breeding Peppers with "dominant heatless"?

So you were referring to C. chacoense (pun-2 pungency genes), not chinense, right? (meaning putting together pun-1 and pun-2). If so, according to the linked paper, non-pungency in chacoense is recessive too, and pun-2 is epistatic to (has an influence on) pun-1. That said, non-pungency will always be a recessive trait. But i could be wrong because after reading that my brain is melting :rofl: so please correct me.
I wasn't, though I thought about that since you asking and the interrelationship of pAMT mutations is an intriguing subject, including the epistatic effect between Pun1 and Pun2/pAMT and how that effects probability distributions in the progeny of Pun1 x Pun2/pAMT crosses. I may post about that elsewhere so as not to disrupt this thread more than I'm about to.

I was thinking of a cross of nonpungent pun1¹ and pun1² varieties, focusing on only the Pun1 locus so no Pun2 locus / pAMT gene involvement. Because nonpungent annuums are commonly the result of pun1¹ mutations and and nonpungent chinense, commonly pun1² mutations, while it may not be the only way to achieve it, it seems an interspecific hybrid could be at least a common way to achieve it.

As to whether nonpungency is always a recessive trait, that seems to get a bit tricky. All the alleles I've seen are recessive, but it's interesting to consider pungency expectations for the pun1¹ and pun1² cross at the Pun1 locus. Considering the F1 generation, the intuitive answer is that because each of pun1¹ and pun1² is a recessive mutation and neither allele pairs, we don’t get nonpungency, thus the F1 hybrid would show pungency. However, in this case the F1 receives one nonfunctional recessive allele from the homogenous P1 parent and a different, but corresponding, nonfunctional recessive allele from the homogenous P2 parent, thus no functional Pun1 allele is present in the F1. The pun1 gene will lack the essential coding for the acyltransferase enzyme allowing for the acylation of vanillylamine, the direct precursor to capsaicinoids, i.e., the gene is fatally flawed as to producing capsaicinoids. This indicates nonpungency. Further, because the required alleles for pungency are not present, all progeny will be nonpungent unless hybridization reintroduces the wild allele. At F1, the cross is already stabilized as to nonpungency.
BTW there were also references to populations of C. eximium to be studied: as C. chacoense they are polymorphic regarding the pungency, so never say never...
It great to see how much scientific attention peppers are getting. I read that PI594141 is a nonpungent pepper which was originally identified as eximium, but was recently reassigned to frutescens, and that it has the pAMT based qualitative loss of pungency. Beyond that I don't know. Lot's to read and it's not always the fastest reading ;)
 
Chili Planet still has Aji Dulce seeds. Aji Dulce 2 is the Habanero-looking strain, so probably also Pepperseeds.eu and Semillas. Welsh Dragon Seeds, Chilli.top, Bienes-Seeds, Pepperseeds.eu, and UK Chilli Seeds have Venezuelan Tiger seeds.
Ahh I see your from Germany too 😁.

From where di you get your seeds and dibyou already grew aji dulce 2? Because some shops may sell crossed seeds
 
Further, because the required alleles for pungency are not present, all progeny will be nonpungent unless hybridization reintroduces the wild allele. At F1, the cross is already stabilized as to nonpungency.
Technically speaking, there would still be the extremely low chance of a crossover directly between the non-overlapping pun1¹ and pun1² mutations that would restore the wildtype gene... :)
 
Technically speaking, there would still be the extremely low chance of a crossover directly between the non-overlapping pun1¹ and pun1² mutations that would restore the wildtype gene... :)
Seems like there's always a chance of something unexpected happening when peppers cross! Do you mean this in a "life finds a way" sense or are you aware of a genetic process by which this could happen. In this case, I'm not aware of a standard mechanism that could result in pungency. Despite that pun1² has the information missing in pun1¹ and even if the frameshift insertions in pun1² don't overlap pun1¹'s deletions in the promoter region or exon 1, each of the alleles exists distinctly from the other and will be separately transcribed to mRNA which will each then fail to produce the protein required to support the pungency pathway.
 
I was talking about chromosomal crossover after fertilization that randomly shuffles chromosome stretches from male and female parents. A shuffle border right between the two mutations in close proximity could combine the healthy wildtype stretches next to the mutations into one chromosome, thereby restoring the wildtype gene. The extremely low chance for that (in general there are less than 10 crossovers per chromosome) is also the reason why you would almost certainly end up with only one of the two mutations in your stabilized line. 🧑‍🏫
 
I was talking about chromosomal crossover after fertilization that randomly shuffles chromosome stretches from male and female parents. A shuffle border right between the two mutations in close proximity could combine the healthy wildtype stretches next to the mutations into one chromosome, thereby restoring the wildtype gene. The extremely low chance for that (in general there are less than 10 crossovers per chromosome) is also the reason why you would almost certainly end up with only one of the two mutations in your stabilized line. 🧑‍🏫
Thanks for your responses. I have some follow up thoughts on the applicability of gene conversion versus crossing over in this case, and realistic probabilities and what not, but I'll save that for another time and place. Cheers.
 
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