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Nickrosis
Manned by Boderators
Reed? :angel:
Sure.
Avirulance factors result in the expression of a number of defense-related genes that are also induced during a more natural and regulated hypersensitive response. That's the principle of Toronto's direction - a common link between the activation of defense gene expression during a hypersensitive response or induced response from a mutated variety. Either way, they trigger the production of active salicylic acid accumulation, which is required for the expression of both that hypersensitive response and systemic acquired resistance, a dirty word in most pathology circles. The Texas Agricultural and Mechanics University adamantly denies the existance of said mechanism so where do we go and who do we listen to?
Infection of plants expressing salicylate hydroxylase, which prevents the accumulation of salicylic acid, or npr1 mutant plants, which are defective in the expression of systemic acquired resistance at a step downstream of salicyclic acid, demonstrated that the signaling pathway activated from disease exposure overlaps with the systemic acquired resistance activation pathway and is salicyclic acid dependent. Interestingly, plants expressing salicyclate hydroxylase exhibited increased sensitivity to infectious parasitic systemic fungi. Those test results demonstrate that disease activates at least two distinct signaling pathways, including a salicylic acid dependent pathway previously shown to be associated with the activation of pathogen defense reactions, and that this latter pathway also induces a protective response similar in nature to tylosis - the compartmentalization of wilt, or it's attempts at. I believe strongly that injection treatments of propocanozole in actively infected trees finds often little uptake and distribution due to this defensive reaction but hey, what do I know...I still maintain that trees have response mechanisms and dirt is something a bit more complex than a holding media for plant growth.
There's no combining the two and as a mutant form of influenza heridotalea triggers the Tcell response in humans, I always thought Toronto's a few steps ahead of the game. Avirulance is a key to disease intervention. All we got to worry about is the competition and marketing skills of the developers.
Aside from that I'm with different trees and a different disease. Only similarities are akin to leukemia compared to melanoma.
Aside from that understanding I haven't injected any E.G. into any elms - ours are healthier than most trees here albeit slightly more native.
Avirulance factors result in the expression of a number of defense-related genes that are also induced during a more natural and regulated hypersensitive response. That's the principle of Toronto's direction - a common link between the activation of defense gene expression during a hypersensitive response or induced response from a mutated variety. Either way, they trigger the production of active salicylic acid accumulation, which is required for the expression of both that hypersensitive response and systemic acquired resistance, a dirty word in most pathology circles. The Texas Agricultural and Mechanics University adamantly denies the existance of said mechanism so where do we go and who do we listen to?
Infection of plants expressing salicylate hydroxylase, which prevents the accumulation of salicylic acid, or npr1 mutant plants, which are defective in the expression of systemic acquired resistance at a step downstream of salicyclic acid, demonstrated that the signaling pathway activated from disease exposure overlaps with the systemic acquired resistance activation pathway and is salicyclic acid dependent. Interestingly, plants expressing salicyclate hydroxylase exhibited increased sensitivity to infectious parasitic systemic fungi. Those test results demonstrate that disease activates at least two distinct signaling pathways, including a salicylic acid dependent pathway previously shown to be associated with the activation of pathogen defense reactions, and that this latter pathway also induces a protective response similar in nature to tylosis - the compartmentalization of wilt, or it's attempts at. I believe strongly that injection treatments of propocanozole in actively infected trees finds often little uptake and distribution due to this defensive reaction but hey, what do I know...I still maintain that trees have response mechanisms and dirt is something a bit more complex than a holding media for plant growth.
There's no combining the two and as a mutant form of influenza heridotalea triggers the Tcell response in humans, I always thought Toronto's a few steps ahead of the game. Avirulance is a key to disease intervention. All we got to worry about is the competition and marketing skills of the developers.
Aside from that I'm with different trees and a different disease. Only similarities are akin to leukemia compared to melanoma.
Aside from that understanding I haven't injected any E.G. into any elms - ours are healthier than most trees here albeit slightly more native.
Nickrosis
Manned by Boderators
Did you just type that in under 3 minutes?
Oh crap, that doesn't answer your question does it?
Since my focus - more so the last fourteen years with the exception of the last three - was concentrated on immune-response and not disease eradication per se, I've had the opportunity to study thousands of abstract presentations on that particular arena of thought. The complexities are quite simple really, learn the plant's response to threat instead of a designed programme to kill the threat. Systemic antibiotic treatments have only recently been examined and only because of detection abilities to "see" the chromosomal adaptations of resistance and find out why - those mean little bacilli are quite adept at change and quicker than we are to emerging threats. Beautiful creatures to study - hopefully we could learn from them but insist we're better so little chance at getting the gold, silver, or bronze in this contest - they are winning.
I've always suggested that the initial attempts of control were responsible for the increase in virulance of this little cutie - oak wilt. I haven't been privy to or too concerned about D.E.D. but my suspicions are similar.
It's a marketing thing, everything in America is.
Since my focus - more so the last fourteen years with the exception of the last three - was concentrated on immune-response and not disease eradication per se, I've had the opportunity to study thousands of abstract presentations on that particular arena of thought. The complexities are quite simple really, learn the plant's response to threat instead of a designed programme to kill the threat. Systemic antibiotic treatments have only recently been examined and only because of detection abilities to "see" the chromosomal adaptations of resistance and find out why - those mean little bacilli are quite adept at change and quicker than we are to emerging threats. Beautiful creatures to study - hopefully we could learn from them but insist we're better so little chance at getting the gold, silver, or bronze in this contest - they are winning.
I've always suggested that the initial attempts of control were responsible for the increase in virulance of this little cutie - oak wilt. I haven't been privy to or too concerned about D.E.D. but my suspicions are similar.
It's a marketing thing, everything in America is.
My ears were buzzing while I was typing it.
You asked my opinion and when I gave it - you asked again while I was busy doing it!!
Same with this last one - some days I'm wired and some I'm not - LOL. You should see what else I got cooking tonight.
You asked my opinion and when I gave it - you asked again while I was busy doing it!!
Same with this last one - some days I'm wired and some I'm not - LOL. You should see what else I got cooking tonight.
