Multiple wall 4 failures

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I have no reference for the trees and decay you are dealing with; however, in regards to odor, it is quite common when bacteria is present. Maybe this would explain some of the complex interactions we see on your cut.

http://rms1.agsearch.agropedia.affrc.go.jp/contents/JASI/pdf/society/47-3060.pdf

Dave

Holy crap. Do you read that stuff often? Fair dinkum I thought my brain would explode! I honestly don't know what the research paper actually means. D mc could you please translate. In human. :D
 
This was the reason for my calling the thread "multiple wall4 failures". Perhaps the wording gave a different meaning to my thoughts than was intended. "Shifting" is exactly what I assume happened. As a portion of the barrier failed so it was recreated further from the pith resulting in the new marks.

I wonder if this has occurred does it mean that both explanations are accurate? That is, as wall4 is formed the wood darkens as noted in ANTB. Later the barrier fails at a certain point where one species of fungi, lets call this one fungiA, proves too strong. The tree then recreates or shifts the barrier at that point, perhaps even adjusting the chemical make-up of the cell structure of the barrier to defend against fungi A. Subsequent failures of the barrier would then perhaps be forced by a different species of fungi, say fungi B. This failure is compensated for by recreating the barrier which is now impervious to fungiA and fungiB but still in the decaying wood is fungiC... and so on. This would result in various "pockets"of differing fungi whilst still allowing the tree to have continued to grow.


I know this is simplified but hey, I'm a simple guy.

I like the way much of that sounds. Tree protection zones are characterized by shifting. This is why this process is referred to "compartmentalization" and not "compartmentation" (a static entity/process). They are also, as you noted, characterized by "successions" of attacks that are at times successful and sometimes not. The virulence of the pathogen, time of year, environment, weather, host vitality, etc., all play into this dance.

But as for Wall 4, the strongest wall and necessarily so, if this fails in the first growth increment within the cambium, then IMO the cambium will be killed and the tree dies if it girdles the stem. If there are attacks and it is later on then much storage space is walled off and similar results can occur with less ability to defend (which is based on storage being sequestered).
 
Holy crap. Do you read that stuff often? Fair dinkum I thought my brain would explode! I honestly don't know what the research paper actually means. D mc could you please translate. In human. :D


LOL. I appreciate your frank honesty. So often in threads, such as this, there is a deterioration from the butting of swelled heads.

Do I read these reports often? Unfortunately, yes. As my wife advances in her studies, these type of things come up in our discussion groups and I must say, even though I have been in the tree business for over 40 years, I am amazed at what I do not know.

I am not a mycologist so I cannot break this report down to simple English. My advice is just to read this report and others like it carefully, primarily sticking to the abstract and the conclusions, you will find yourself understanding more and more. This was posted just to illustrate the complexities of the interactions between fungi and bacteria which can leave their tracks for those of us caring to try to decipher.

Dave
 
LOL. I appreciate your frank honesty. So often in threads, such as this, there is a deterioration from the butting of swelled heads.

Do I read these reports often? Unfortunately, yes. As my wife advances in her studies, these type of things come up in our discussion groups and I must say, even though I have been in the tree business for over 40 years, I am amazed at what I do not know.

I am not a mycologist so I cannot break this report down to simple English. My advice is just to read this report and others like it carefully, primarily sticking to the abstract and the conclusions, you will find yourself understanding more and more. This was posted just to illustrate the complexities of the interactions between fungi and bacteria which can leave their tracks for those of us caring to try to decipher.

Dave

Oh boy. You mean I have to read more of these. Owww. This is worse than ice cream brain freeze.....

Thanks for the link mate. I will try again with a strong coffee under my belt and matchsticks under my eyelids... :)
 
This was the reason for my calling the thread "multiple wall4 failures".

To have a wall 4 there must be an injury and infection (as there always with injury). This gives the "wood formed prior to injury vs wood formed after the injury".

There are 2 distinct wounds evident in this section of the tree and this is where the wall 4 has to exist in that inter growth increment space. There will be woundwood originating in the area of the wound to identify the growth increment. The wound can even be identified as to what month the injury occurred I have read unless it occurs in the dormant season.

I do not think you had any idea what/where wall 4 was when you started this thread and when I asked you to identify your premise.
 
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threads, such as this, there is a deterioration from the butting of swelled heads.

As interesting a concept as CODIT....the knowledgeable arborist devoid of ego. Have you reached that plateau?

Do I read these reports often? Unfortunately, yes. As my wife advances in her studies, these type of things come up in our discussion groups and I must say, even though I have been in the tree business for over 40 years, I am amazed at what I do not know.

I'd be interested in what you (and your wife) DO know (as opposed to "do not know")....in regards to the thread subject.

So often this/these threads reach a certain point and posters go on tangents and fire up links, etc., and some are reticent to post anything for fear of being inaccurate. Then they end and time lapses and somebody else with knees knocking wades into it again and it is just like "Groundhog's Day".
 
To have a wall 4 there must be an injury and infection (as there always with injury). This gives the "wood formed prior to injury vs wood formed after the injury".

There are 2 distinct wounds evident in this section of the tree and this is where the wall 4 has to exist in that inter growth increment space. There will be woundwood originating in the area of the wound to identify the growth increment. The wound can even be identified as to what month the injury occurred I have read unless it occurs in the dormant season.

I do not think you had any idea what/where wall 4 was when you started this thread and when I asked you to identify your premise.


I had an idea TV but I am beginning to think it was the wrong idea!

I initially believed that the red line in the photo below would indicate the approximate position of the first wall4 formed. (Pardon the liquid paper!)

attachment.php


I believe the injury to have formed as far back as 20 years ago and that the original pith has become the smelly brown stuff you see above.

Exactly where this barrier of modified cells COULD form is a topic much discussed between jobs and over lunch. I have ass-u-me-d that only undifferentiated cells could form this barrier so this would mean that wall4 would form on the inside of the cambium in the months following injury. Of course this assumption then led to even more heated debate over what then happens to the xylem and how does the tree draw water upward if the xylem is compromised every time the tree forms wall4.

As you can see, I am not without ideas. But your signature applies rather well here I think. I do enjoy everyone's input on this fascinating (to me) topic and I can assure you I do not take offense when you shine a spotlight on the gaping holes in my knowledge. :cheers:
 
So, which is it, that differentiated cambium cells form wall4 or wall4 is some keno reaction barrier zone independent of callus/cambium? Seems you have hedged your bets on both animals.

Barrier zones, reactions zones and wall4 ... not all the same animal and the variety plus inconsistencies I see and read validate this, just like the one written above.

Wall 4 is a tricky one. It is a physical and biochemical response that is formed by cambium cells present at the time of wounding.

Kino itself is not a wall 4 response but Kino bands are. When Shigo first visited Australia he pointed out that burning caused kino bands and that this injury was turning premium grade wood into pulp timber. The anatomical differences in a kino band can be easilly observed with a loupe.

Unlike any other walls, wall 4 is an actual wall or barrier rather than being just part of a model. As a result it gets called a reaction zone (since it involves various chemical and anatomical reactions) or a barrier zone (since it forms a very strong barrier to the outward spread of decay).

Hopefully that clarifies things
 
I feel another brain freeze coming on. I will read a little more then throw out some questions.

And congratulations on your thread necromancy skills Corymbia!
 
To have a wall 4 there must be an injury and infection (as there always with injury).

Wall 4 requires an injury to live xylem tissue ... it does not require an infection althought an infection is almost inevitable since there are normally stored sugars in the sapwood
 
You can see one of the many burls(?) in the top left hand corner of the photograph. I forgot to take any good photo's pre removal so all I have is a couple of pictures from my phone but this tree had numerous tumour like lumps all over the bark. When we dissected them there was no obvious evidence of why they started but I am sure someone wiser than I will have an idea.

What you're mistakenly calling burls and tumors, is in reality buttressing wood, and it's perfectly natural and expected on mathure S. molle, along with hollow cores.

jomoco
 
I had an idea TV but I am beginning to think it was the wrong idea!

I initially believed that the red line in the photo below would indicate the approximate position of the first wall4 formed. (Pardon the liquid paper!)

attachment.php


:

I could be wrong but you are getting the action of fungi mixed up with wall 4. The fungal activity that you are seeing could have originated elsewhere since wall 1 is very week. There is a clear wound to what appears to be a root (or branch) stub. The reaction wood indicates this wound is fairly recent.

The tree appears to be a poor compartmentaliser so I am guessing it is a Shinus? The fungus is repeatedly breaking through and forming new boundaries. To survive the fungus needs to win or reproduce. With shinus it can do both.
 
What you're mistakenly calling burls and tumors, is in reality buttressing wood, and it's perfectly natural and expected on mathure S. molle, along with hollow cores.

jomoco

I make lots of mistakes Jomoco and this time it was not taking enough photographs. Other than what you can see here, there were indeed isolated "lumps" of wood where no buttressing wood normally forms. There was, in addition to those "lumps", the quite normal basal flaring that is commonly associated with Schinus molle

Corymbia I thought that the ongoing battle between the outer "healthy" wood and the inner rotten wood was repeat failures of wall 4. I posted the few photographs I took as a question rather than a statement of fact.

I have a rough idea of CODIT but as you can see, not much experience at seperating different processes occurring in trees.

There are very few S.molle in Perth but it seems that what I took to be unusual in this tree is in fact quite common in the species. I have noticed similar development in other specimens but as they are demonstrably younger it is less obvious.

Ah well. If I had not opened my mouth I would not have revealed my ignorance but then I would have remained ignorant too.
 
I think I see the issue. What you are seeing is the spread of fungi along with new barriers and breaching of the barriers by the fungi. These are not wall 4's. The injury elsewhere and you are looking at are probably breaches of wall 2 which is not very effective on Shinus. As a result they are prone to extensive decay.

In addition wall 1 is very weak and when wall 2 is also weak you can end up with the fungi being further inside than where it started and then moving in and out from that point. Those who rip timber will often observe this.
 
Kino bands in detail

.
Kino itself is not a wall 4 response but Kino bands are. When Shigo first visited Australia he pointed out that burning caused kino bands and that this injury was turning premium grade wood into pulp timber. The anatomical differences in a kino band can be easilly observed with a loupe.

My mum told me to play nicely with the other children and to add a picture or two. (I apologise for not prepping the samples properly but I wanted to get home early)

The first image is the start of the kino band (transverse section) you can see the immediate change in the structure.The xylem goes from anisotropic to isotropic (much like wound wood), no vessels are formed and rays are essentially defunct. The cells are small and dense. The kino fills the voids and limits connectivity between the pre-wound and post-wound tissue.

By comparison the outside of the kino band "Kino band (1)" xylem transitions more gradually back to the formation of typical anisotropic tissue.

Let me know if this helps or if you need me to prepare up and stain full samples to make it clearer.
 
Allow me to speak for the other knuckle draggers here when I say, Fark this kino, where do I put my chainsaw!

This is the greatest strength of our forum IMO.

I honestly am a little confused by the differences between kino and kino bands but I know Corymbia will do his best to educate me. I may be a lawn mowing wannabe but who knows, perhaps a little wisdom may rub off.

Give me a couple of days and I will have some more intelligent questions.

:cheers:
 
Sometimes using correct rerminology is less than helpful...

From almost a year ago
I strongly suspect what you are looking at in the dark lines through the cross section of the stem are demarcation lines from competing fungi.

The less than helpful correct terminology is....

You are more than likely looking at zone lines produced at the edge of pseudo sclerotial plates. :dizzy:

The fact that wood decay fungi create protected boundaries around the volume of wood tissues they are consuming is not really all that surprising.

When it comes to Kino channels/vessels/canals it can be equally confusing to get lost in jargon.

Whilst it is tempting as Australians to feel that Kino channels are something special to Eucs they are not, and more experienced commercial forestry harvesters will know only too well the significant losses in merchantable timber associated with the formation of traumatic resin canals in pines.

There has beensubstantial research carried out in an attempt to develop greater understanding of what processes are going on following wounding that result in the resin canals, kino channels....

From my limited level of understanding it is more accurate to recognise that the formation of kino channels is often a function of traumatised parenchyma, and not derived from the vascular cambium. This (in younger trees) is often produced from the meristematic activity of the inner phloem parenchyma..this also involves the parenchyma rays.

Despite all the money poured into this kind of research by the pulp industry (kino channels are not what they need in their production process) to me at least more remains unknown than known regarding the chemical control over kino channel production.
 
Allow me to speak for the other knuckle draggers here when I say, Fark this kino, where do I put my chainsaw!

This is the greatest strength of our forum IMO.

I honestly am a little confused by the differences between kino and kino bands but I know Corymbia will do his best to educate me. I may be a lawn mowing wannabe but who knows, perhaps a little wisdom may rub off.

Give me a couple of days and I will have some more intelligent questions.

:cheers:

LOL, that's me.

I do have a basic understanding of CODIT and how it works but no where near on the level as some of these guys around here.

Thanks for an interesting, thought provoking thread. :cheers:
 

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