Yes I read that, a link would be appreciated though as it is on the thumb drive housing a massive majority of my journal article hoard, I would like another copy of the paper if anybody could oblige.

Nasty stuff, but for 100% increase in yield, damn, I'm game, strain dependent, that could equal another gram and a half of crude alkaloid per liter, which is going to equate to quite a lot of lysergic acid, and a great fucking big migraine for the local law enforcement donut gobblers.

If it is C.Purpurea, the weak H2O2 solution will be fine.

Bio 101 (failing to mention 'superoxide radical');

Hydrogen Peroxide

Plants release hydrogen peroxide (note;And superoxide radical, but it or its mechanism are not mentioned here)in response to the presence of a fungal invasion, which attacks by piercing the cell wall of a plant and breaking it down.

This hydrogen peroxide (chemical symbol H202) is a double edged sword in its defence against the antigen.

One Way : Hydrogen peroxide stops the breakdown of the cell wall

Certain pathogens will use pectinase, a digestive enzyme, to break down the cell wall barrier and invade the plant. The pectinase released by the fungus must be stopped. H202 is involved in halting the action of this pectinase in the following example;

The H202 is created and moves to the cell wall - the site of the invasion.
It reacts in contact with and enzyme called peroxidase, which promotes the breakdown of pectinase.
The foreign chemical is rendered useless.
Threat of the cell wall being compromised is removed.

Another Way : Some of the H202 triggers the creation of phytoalexins

Phytoalexins are similar to the antiviral proteins previously mentioned as a secondary line of defence. Phytoalexins are a family of hormones that inhibit protein synthesis and thus "shut up shop" in the event of a pathogenic attack by halting the protein production process in our cells.

Chemicals released by the fungus that are being used by it in its attack trigger a chemical response in the plasma membrane that makes the plant aware of the pathogens presence.
Hydrogen peroxide from the plasma membrane triggers a chemical response to inform the nucleus of the infected cells of the current situation.
mRNA from the nucleus is transported to ribosomes, as described in the protein synthesis section, where phytoalexins are to be produced (essentially protein synthesis coding for phytoalexins).
The phytoalexins then take on a role similar to that of antiviral proteins, where the presence of a phytoalexin in a cell inhibits protein synthesis and therefore preventing growth of the foreign agent by removing all possible avenues of invasion for the pathogen, thus eliminating the threat.

http://www.biology-online.org/1/12_cell_defense_3.htm

As such effective plant pathogens such as C. Purpurea have a natural ability to decompose peroxides.

Ergot, the genus Claviceps;

"Since infection-induced H2O2 production has been shown to occur outside host cells (Mehdy, 1994), we suggest a multiple function of fungal catalase in pathogenesis due to its hydrogen peroxide decomposing activity: (a) Cytotoxic effects to fungal cells are prevented. (b) Mechanical barrier formation during host defense reaction,
i.e., H202-mediated cross-linkage of cell wall components during oxidative burst or lignification, are suppressed. (c) In particular, in grass cell walls, a phenolic cross-linkage of polysaccharides is supposed to occur while cell walls expand during their ontogeny causing high cell wall rigidity (Carpita and Gibeaut, 1993). By suppression of those reactions, ergot fungi might maintain a convenient habitat for colonization. In the rachilla, infection induced cross-linkage of phenolics (see above) forestalls fungal colonization and, therefore, might efficiently control fungal growth."

this is what ive found too vesp actually getting your hands on a good fungi is very very hard.

still im always looking.

Mine are a bit old, ut hopefully still viable, they wouldn't be if they had been in the dirt naturally at the moderate temperatures they have, but since they have been kept buried in plastic bags in a sealed box underground and another batch in a fridge, hopefully that shouldn't apply.

Either way, I'l be going hunting again soon as its almost the season for sclerotia germination.

At least one species, quite unusually for a rust/smut fungus is eaten, Ustilago maydis is apparently sold in cans.

And yes, its JUST coming into season, so its time we got our arses out into farmers fields, canal banks, hell, last year a few sclerotia turned up in my back garden growing on Lolium species.

this is the thing how to select the right strain?
do you culture each one and do qauntitative anal. on each extract?

I don't believe extracts are needed, at least not at first.
One uses a solution that changes colors, such as blue -- the more blue it is, the more alkaloid there is present... thus it determines the best strain under those conditions, sort of a pseudo-quantitative method.

To mutate the strains for a better one -- you just add some mutanogentic chemical, and culture and test the tons of samples that are produced testing with the indicating solution. Isn't there a link or PDF of this on the thread? I thought I uploaded it, but perhaps that was somewhere else...

Ethyl methanesulfonate has been used, as has N-nitro-N-methyl-N-nitrosoguanidine.

Any other suggestions?

Personally I am not sure I would put my trust in things that just might make cultures a little more prone to mutation, that is to say, I am not convinced of the possible results, unless shown, and if it is something I am prepared to drink (not counting the fact that caffeine disagrees with me) then it can't be THAT strong of a mutagen.

Although I haven't yet checked the scimad thread.

I went and had a look along the local canal towpath yesterday, where there were quite a lot of sclerotia last year, and was quite annoyed, it seems those do-gooding fuckpots at the local council decided to spruce it up with a new surface, and obliterate the stands of Lolium and Bromus grasses that grew there.

Which will mean hoping my current batch from last year are still viable, although they should be, and going quite some distance to check another location.

As far as chemical mutagens go, they do indeed have differing modes of action, some swapping pyrimidine bases around, some intercalating, etc.

That sounds like said FOAF was full of shit, TBH, ergot feeds off the sugary juices flowing throughout the growing tissues of the plant, I doubt it would parasitize DEAD rye, infection starts at the immature flowering stage, then progresses as it matures.

Seems far too....ghetto for it to work.

And C.purpurea sclerotia need a cold spell to germinate, but actual temperature for GROWING is optimum at 20C.