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Oh my giddy aunt, Science Week


Marcus B-T
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Just had a conversation with a top mycologist at Cambridge University about why things like Meripilus (No the network hasn't died that was one of the reasons I made contact with her) become pathogenic. And my giddy aunt is it all potentially complicated but realy interesting. I am going to try to distill the info down into something that makes scence to everyone (including myself), but just to say our perception of what is going on is likely to be so wrong it's frightening. Also would like to say if you ever want something to get the kids interested in science and learning get them along to the Cambridge Science Festival (actually if you don't have kids and you want to learn more about science get yourselves along) there is loads of stuff going on tomorrow Saturday 21st. Google Cambridge Science Festival and loads of stuff will come up.

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No the network hasn't died that was one of the reasons I made contact with her)

 

 

 

but just to say our perception of what is going on is likely to be so wrong it's frightening.

 

 

 

Awaiting some dates from you Marcus

 

 

Intriguing :confused1:

I'm all agog with anticipation :001_smile:

 

 

 

 

.

Edited by Monkey-D
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Right here goes. Now you have to understand two things before you read on. Firstly I am not a mycologist so I am simplifying as much for myself as for you who are reading this. Secondly it is simplified since if I went in to details it would be a very long posting.

 

The fungi like basidiomycota (your mushrooms and toadstools) can produce sexual spores (male and female bits) and when these come together they form a new fungi. Now both spores could come from the same fungus but they could come from other fungi. Some fungi will exclusively cross fertilise with other fungi, this means there is potential for a large amount of genetic variation, because each time two fungi get togther they share thier genes and produce a whole range of new fungi that represent the genetic makeup of both of them (this is fairly straight forward and if you think about how kids share their parent genes you will get the picture here). Now this means that rather than their being one type of fungi or two types or what ever, there is a range of fungi of the same species. Some may prefer to be saprophytic and live on dead material, others will prefer to take this a stage further and invade the 'dead' materail in the centre of large trees, others will be truely pathogenic and look to invade the living parts of trees. But remeber we are potentially still talking about the same species. Howevere, when the prefered food source is used up the fungus will look to what is still available, and because it has some of the genes that allow it to use these other sources it switches to them, but it isn't as good as others and so its use of the resources is slow waiting for the tree to become stressed perhaps, or waiting for dead material to be partly broken down. If the tree is invaded by a pathogen it can react and counteract the presence. The success of this process is partly then down to the genetics of the tree but also the genetics of the fugus, i.e. how pathogenic it is.

 

When I heard all this a little light bulb went on in my head. Because what this will manifest itself as to us with visual symptoms is 'variability' and 'uncertainty' as to what is happening. And isn't that just what we see in our day to day observations of trees and fungi? We have perhaps what we might call expected or usual symptoms with a particular fungi and tree association, but then we have a number of other examples that just don't seem to fit. This is genetic variation of fungi and hosts in action.

 

So you might think this makes it imposible to call what is happening, but no. If you can understand the way in which genetics and environment interact in these systems then they become understandable, i.e. you understand why the variations happen and the mystery is removed.

 

Please do reply and coment on this.

 

Regards

 

M B-T

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So it could well be that G. applanatum and G. adspersum/australe are quite possibly one and the same, varying their decay stratergies and form according to situation.

 

Would make a heap of (up till now unquantified) sense.

 

Possibly why there is no diffinitive within the community (Londsdale,Butin,Green,Mattheck,Strouts,Jordan,Kaizer et al) to Id'ing these individually and positively.

 

Also the possible two different forms of Merip, that JFL talks on, would fit in neatly to this hypothosis.

 

 

 

Interesting post Marcus, would be keen to hear Andrews view on this.

Anychance you could nudge him along :wink:

 

 

.

Edited by Monkey-D
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Not just two forms but thousands of forms. If you imagine it more as a sliding scale rather than either or, this is probably close to reality. The are things called Quantitative Trait Loci (QTL) and these are genes that don't just switch on and off but are expressed more and less in reseponse to changes in the environment. It is highly likely that both the trees and the fungi have them, and so as the environment, the trees and the fungi change, the expression of the QTL will change.

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