GIG RACING is a peculiarly Cornish sport. The dangerous coastline in this corner of England always provided plenty of work for the swift, open boats -both in guiding sailing ships into port and rescuing their crews when they foundered. Today, rowers compete in weekend gig races, in boats crafted from Cornish elm planks according to the original design. Or at least they did until now. Today, Cornish craftsmen like Ralph Bird, who builds gigs at his yard near Truro, have a problem that could end the tradition.
Cornwall鈥檚 elms have all but disappeared. 鈥淲e always built with elm,鈥� says Bird. 鈥淚t was traditional, and there was always plenty of it about. We didn鈥檛 have to look elsewhere. Now the trees are almost totally wiped out.鈥�
Around half a million Cornish elms have now succumbed to that scourge of the 1970s: Dutch elm disease. But it isn鈥檛 only the gig-builders who mourn the passing of the trees. Since the epidemic hit Britain in the late 1960s, more than 25 million of the country鈥檚 30 million elms have fallen victim to the disease, caused by the fungus Ophiostoma novo-ulmi, that swept across the country aboard an army of small, brown beetles. Nor was Britain the only victim. The epidemic spread both east and west across the US from the Great Lakes, and raced eastward through Europe to the borders of China. The worldwide trade in timber accelerated the spread and it eventually reached even the ocean-bound outpost of New Zealand.
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Although the disease faded from public consciousness, it never disappeared completely. After cutting a swathe across vast areas, the disease holed up in surviving pockets of elms. In these reservoirs, both beetle and fungus hung on until the next generation of elms grew large enough for them to breed in. Now the disease is back with a vengeance. In Britain, the first hint of its return came in 1990. Since then almost 90 per cent of the young elms around London have died. And, to the consternation of the gig-builders, last summer saw a resurgence in Cornwall. This new wave of disease is also on the move in continental Europe and North America. The cycle could keep rolling on and on, warns Clive Brasier of the Forestry Commission鈥檚 Forest Research Station near Farnham in Surrey.
New wave
With this latest phase of the epidemic hanging over their heads, forest researchers are looking to biotechnology and biocontrols for the weapons they need to fight the fungus. Despite decades of research, no one has yet found a way to stop the killer disease in its tracks. Most efforts to control its spread relied on prompt identification and removal of infected trees. Attempts to kill both beetles and fungus with chemicals proved costly and ineffective. In the 1970s, researchers experimented with pheromone-laced beetle traps, and with injection programmes for trees, but had little success.
Tree breeders, particularly in the US and the Netherlands, are having better luck creating resistant trees by crossing local elms with species from Asia that have some natural resistance. But these hybrids are unlikely to repopulate the British countryside. They bear little resemblance to British elms and are poorly suited to the climate.
鈥淭he huge explosion in biotechnology offers us some radical alternatives,鈥� says Brasier. One approach is to try to fight disease with disease, harnessing the power of virus-like agents called d-factors. These pathogens, which Brasier discovered a decade ago, attack the Dutch elm fungus, sapping its vitality. D-factors also stop its spores from germinating, reducing a normal rate of successful germination of around 90 per cent to 20 per cent. D-factors consist of multiple stretches of double-stranded RNA, but are not classed as viruses because they lack a protein coat. Similar agents are quite common in other fungi-chestnut blight fungi have their own 鈥渉-factors鈥�, for example-but only a few cause sickness in their hosts.
A second tactic is to equip trees with genes that manufacture antibeetle or antifungal chemicals. Behind both lines of investigation is a search for the origin of the fungus that began back in 1979. If Brasier and his team can find the fungus鈥檚 natural home, they might be able to explain how it became the most destructive tree disease ever known. In its natural haunts, perhaps somewhere in Southeast Asia, Brasier suggests, the fungus is probably fairly tame, kept in check by local predators and pathogens. If the researchers can identify such controls, they might be able to put them to work against the fungus.
Paths of destruction
Dutch elm disease, first appeared in Northwest Europe around 1910, and reached North America in the 1920s. The fungus responsible for this first outbreak was Ophiostoma ulmi. By the 1940s the epidemic died down in Europe, possibly after widespread infection with d-factors. But this did not happen in the US because of a complex interplay of factors, including the differences in vectors and the greater susceptibility of the American elm.
Then, in the late 1960s, came a new and far more destructive outbreak. This time the fungus was distinctive enough to merit a new name, Ophiostoma novo-ulmi. Europe鈥檚 elms had almost no resistance to this new attacker, and keeled over as the disease swept across the continent. In North America the new disease was less noticeable because the original epidemic was still active. On both sides of the Atlantic, the new fungus quickly ousted its predecessor, O. ulmi, driving it towards extinction.
Ophiostoma novo-ulmi is spread by small beetles belonging to the genus Scolytus, which breed beneath the loose bark of dead or dying elms. The fungus grows in the 鈥済alleries鈥� that female beetles drill out of the nutritious inner bark, or phloem, to create nursery tunnels for their larvae. Inside the galleries, the fungus forms a network of threads, or hyphae, and produces spores, both asexually and, when conditions are right, sexually. When the new generation of beetles eventually emerge from their galleries in the dead tree to look for a new place to breed, they carry spores with them. If they don鈥檛 find a dead tree immediately, they stop off to feed in the crown of a healthy elm, shedding spores as they bite into the bark.
The fungus germinates and grows in the feeding wounds, penetrating the xylem vessels that transport water around the tree. Once in the tree鈥檚 plumbing system, the fungus spreads quickly, blocking the vessels and producing a powerful toxin. The tree鈥檚 leaves wilt as it dies back from the tips of its twigs towards the trunk, and the entire tree may be dead before the summer is out.
In Europe there are two main carrier beetles. 鈥淭he larger one, Scolytus scolytus, is more efficient at hauling spores,鈥� says Joan Webber of the Forest Research Station. Some of these bigger beetles carry as many as half a million spores although most manage only a few thousand. Webber鈥檚 experiments have shown that at least a thousand spores are needed to successfully infect an English elm through a feeding wound. This makes the smaller species of beetle, S. multistriatus, a much less effective vector: few carry more than a hundred spores. But the beetle does the job well enough in North America, where it is the only species present, because the American elm is much more susceptible to the fungus and far fewer spores are needed to start an infection.
Reducing the potency of the fungus鈥檚 spores by infecting them with d-factors could help to slow the spread of the disease. The virus-like agents spread from fungus to fungus when individual hyphae fuse together. The best studied of the 40 d-factors isolated from the fungus, called d2, interferes with the activity of the enzyme cytochrome oxidase, which is vital to the respiratory process. This slows the growth of the fungus and causes it to age unusually fast. 鈥淲e don鈥檛 know precisely how it does that yet,鈥� says Kenneth Buck, a molecular biologist working on d-factors at Imperial College, London. 鈥淣ot all d-factors work this way but it seems to be a common mechanism.鈥� Buck and his colleagues are cloning genetic material from the d-factors to try to identify which of their proteins interfere with the growth of the fungus.
D-factor dilemma
At the Forest Research Station, plant pathologist Louise Sutherland is checking out the characteristics of as many d-factors as she can lay her hands on, in the search for suitable candidates to control the fungus. Pick one that is too vicious and the fungus will soon evolve to resist infection; pick one that鈥檚 too weak and it may have little effect. 鈥淢aybe you should release a moderately severe one so it doesn鈥檛 put so much pressure on the fungus to change,鈥� suggests Sutherland.
Webber鈥檚 experiments have shown that d2 reduces the potency of fungal spores so much that at least 50 000 spores are needed to cause infection. Few beetles carry so many spores: they have no special organ to transport them and the spores simply cling to the bristly, pitted surface of their bodies. But if bark beetles are transporting enough spores to keep the current epidemic rolling, they could also be harnessed as carriers of d-factors, spreading the fungus鈥檚 own disease into the wild population, says Brasier. It would be simple enough, he suggests, to breed beetles in the laboratory, contaminate them with spores infected with suitably potent d-factors and set them loose in areas with Dutch elm disease.
Fighting disease with disease should work in theory. But there is a hitch. Under natural conditions, the main route of transmission for d-factors is from the cytoplasm of one fungus to another, during fusion between fungal threads. At the fast-moving epidemic fronts, the fungus is essentially a clone produced by asexual reproduction. Where the fungi have an identical genetic makeup, there is no obstacle to fusion and d-factors pass readily through the population. But Brasier and his colleagues have found that as the fungus becomes more established and reproduces sexually, its population grows genetically more diverse. With diversity comes 鈥渇usion incompatibility鈥�-the threads of a fungus will not fuse with those of a genetically different individual. 鈥淰egetative incompatibility limits the dissemination of d-factors in the wild,鈥� says Buck.
This means that releasing carefully selected d-factors into the population should work at the leading edges of epidemics but will have little impact where genetic diversity is high, as in most of Europe. To compound the problem, the fungi also have some mechanism for eliminating d-factors from their cytoplasm when they reproduce sexually. To overcome both of these problems, Buck and his team want to insert the d-factor鈥檚 genes into the fungal nucleus, where it would be inherited like a single gene. When the fungi 鈥渕ate鈥� during sexual reproduction these d-factors would now pass safely into the next generation. And, because genetically different fungi can crossbreed, the process would spread d-factors into strains that would normally be protected by vegetative incompatibility. Three years ago, American researchers succeeded in inserting genes from an h-factor into the nucleus of the fungus that causes chestnut blight, and are now testing it out in the field.
But will the idea work in the wild? There are at least three places that would make ideal 鈥渓aboratories鈥� for testing the effectiveness of d-factors. In the outbreaks around Auckland in New Zealand, in Washington DC and in Oregon, the fungus is a single clone and, for some unknown reason, there is no natural infection with d-factors in any of these places to confuse the trials. In Washington DC, a city renowned for its magnificent elms, the National Parks Service is open to the idea. The incidence of Dutch elm disease has been kept at around 1 per cent by conventional management. But the city is broke and some authorities have more urgent calls on their budgets, raising the prospect of a flare-up of disease. Jim Sherald, of the National Parks Service鈥檚 Center for Urban Ecology in the capital, is responsible for around 6000 elms along the Mall and on other National Parks land in the city. 鈥淎merican elms are beautiful trees and we would like to keep them,鈥� says Sherald. He is interested in any possible new addition to the armoury. 鈥淥ur concern at the moment is that the better d-factors may not be native ones and we are worried about using an alien one. The solution is to find one that is from the US, one that we feel comfortable with.鈥�
Repellant ideas
Another radical strategy, made possible by advances in genetic engineering, is to provide trees with their own defences. They could, for instance, be fitted out with genes for producing toxins that kill the beetle, or chemicals the beetles find unpalatable. 鈥淲e are a bit cautious about the first approach because it would work against other insects too,鈥� says Brasier. Creating unpalatable trees also has its drawbacks. A beetle that dislikes the taste of one tree is likely to visit, and perhaps infect, several before it starves to death. A safer bet is to repel the fungus by equipping the tree with some sort of antifungal agent.
But creating fungus-resistant trees is a long, slow process. The challenge is to identify a suitable repellant in a plant and find the gene that controls its manufacture. 鈥淵ou look for something that will slow or inhibit the fungus. You search the literature, listen out on the grapevine, make contacts in companies-and use a lot of inspired guesswork,鈥� says Kevan Gartland of Abertay University in Dundee. He and his colleagues have half a dozen candidates, the identity of which is covered by secrecy agreements with companies that have supplied them. 鈥淲e have some we are cautiously optimistic about,鈥� says Gartland.
Transforming trees
But what repels the fungus in the lab must still prove its worth in a full-grown tree. That means developing a reliable method of raising elms from cultured cells, and perfecting a technique for inserting the required genes so they end up in every one of the tree鈥檚 cells. Once you have trees you can put their new defences to the test by unleashing spore-carrying bark beetles onto them.
Last year, the group at Abertay became the first to successfully insert foreign genes into elm cells. Like other plant biotechnologists, they employed the natural genetic engineering skills of Agrobacterium tumefaciens. In nature, the bacterium injects its own genes into a host鈥檚 genome to set off massive cell division, creating a tumour or gall.
Gartland and his team have 鈥渄isarmed鈥� one particular strain of Agrobacterium so that it ferries the genes they choose minus its own growth modifying genes. Elm tissue infected this way can then be induced to sprout shoots and roots with a judicious addition of hormones, producing a 鈥渢ransformed鈥� plantlet. Once Gartland and his team find the right genes, they will be able to produce a limitless number of trees for planting schemes. 鈥淲e can grow up thousands of trees from culture,鈥� says Gartland.
While the teams at Imperial College and Abertay have been at work, Brasier has been pursuing a third line of attack-hunting for the origin of the fungus. Annual expeditions have taken him from Iran and Central Asia to China and the remote Himalayas, but he has still not found the mysterious progenitor of Dutch elm disease.
In 1993, Brasier discovered a fungus, living with local bark beetles in the native elms of a remote Himalayan valley. Kept under control by its natural enemies, this fungus did little damage to the elms. Could this innocuous fungus have escaped from its Himalayan valley and developed into the aggressive pathogen that had swept the world?
Disappointingly, the answer turned out to be no. Brasier failed to persuade the new fungus to interbreed with O. novo-ulmi, suggesting that it was a separate species. Molecular studies confirmed that the Himalayan fungus was a distinct species, now called Ophiostoma himal-ulmi. Nor could it have given rise to O. novo-ulmi in the recent past, perhaps, by hybridising with O.ulmi. But the Himalayan discovery could provide clues to useful new biological controls, perhaps in the form of a rival fungus that competes for space under the elm bark, or a parasitic nematode or a virus that keeps the number of beetles down.
Brasier鈥檚 Himalayan discovery did reveal the existence of a novel tree pathogen which could start a new epidemic should it ever escape the confines of its natural habitat. And it is unlikely to be the only one. With trade penetrating ever more remote areas, it could be just a matter of time before one of these unknown pathogens turns up closer to home, says Brasier. Such threats make the search for new weapons against forest pathogens such as the Dutch elm fungus all the more urgent.
Transatlantic threat
One terrible threat is already too close for comfort. This is a fungus called Ceratocystis fagacearum, which causes a wilting disease of oak trees. The disease exists in North America, where it is transmitted by sapfeeding beetles. These are so inefficient that the disease has never reached epidemic proportions. So far, the disease has not crossed the Atlantic. 鈥淏ut we are very keen to keep it out of Europe,鈥� says Brasier. Europe鈥檚 oak trees could be highly susceptible to the fungus, and once here there is a danger that it would hitch a ride with the native oak bark beetle, Scolytus intricatus, which is likely to be a highly efficient vector. 鈥淭his gives it the potential to behave like a Dutch elm disease type fungus,鈥� warns Brasier. Likewise, the US has every reason to fear the accidental introduction of Europe鈥檚 larger elm bark beetle, which might turn its low level disease into an epidemic. 鈥淭he risks operate both ways,鈥� says Brasier.
Perhaps even more than the elm, the oak tree is a vital and much-loved part of the European landscape. 鈥淚f oak wilt arrived in the Caucasus today, it could be on our doorstep in five years鈥� time,鈥� says Brasier. 鈥淎nd like Dutch elm disease, it could have a catastrophic impact across Europe.鈥�
