for a wide array of foreign pathogens to be resisted and accounts for differences in disease resistance among individuals.  Thus, populations with low or no variation at MHC genes are potentially susceptible to disease epidemics, as all individuals in the population will be equally susceptible to novel diseases.   

Devil populations in eastern Tasmania have low levels of genetic diversity due to reductions in population size over the last 150 years.  DFTD is so virulent in these populations because the tumours have the same MHC type as healthy devil cells.  Being an infectious cancer, transmission of DFTD between individuals is a bit like a skin graft or organ transplant. If the tissue’s MHC type matches, the transplant is accepted, if not it is rejected.  Because the MHC types of the tumour and the devil match, DFTD cells are not recognised as foreign so no immune response is mounted.  And because of the low genetic diversity, all devils in the population have similar MHC types meaning the disease can easily spread from one individual to another. 

DFTD has spread rapidly throughout eastern Tasmanian populations, causing a 90% decline in total devil numbers.  However, a population at West Pencil Pine in northwestern Tasmania has much lower prevalence of DFTD, suggesting this population harbours animals that are resistant to the disease.  New research by Belov’s lab published in Proceedings of the Royal Society of London last month shows that these populations have differences in their MHC makeup that appear to allow them to resist the disease. 

Here the story gets a little (more) complicated: Tasmanian devils have multiple MHC genes (up to 7 genes each), which fall into two groups on the basis of their DNA sequence.  The tumour cells have both group 1 and group 2 variants, as do the individuals from the susceptible eastern populations.  However the northwestern populations harbour a greater diversity of MHC types, and many individuals from these populations have MHC types which have only either group 1 or group 2 sequences.  None of these individuals have succumbed to DFTD, suggesting they are resistant to the disease.  Belov’s group proposes that in individuals with only group 1 sequences, the immune system will recognise the group 2 sequences on the tumour as foreign and resist it (and vice versa for individuals with only group 2 sequences).   This has yet to be tested in practice, as it is obviously difficult to get permission to infect an endangered species with a deadly disease.  However, these findings are promising for the continued survival of the species and may have a significant impact on their conservation management.

Siddle HV, Kreiss A, Eldridge MD, Noonan E, Clarke CJ, Pyecroft S, Woods GM, & Belov K (2007). Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial. Proceedings of the National Academy of Sciences of the United States of America, 104 (41), 16221-6 PMID: 17911263

Siddle, H., Marzec, J., Cheng, Y., Jones, M., & Belov, K. (2010). MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer Proceedings of the Royal Society B: Biological Sciences DOI: 10.1098/rspb.2009.2362

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