Alright, it is kind of long so I am going to copy and paste my post from another forum:

"Would it be possible to acquire a lab source with a license to handle ergot fungi? You could potentially supplement N-ethyl-L-tryptophan to produce ETH-ergotamine, then possibly do a peptide coupling reaction using COMU as reagent, sym-collidine as Lewis base, and DMSO (instead of DMF) as solvent?

I know you were (understandably) wary of the idea because I couldn't find use of biosynthesis in ergot itself. However, i did find lots of resources using biosynthetic methods, including penicillin, yeast, e coli, and flavobacterium (http://www.google.com/patents/US4016037 here they made biosynthetic 3,4-methylenedioxy-L-phenylalanine starting from a semisynthetic hydantoin; hydantoin is an antibiotic, the bacteria are resistant to it, and so they break it down into amino acids)

Anyways, I did find one mentioning of biosynthesis in ergot culture! Check it out:

https://psychonautwiki.org/wiki/LSA_adducts http://www.nature.com/nature/journal/v187/n4733/abs/187238a0.html http://www.nature.com/nature/journal/v192/n4802/abs/192552a0.html

It states that adducts with LSA, an amide, can form adducts with aldehydes. In the paper it is stated that after submerging a culture of ergot in fermenting liquor, which has extremely high levels of acetalhyde, the resulting ergot had especially high levels of LSH, lysergic acid hydroxyethylamide, which is usually highly unstable and occurs only in trace amounts even in the most LSH-rich ergot strains. Generally it is known that aldehydes can do this with amides without a catalyst, but the reaction is reversible. In ergot, it seems to happen biosynthetically (catalyzed by enzymes, that is) because LSH typically degrades rapidly within minutes into LSA. Therefore, if it were just occurring as a natural reaction on its own, it would be reversible and all the LSH would eventually breakdown entirely over time. Since the highly elevated LSH levels were recroded after the full ergot life cycle, which is several weeks, if seems that the enzymes in the ergot are biosynthetically using the acetaldehyde to produce LSH at levels otherwise unattainable! This makes sense because the major ergot alkaloids--ergotamine, ergocristine, etc--are adducts between the amide LSA, and beta-peptide proteins.

So I think this could lend a lot of support to the idea of biosynthetic ergot manipulation!!

One argument at this point, could be that the N-ethyl itself could cleave off, that the ring cyclization steps would possibly cleave any substitution, barring any N6 ergotamine analogs. However, I found some a reference that supports evidence in favour of N6 ergot biosynthesis:

http://metacyc.org/META/new-image?type=PATHWAY&object=PWY-6503

In this bionsyhtetic pathway for ergotamine in ergot fungi, it shows that L-tryptophan is first converted into 4-dimethylallyl-L-tryptophpan, which then becomes (in a separate, N-methylation step) 4-dimethylallyl-L-abrine (abrine being n-methyltryptophan).

After this point, many steps involving ring cyclization follow without disturbance of the N-methyl group. Although the N-methyl is way more stable than say, an N-ethyl placed there, it does indicate that the ring cyclization steps occur without cleaving N-substitutions on the tryptophan.

It also seems that the alpha-carboxyl on tryptophan is important for the ring cyclization steps, so it cannot be a basic tryptamine. There are two other ways I can think of to (maaayybbeeee) improve potential yield and maximize full conversion:

1) I imagine it would be a far more expensive synth, but something like 4-dimethylallyl-N-ethyl-L-tryptophan would bring the biosynthesis a significant step closer to the final step, although it's quite likely (even probable) that producing it synthetically would lower the yield more than just adding simple N-ethyl-L-tryptophan and simply letting it to go through the enzymatic step.

2) In the paper where they biosynthetically made ethocybin from DET in magic mushrooms, they said the mushrooms took a few weeks longer to fully grow. It seems adding it right from the beginning resulted in the mushroom's enzymes having to catch up--after all, the enzymatic process I am sure occurs in sequential order. This is further confirmed because they added NMT into the culture, and instead of producing more psilocybin, it instead produced highly potent levels of baeocystin, with almost no psilocybin whatsoever. This implies that the process goes in sequence--sure, the mushroom has N-methyl transferase enzymes within it, but once it is saturated with NMT and recognizes it has an already substituted tryptamine on its hands, it doesn't bother. It recognizes that biological step is done and carries on in sequential order to the next. The paper for that is here:

http://files.shroomery.org/cms/Biotransformation_of_tryptamine_derivatives.pdf

Basically, this all leads up to the idea that, perhaps if you supplemented the tryptophan analogue later into the erogt life cycle (perhaps one week after growing, maybe 3 weeks, or something), the yield will be higher simply because the fungus will be at a stage in its life cycle where it is producing more of the necessary enzymes. Also, in the case of the DET, which seemed to stall mushroom growth, this seems to imply that the DET sat in the culture, being totally unused, simply degrading! Maybe then if you add the analogue later on, the fungi will be ready to pick up on it by then, because it will already be in the midst of producing its own abrine analogs itself.

Therefore, if it were done, the ergot trials could be split into different control groups, where the analog was added into culture a week into life cycle, 2 weeks, 3 weeks, et cetera, and then the comparative yields could be used to determine the best point of supplementation. it should also be mentioned if the biosynthetic route worked, you could make equally large yields of 5-MeO-LSD and 5-Bromo-LSD! By the way, there's a reference on the internet for 5-HO-LSD, which has the internal moiety of bufotenin (as opposed to DMT in LSD). They refer to it as 12-OH-LSD:

"The process (which follows) is somewhat complicated and an easier dehydrogenation process may work. 2,3-dihydro-LSD can be converted directly to 12-hydroxy-LSD, which has about the same activity as LSD and this process is also given below."

https://www.erowid.org/archive/rhodium/chemistry/psychedelicchemistry/chapter7.html

Also as indicated by the quote above, they seem to have found 5-HO-LSD to be very similar to LSD, although I imagine it would be a rather gross and nasty trip. The reaction involved is based on the same process in which indoline is reacted to form 5-hydroxyindole. They used Fremy's salt as the oxidizing agent. There are other papers indicating that palladium (II) acetate would have a much higher yield than Fremy's salt as the oxidizing agent."

Basically, we found a paper confirming that 5-methyltryptophan was supplemented into ergot, and successfully converted into yields (http://jb.asm.org/content/125/1/158.full.pdf)