This is exactly what I am after I think. I would be happy for a 1:1 at this stage by no means am I a breeder and understand anywhere near enough to even go down that path but a simple cbd dom x’ed with a thc dom if that makes a 1:1 then I’m ok with that.
At least i can get some interesting 1:1 which is fine.
So lets go a little further down the rabbit hole then if I may.
If I took the seeds from the first cross (1:1) and planted 2 more reversed one and pollinated the other from the first generation is that where things start getting all over the place? by that I mean differing ratios and cbd dom or thc dom etc…?
Yes exactly. Since chemotypes segregate as if there is a single locus (B), you can do a simple Punnet’s square to figure out a 1:2:1 ratio of THC dom (~20:1), intermediate (~1:1), and CBD dom (~1:20) plants). That is definitely simplified because you can also end up with plants with weird ratios like 1:5, 1:10, 1:50.
You could always just keep the ones with the effect you like, and not worry about their ratio. It’s just that if you like an intermediate type, then you can’t stabilize it in seed form, without also spitting out THC and CBD dom plants. (The exception to that would be if there were an extremely rare crossover within the B-locus that brings together functional CBDAS and THCAS genes. In which case they would be linked together and you could have a true breeding intermediate. Supposedly Medicinal Genomocs has such a line.)
That’s about CBG inheritance. Type 4 plants (CBG dominant) occur when both the THCAS and the CBDAS genes are nonfunctional on both copies of the genome (recessive). If you have THC or CBD dominant parents, they have at least one copy of functional THCAS/CBDAS. This would only be relevant if one of the parents has a hidden recessive B-locus with nonfunctional THCAS/CBDAS.
Thanks that’s what im after a good mix of both to see what the medicinal effects are with differing strains that aren’t being crossed that I may have some interest in crossing.
Do you hold classes? Lol. Great info… but tough learning. Can you recommend any books on the subject? I find this fascinating. So, if by blind luck I happen to breed two ( non stable) 1:1 ratio plants, does that ratio happen in 2 out of 20 the next round of growing if it was 1 out of 20 the first generation? And with another lucky round 4 out of 20? It does seem nearly impossible if thats the case to do with luck alone. I see now why these ratios are hard to come by in predictable fashion.
If you have a 1:1 plant that is the offspring of a CBD dominant and THC dominant plant, it has one functional THC allele and one functional CBD allele. They are codominant. The parents are Bt/Bt x Bd/Bd; the offspring is Bt/Bd.
Assume the following: (I don’t know how to do subscripts on here so I made an image)
It can be treated as a simple, single locus cross in a Punnet’s square (ignoring very rare crossover events):
The original F1 cross being Bt/Bt x Bd/Bd. All offspring are Bt/Bd:
The F2 cross of a 1:1 ratio plant is Bt/Bd x Bt/Bd. Offspring will be 1:2:1 Bt/Bt:Bt/Bd:Bd/Bd. So a 1:1 crossed to a 1:1 (or selfed) gives you a 1 in 2 chance of having intermediate progeny in the next generation, not 1 in 20. If you choose two 1:1 plants from the parent population, the rarity of those plants among the parent population doesn’t matter anymore.
Is this based on one gene controlling both THCA and CBDA production?
That’s what it looks like with pairing of allele and the co-dominant behaviour you are describing.
THCA and CBDA genes are found on chromosome 6 have been found to be two distinct genes.
In your case above you would be assuming both allele from each gene would be dominant and homogeneous; if each gene carried one dominant and one recessive allele the probability becomes less; if the two alleles for each gene are co-dominant this becomes much more complicated.
To be fair there were two theories, one in 2003 (de Meijer et al. 2003) and one in 2006 (Kojoma et al. 2006). It wasn’t until the genome was recently mapped until they found it was two different chromosomes.
Could you explain this? Its very confusing to me. Not your wording by any means, just this part. Your explanation of the Bt/Bd alleles was great, and I’m starting to get that part of it, thanks… So you’ve got 20 plants and 1 is thc dom(20:1.) You have another 20 plants and one is cbd dom(20:1)and a 1:1 ratio of intermediates? How do you get 1:2:1 ? Or am i completely lost?
I get this part. I may have misinterpreted your earlier post. Difficult stuff. I’ve been reading a book on that, but i really need to read something like that many times.
There are two genes that are very closely linked and rarely cross over. For practical purposes you can pretend they are one gene.
They are codominant. If both THCAS and CBDAS are expressed, you get intermediate plants. If you have plants with functional THCAS and CBDAS on the same chromosome, the punnet square I made doesn’t apply. But when starting with a THC dom plant and a CBD dom plant, we know that each parent can only donate a functional THCAS linked with nonfunctional CBDAS, or functional CBDAS linked with nonfunctional THCAS, respectively. Since these rarely cross over, we can treat it as a single locus. To find the rare crossovers, you would need to grow many, many plants, then either perform molecular tests on them or inbreed them and find stable, intermediate lines.
If you have a THC dom plant and cross it to a CBD dom plant you will get a 1:1 ratio I’m all progeny. The subsequrnt F2 progeny of that cross will yield a 1:2:1 ratio. If you make that cross and get 20 offspring, you can expect ~5 THC dom, ~10 1:1, and ~5 CBD dom.
Two competing theories are supported by existing data:
In one, CBDAS and THCAS are mutually exclusive alleles (i.e., very different isoforms, as the protein sequences are only 84% identical). Genetic analysis supports this model, with approximately 1:2:1 segregation of chemotypes in a cross of drug type versus hemp (de Meijer et al. 2003).
An alternative model is that THCAS and CBDAS are closely linked (i.e., adjacent on a chromosome), and one or the other is inactivated in drug-type or hemp strains. This model was motivated by the discovery of a THCAS -like gene in hemp plants (Kojoma et al. 2006) and is consistent with the possibility that these related genes are derived from an ancient tandem duplication.
Evidence from the genome suggests the second theory is correct.
Either way I have kits on the way, I’m sure everyone does different tests. The main trade off is genetic testing ($$$) saves time and space from having to back cross & sibling cross to find traits in their children.
Yes, I have read that paper. There are definitely two different, tightly linked genes that rarely cross over. (Laverty et al, 2018). They can be treated as mutually exclusive for practical purposes for simple breeding projects, but they are actually not.
One thing to note about the notion that this “should make it possible to separate them during breeding to grow plants without THC.” is that cloned CBDAS has been shown to produce small amounts of THC from CBG in vitro (I am having trouble finding this reference at the moment). These ezymes can be “leaky” which makes sense, given THCAS likely evolved from CBDAS. Different variations of CBDAS are likely more or less leaky than others. There is also potential that CBCAS also produces some THC.
Okay, they are only theories. Personally I wouldn’t use Punnet’s square for anything other than dominant and recessive allele. Not co-dominant or linked genes as they challenge Mendel’s law.
With your theory you will get a 1:1 THC/CBD ratio; 1:2:1 ratio of offspring. Not all offspring will be 1:1 and a test kit will be required to find the ones that are.
The chromosome map and the McKernen paper
discussing a stable intermediate line, are convincing lines of evidence (to me at least) to support that that the hypothesis that THC/CBD determination was a single, mutually exclusive locus is wrong, and there are two distinct, nonmutually exclusive genes. But they, and I, could be wrong. Regardless the crosses act as if it’s a single locus, so for all but the most rare circumstances (and definitely for the purpose of the original question asked in this thread), you can assume it will act as a single locus.
In the first generation (F1) of a CBD dom and THC dom cross ALL will be 1:1 (unless, say there is a super rare null, recessive B-allele but this can be assumed not to be present unless you know it is in your genepool (ie CBG plants when homozygous)).
Codominance is fully in line with simple Mendelian genetics and Punnet squares. THCAS and CBDAS are codominant when expressed together. They compete for, and share the CBG precursor, with some variation for enzyme affinity or possibly expression levels.
Linked genes are are a known exception to the Law of Independant Assortment. Why wouldn’t you account for that since we know these are linked?