Some similarities to : other
Japanese Larch is a
monoecious plant with separate male and female flowers on the same plant. It is member of the Pine Family of trees having deciduous needles, it is therefore a deciduous conifer. It turns a golden brown in autumn before the needle leaves drop off.
Forestry plantations of Japanese Larch in South West England have been dying in 2010 due to the pathogen Phytophthora ramorum.
The Sesquiterpenes (-)α-Cadinol and Oplopanone are found in the leaves.
α-Cadinol is an aromatic hydrocarbon present in a number of plants including Yarrow,
Jasmine, many species of Juniper, and some species of St Johns Wort. It is one of the many anti-fungal agents employed by the plant in defence against pathogens.
Cadinol is a derivative of α-
Cadinene a sesquiterpene first identified in Cade juniper, hence the names. It has a chemical structure very similar to Muurolene and is used as a flavouring agent and perfume.
Rhododendrons now harbour a disease caused by the fungus Phytophthora ramorum which was first found in the UK late 1900's and which is also deadly to some species of trees. Uprooting these rhododendrons is becoming much more imperative. Ramorum disease hosted in Rhododendron pontica is now spreading to other trees such as
Douglas Fir, Western Hemlock amongst about 220 other vulnerable trees. This includes
Japanese Larch, which is extensive in forestry plantations.
The disease was first spotted in Larch trees in 2009 in South West England. Since then it has spread rapidly and is now found, mainly in the West, in Devon, West Somerset, Wales, and with pockets in Lancashire, Cumbria and Western Scotland. All infected trees are being felled as a matter of some urgency, which is having a devastating effect on the plantations; the wood cannot be used for fear of spreading the fungus further afield. Infected Japanese Larch trees are especially prone to release high levels of the fungal spores in spring and summer. In moist air (such as is likely in the West) the spores can spread significant distances to infect other trees, even in gardens and parks. Infected Larch trees shed their needles early, well before autumn. The shoots visibly wither and the needles go black, branches die back and the upper trunk can bleed resin. The fungus infects the tree just beneath the bark; infected trees show an identifying wine-red stain if the bark is peeled away.
FUNGAL ATTACK and RESISTANCE
Your Authors thoughts
Fungi aren't usually able to attack and consume living trees, for trees actively produce a cocktail of fungicides which are usually effective in preventing any fungal infestation taking hold. Trees accomplish this in a variety of ways. They may produce a plethora of fungicides even when not under fungal attack. The way that they synthesize the fungicides, creating a great many with nearly the same chemical structure but with various additional groups scattered all over the place, usually ensures that even if the fungi evolves resistance to one particular chemical, it would have great difficulty evolving resistance to the plethora of differing fungicides simultaneously.
However, synthesising a plethora of fungicides that are active all the time, is for one thing, a waste of the trees precious resources, and for another, it tauntingly dangles the chemicals continually exposing them to fungi, which may then have greater opportunity to evolve resistance; far better to hide the fungicide from view in an in-active form which the fungi cannot normally sense. In certain cases, mechanisms exist which will switch an in-active form of fungicide into an active form when the tree is under the stress of a fungal attack; a stress activated switch. The fungus will have a harder time developing resistance to this form of fungicide when it cannot 'see' it all the time. This hidden form of the fungicide still requires use of the trees resources to manufacture; far better if the tree can only synthesize the fungicide only when a fungal attack is well underway. This strategy is also employed in certain cases, triggered by the products of fungal attack, and makes much more efficient use of the trees resources.
If the fungus is able to develop resistance to enable it to evade these mechanisms, the tree then has little defence against such an attack. It could possibly take evasive action by jettisoning an infected portion of itself before it reaches the bole, and this mechanism is used in some instances, more as a last resort. It could also physically block off infected portions with some resin which hardens, perhaps temporarily preventing further spread of the fungus. When all such measures fail, the tree is doomed, and so too all identical trees around it, for not only can fungi spread from nearby tree to nearby tree by underground mycorrhizomes, it can also spread by releasing lightweight wind-borne spores which can travel great distances.
Felling infected trees is probably a damage limitation measure; for if the fungus initially started from one tree, and is now infecting tens of thousands of similar trees throughout differing regions, then even if it were possible to fell all infected trees, it only needs one stray bit of infected wood, one remaining mycorrhizome, or one stray fungal spore to start a new infestation. Such a felling strategy is doomed to failure. The only hope is that, on the way, the fungus evolves into a less virulent form, or the species of tree develops resistance to the fungus.
When it takes a few years for one tree to beget another, resistance by way of genetic mutation is just a yearning hope that may take decades to materialise. But faster ways of developing resistance exist. The tree may in the past have already been able to synthesize a potent fungicide that will stop the dead fungus in its tracks, but has (for instance) lost the mechanism to switch on this synthesis. Here, a mutation in the tree cells could switch it back on again, and the tree may once again able to repel this fungal intruder. How fast this mechanism is able to be propagated within the infected tree itself and in other trees around the forest will decide if the forest is able to survive. Other trees may develop resistance in the very same way, perhaps initiated by the fungal attack itself.
Your Author surmises that resistance might be transferred from tree to tree in many ways that researchers have not yet dreamt; for instance by pheromones released by the infected but now resistant tree to which other trees are able to respond. It is now known that pheromones and air-borne hormones released by plants under the attack of predators (for instance insects or pathogens) are able to switch on various plant defence mechanisms in nearby and as yet un-affected plants, forewarning them of impending attack, and predisposing them to generate their own defensive chemicals. See Plant Hormones, Lodgepole Pine and Auxins.
Or resistance might be passed on from tree to tree by siRNA's, small snippets of RNA that can infiltrate every cell of plants and alter the expression of the plants genes.
Abietane diepoxides such as shown left have been isolated from Japanese Larch and exhibit anti-tumour activity. Note the similarity to Phyllocladene.
Strictly speaking, Larixol, with a broken third ring, is not an Abietane Diterpenoid, but rather a Labdane Diterpenoid.
Some diterpenoids are also found in the leaves: the labdane diterpenoid Larixol, as well as several derivatives of
dehydro-Abietic Acid such as
dehydro-Abietinol, 7-oxo-dehydro-Abietinol, 7-oxo-dehydro-Abietic Acid, 9α,13α-epidioxy-Abiet-8(14)-en-18-oic Acid, 9β,13β-epidioxy-Abiet-8(14)-en-18-oic Acid,
dehydro-Abietic Acid, 7α-hydroxydehydro-Abietic acid, 8α,9α,13α,14α-diepoxy-Abietan-18-oic acid and 15-hydroxydehydro-Abietic Acid.
The leaves contain two deformed abietanes,
Karamatsuic Acid (9,10-seco-9,10α-epoxy-Abieta-8,11,13-trien-18-oic Acid) and
Larikaempferic Acid (9α,13α-epoxy-8-oxo-9(8to7)abeo-7β-Abietan-18-oic Acid).