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rockyfungus
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Endochitinases (E.C 3.2.1.14) and exo-chitinases. The endochitinases randomly split chitin at internal sites, thereby forming the dimer di- cetylchitobiose and soluble low molecular mass multimers of GlcNAc such as chitotriose, and chitotetraose.[19] The exo- chitinases have been further divided into 2 subcategories: Chitobiosidases (E.C. 3.2.1.29),[20] which are involved in catalyzing the progressive release of di-acetylchitobiose starting at the non-reducing end of the chitin microfibril, and 1-4-β-glucosaminidases (E.C. 3.2.1.30), cleaving the oligomeric products of endochitinases and chitobiosidases, thereby generating monomers of GlcNAc.[19]
Our meds tend to target steroids, cell walls, or protein production. Went down a rabbithole of trying to find what bacteria we used to develop anti-fungals and what their mechanism of action is.
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007184
Best I could find. I like cell biology and microbiology...
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rockyfungus
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Speaking from a human physiology point of view. Scalloped edges, uneven borders, thicker borders, raised areas, change in colors, etc are not NORMAL. Basically things that human pattern recognition software picks up. Are these abnormalities idiopathic (genetics for simple sake) or true pathology?
Something is either impeding growth, taking up mass, stealing nutrients or blood (let's call it water?), or hacking cellular mechanisms. Obviously these mycoparasites like most human pathogens don't want to kill the host outright. They need to parasitize a host but not disrupt it's lifeblood.
We are only talking about "biotic" life here aren't we. What about the billions of viruses that most likely causing issues as well.
Wouldn't a germination plate have the highest concentration of microbes if we are working in true aseptic fashion?
We try and grab way from those notches as best chances are far away from the "odd" part. Did those clean plates come from anywhere near the notch?
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rockyfungus
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I could be completely off base. For commercial growers they just transfer these known commercial strains? Are they reaching senescence and weakening the "immune system" of the myc.
Like my 3015 is god knows how far out it is? It came from agar, I've received LCs for gourmet. I've tried to go back to spores from own grows but at that point it's not 3015 I'd imagine.
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rockyfungus
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Didn't read the whole thing just what you got. Viruses are in you, part of your DNA. Probably along those lines.
All this genetic material is prayed on by viruses. So spores are a honeypot I guess.
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rockyfungus
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Re: Mycoparasite/Mycovirus Discussion [Re: Stipe-n Cap] 1
#27526825 - 11/01/21 07:36 PM (2 years, 2 months ago) |
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rockyfungus
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What's the NM on that thing? UV leads to reactive oxygen and nitrogen that damages major cellular pathways. DNA and lipid membranes mainly. This leads to cytotoxicity (cell death), mutations, and alterations in cell signaling.
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rockyfungus
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 Not sure if mycovirus. Hispanica I keep germing and getting a feathery appearance with zones of clearing as it grows. It never forms a nice round colony just feathers.
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rockyfungus
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I'll keep it short as I'm not 100% sure on the language and only read your excerpts. Also nothing is a "virus" in the study. It's a parasite they took genetic info from and inserted into a bacteria (plasmid)??
Mycoviruses don't traditionally hijack a cell extracellularly. Viruses typically find a receptor attach and inject genetic material.
Fungal viruses are active in hyphael networks and spores? How do they get in?
The 2nd blurb is how they got the genetic material in. They had to destroy the cell walls of a parasite so it could take up genetic info and form spheroblasts. Sphereoblasts could only enter a (damaged?) hyphal network. They destroyed the hyphaes and rebuilt them? Which I suppose this parasite is resembling the mycovirus to prove they can only infect through those processes?
So where in growth does hyphal colony have shedded cell walls that can be infected. Or how do spores get infected? Basically is there a place in fungal reproduction where it's hyphael network is bare and exposed?
Rambled if you have a direct question I can try and break it down. Or if you want a term broken down. I hate explaining stuff to other mycologist like they don't understand science. I've done a fuck ton of biology so some words are standard. The more educated people get in a singular field the less they understand what normal people know. So if you need it explained like your 5. No worries I'll try.
Edited by rockyfungus (02/23/22 08:28 AM)
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rockyfungus
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Someone should send you a known culture already colonized, see what happens? Or flip. Work somewhere else with fresh clothes, tools, print. Fruit at normal place and elsewhere and compare?
Or you just picked a turd or need to dial those conditions in
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rockyfungus
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Unrelated but possibly related? Was reading about the parasites I may come in contact with in my line of work. The trophozoites are mobile and consume bacteria (which allows for the diagnosis on E. coli plates). The trophozoites form double walled cysts which are incredibly resistant to methods of eradication (including freezing, heating, and irradiation).
Not going to dig but do they eat fungi?
https://en.wikipedia.org/wiki/Trophozoite
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