Dear Luke,
1) Thank you for taking the time to reply although it appears to me that you
are opening more questions than answering existing ones.
1) Would you be so kind to answer my questions first before posing new
questions to which you expect an answer ?
2) Have you any thoughts about competition between different species
mycorrhizal fungi for soil volume ? For example ericoid mycorrhizae
associated with heather competing with ecto and VA mycorrhizae associated
with trees ?
2) Yes, I have and they will be published in my Dutch book on the tree
species specific ecosystem in September 2012.
3) Lonsdale (1999, p. 99), Schwarze et. al. (2000, p. 76-81) and Butin (1995,
p. 163). Schwarze et. al. (2000)
3) Isn't this all literature based upon in vitro research of dead wood ? And
does any of the authors explain where the acid in the fruitbodies of F.
hepatica comes from, why F. hepatica is restricted to "white oaks" such as Q.
robur/petrea and to C. sativa and what process or pathogen other than F.
hepatica causes the typically shaped morbid growth and necrosis of living
tissues and bark, that only occurs in these tree species while being
colonised by F. hepatica ?
4) Sapwood redundancy may occur after loss of root function or crown volume
and associated foliage.
4) Which IME never is the case with, nor the effect of an infection of living
tissues by the mycelium of F. hepatica.
Regards,
Gerrit
First some general remarks and questions :
- Where does the sour vinegar taste of fruitbodies of the often guttating
"poor man's beefsteak" F. hepatica come from, that makes it necessary to soak
it in milk or wine overnight before it can be consumed, if not from the acids
the sapwood of Q. robur/petrea or C. sativa secretes when living tissues are
invaded and "tapped" by the mycelium of F. hepatica ?
- As I said before, it has been assessed, that F. hepatica "feeds on" the
sugar rich acids produced by the sapwood, acids that are no longer present in
dead heart wood of white oaks and sweet chestnut, and that is why Laetiporus
sulphureus can easily invade, dry brown rot and hollow the heart wood of
these trees.
- What other pathogen do you suggest is responsible of the typical living
tissue and bark morbid growth and necrosis that is always associated with the
presence of the mycelium and/or fruiting of F. hepatica inside and/or on the
tree ?
- Even when constricted to (necrotrophic) parasitic bracket fungi, the tree
species specific ecosystem of white oaks is far more complicated than you
present it. Along with F. hepatica and Laetiporus sulphureus, Inonotus
dryadeus, Phellinus robustus, Daedalea quercina and Piptoporus quercinus,
among which competition for territory and sugars takes place, play a just as
important role in old white oaks becoming veterans on the long run.
- F. hepatica produces an atypical brownrot of (dead) sapwood, L. sulphureus
a dry brown rot of heart wood. Inonotus dryadeus produces a soft rot of
living tissues and a white rot of dead wood, Piptoporus quercinus and
Daedalea quercina a brown rot of heart wood, and Phellinus robustus a
simultaneous white rot.
1) The paragraph quoted above appears to indicate that you consider that
Fistulina hepatica can kill sapwood and cambium. I'm afraid that this is
quite different from my understanding that F. hepatica is purely a saprotroph
that is specialised to colonise and gain its nutrition from heartwood.
However, I'll accept that it may also be able to obtain nutrition from dead
sapwood if not 'out-competed' by wood decay fungi that are more able to
utilise this substrate. I'm sure that we are all aware that sapwood and
cambium may die for a multitude of reasons: biotic, abiotic, but most often a
combination of a number. My understanding was that, once dead, F. hepatica
maybe able to utilise the newly available substrate as a secondary
saprotroph. If it's not too much trouble could you please recount the steps
you've taken to eliminate these potentially primary reasons for sapwood and
cambium death and enabled you to come to your conclusion.
1) All continental European scientific literature lists F. hepatica either as
a wound parasite or as a (weak) necrotrophic parasite and states that F.
hepatica is unable to infect, colonise and fruit from completely dead laying
down or standing up wood of Q. robur/petrea or Castanea sativa, if the
mycelium has not occupied a foothold in the tree while the tree was still
alive, which - according to my understanding - is correct.
2) My understanding is based on trees being balanced, as are all plants. If
something occurs to one part of the plant ramifications occur throughout it.
For instance, if we experience drought, tree roots won’t be able to supply
sufficient water and nutrients, leaves wilt and potentially die. When this
occurs, and the foliage area of the tree is significantly reduced, some roots
and sapwood will also become physiologically dysfunctional.
2) My understanding is based on my concept of (the dynamics of) the tree
species specific ecosystem with its tree species specific life cycle, tree
species specific soil food web and tree species specific parasitic,
saprotrophic and (ecto)mycorrhizal (macro)fungi, which are for the greater
part responsible for the uptake of water and nutrients and for protection of
the tree roots and the tree as a whole against drought, toxics and attacks
from (soil) parasites with self-produced antibiotics and fungicides.
3) Another example is when foliage is removed, potentially by storm damage or
chainsaw. With a reduced amount of foliage the tree has reduced requirements
for water and nutrients so some of its roots and sapwood become redundant and
eventually physiologically dysfunctional. The same can be said if roots are
removed by either trenching or root diseases: the remaining roots won’t be
able to supply the requirements of the amount of foliage present prior to the
root death event so some of that, along with some sapwood, will die and
become available for colonisation by saprotrophic decay fungi. Some buffering
can occur but I imagine that this depends on the tree’s energy reserves.
3) What role do (tree species specific) ectomycorrhizal macrofungi play in
your example, how do they affect this process and how does this process
affect the ectomycorrhizal symbionts ?
4) There are numerous ash pollards.
4) Being associated with endomycorrhizal microfungi, ash has a completely
different tree species specific ecosystem and life cycle than tree species
associated with ectomycorrhizal macrofungi - such as oaks and beech - have.
5) I’m sure that you probably know better than most that soil is chocka-block
with organisms including some that feed on live roots such as native species
and strains of Pythium and Phytopthora. I have a friend who did his PhD. On
these at Aberdeen University. Under normal conditions the tree can tolerate
their presence but, if conditions alter and become ‘stressful’ for the tree
or beneficial for an organism that is normally only a weak pathogen, it may
kill a significant amount of tree roots. If this were to occur the tree may
appear drought stressed, its foliage cover reduce and portions of its sapwood
may become dysfunctional and available for colonisation by saprotrophic wood
decay fungi.
5) Did your friend also study the role (ecto)mycorrhizal (macro)fungi play in
the soil food web and the influence they have on the development or
inhibition of soil pathogens ?
6) I’ve previously considered that the ‘morbid growth and necrosis of Living
tissues and bark’ were caused by stresses to the tree – biotic, abiotic, or
more likely a combination of a number of stressing agents – and F. hepatica
colonised those tissues once they became unviable. If this is correct F.
hepatica is a saprotrophic species.
6) See 1).
7) I’m afraid I don’t know the answer to your second question but I would
love to hear yours.
7) I already said, that other than white oaks such as Q. robur/petrea and
Castanea sativa, red oaks, such as Q. rubra, lack the acids in their living
tissues the mycelium of F. hepatica needs to "feed on".
Best wishes for 2012,
Gerrit
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