UKTC Archive

RE: Ganoderma applanatum/australe on n.maple - implications

Subject: RE: Ganoderma applanatum/australe on n.maple - implications
From: luke steer
Date: Dec 29 2011 22:17:47
Dear Gerrit,
I trust that you are continuing to find our discussions interesting but if 
not maybe we should desist.  

Regarding point 3 below my understanding is that the statements in the quoted 
references of F. hepatica principally colonising heartwood are based on 
observations.  However I know that in 2000 Schwarze, Balm and Fink published 
a paper in Mycological Research with the title: Dual modes of degradation by 
Fistulina hepatica in xylem cell walls of Quercus robur.  I found it very 
interesting.

I may not be totally understanding your use of the term: 'typically shaped 
morbid growth and necrosis of living tissues and bark.'

Originally I took it to mean wood with reduced vitality, dead areas of wood, 
and bark in declining health leading to death.  Is this correct?

Regarding the sour vinegar acid you refer to I have found no references to 
that so I'm not in a position to comment.  However Desch and Dinwoodie (1996, 
Timber - Structure, Properties, Conversion and use: page 43) state that wood 
is acidic and the level of acidity is considerably higher in heartwood 
relative to the sapwood.  They go on to say that the level of acidity varies 
considerably among different woods but values of pH 3.0 have been recorded in 
the heartwood of oak, sweet chestnut, eucalypt and western red cedar.  Papers 
that I've read indicate that F. hepatica can grow on the first three of those 
species.  It strikes me that the acids found in heartwood could be the source 
of the 'vinegar acids' you refer to?  Something else to eliminate from your 
research to enable you to reach conclusions.  

I've also found references to F. hepatica having the ability to produce 
phenoloxidases and in particular tanninase which allows it to break down 
tannin and utilise the released sugars.  Apparently it can grow on substrates 
that contain up to 1.25% oakwood tannin which inhibits the growth of many 
other wood decay fungi.  

Could the process of digesting white oak heartwood and the tannin and acids 
that it contains enable the fungus to produce chemicals, potentially vinegar 
acids, as secondary metabolites to reduce the palatability of their fruit 
bodies and mycelium for other organisms?

Many thanks for your commitment to improve our knowledge of relationships 
between trees and fungi.  

Regards

Luke  

-----Original Message-----
From: Viper Snake [mailto:snake24@xxxxx.nl] 
Sent: 29 December 2011 20:59
To: UK Tree Care
Subject: RE: Ganoderma applanatum/australe on n.maple - implications


 
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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