This post continues my look at the genetic code with the
idea that dimers may have had a major impact on its
development (Dimer being between any two pyrimidines on the
same strand of RNA caused by UV light damage.)
The stop codons are UAA, UAG, UGA UGG (is tryptophan and may
well have initially fit in here too)
Note all the above have
1. U+purine+purine That suggests that the anti codon on the
tRNA had the complementary base pairing of
A+pyrimidine+pyrimidine and those two pyrimidines would be
a likely candidate for a dimer damage thus stopping the
coding process.
Therefore stop codons may stop because it sets up two
pyrimidines in a row - and they turn into a dimer that can't
be coded. End of genetic message.*
2. No C That suggests why CAA, CAG, CGA, CGG, the other
pyrimidine, +purine+purine are not stop codons.
Deamination may well have turned C to U and kept C out of
the code at the start - at least until this was frozen.
***
And what about the start codon?
It may also have a possible dimer clue. Start = AUG This is
purine,pyrimidine, purine, (and again no C)
Note: there is no chance for two pyrimidines to be adjacent
in the codon or with the bases on either side of the
codon. (though it is also true that GUA should work
and it does not)
All this is certainly speculative, yet it seems to also be
falling into place quite nicely.
How do others feel about dimers as being a key to the
development of the genetic code from this and the numerous
other posts exploring this possibility?
*One comment was that dimers could not be replicated. Yet
thematching strand can be, and IF the dimer was on the
anticodon - tRNA side, any coding would probably work
reasonably well.