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.
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