I.

The Missing Genetic Code

A. Ribonucleic Acid Anabolism
1. Replication
2. Translation
B. Nucleotides
1. molecular structure for nucleic acids, codons and genes
2. three component structure ( base, sugar, phosphate)
3. molecular structure for encoding genotypes for all genomes of all organic life forms on
 earth
C. Purines
D. Inosine Wobble Codes
1. Only purine or pyrmidine nucleotide or nucleoside which can form covalent hydrogen
bonds with three other purine-pyrmidine members of the genetic code set; I can pair with
Uridine, Cytidine, and Adenosine; distinct competitive advantage for genotype inclusion
since it reduces the numbers of tRNA synthesases needed to decode the genetic primer
2. Poly A and Poly I can form double helixes and were perhaps the first two purines
synthesized in The RNA World prebiotic period of evolution, HCN can generate adenine
and adenosine can deaminate to form water and inosine
3. Inosine with the OH side group begins purine oxidation and reduction processes while
creating a water molecule
E. Purine Metabolism
F. Amino Acid Synthesis
1. The Inosine Family
a. First Closed Purine Nucleotide Ring
(1) IMP
(a) Purine Nucleotide Metabolism
i) Purine Families
ii) The Adenosine Family
(1)
(2)
(3)
iii) The Guanosine Family
(1)
(2)
(3)
2. Inosine Wobble Amino Acids
a. Purine Nucleotide RNA Anabolic Starter
(1) Salvage Switch
(a) HPRT
(2) Catabolic Finisher
(a) XMP
(b) Xanthosine Oxidase
 (c) Uric Acid
G. Deoxyribonucleic Acid Catabolism
H. Pyrmidine Metabolism
II. Genetic Code
A. Genes
1. DNA
2. RNA
3. Inosine Wobble Amino Acids
a. tRNA synthesase for 8/20 standard amino acids can recognize inosine wobble anti-
codons (ala, arg, ile, leu, pro, ser, thr, & val) and either modify the amino acid peptide
chain post translationaly
b. A to I post transcriptional mRNA editing occurs before intron-extron splicing,
modyfying original DNA command and changing amino acid modules for glutamate,
which generates 95% of the Central Nervous Systems Post Synaptic Messages
c. three amino acids are part of the closed purine ring (gln, gly, asp) which is the most
basic and first molecular substrate for DNA replication and cellular stem cell mitosis
and meiosis
4. Amino Acids
5. Amino Acid Mutations
a. Single Nucleotide Mutations (SNPs)
(1) Guanine & Adenine Substitution Mutations
(a) 61% Of the "almost universal" genetic code is caused by the GA mutation
which changes the amino acid synthesis scheduling, mostly to a stop signal
(b) GA account for almost 50% of amino acid mutations found in genetic and
metabolic diseases
(c) I should be added to GA since it metabolic role is central to the cross signaling
of Adenine and Guanine
b. ATGC is transcription code; IUGC is translation code , ATUI is replication code
c. Guanine and Adenine GA or AG substitutions at the wobble position causes mutations;
inosine should be nucleoside with small hydroxyl group
d. 40% of amino acids are "at risk" for missing inosine instructions codes and covalent
pairings (I-U); (I-C); (I-A)
e. A to I post transcriptional mRNA editing changes glutamate calcium ion channel
receptors from glutamine to arginine; glutamine is primary ammonia and amino side
 group carrier; begins purine synthesis de novo which terminates the most complex (12
catalytic steps; di and trifunctional enzymes) synthesis in nature; the purine nucleotide
closed ring structure, the fundamental aromatic, hexagonic, heterocyclic for dna and
rna nucleic acids; photochemical and electromagnetic ciruit of DNA and RNA
B. Is incorrect, uses wrong mathematical operator; should use addition not substitution; ie. add
inosine as third purine nucleotide base, and donot substitute uracil for thymine in amino acid
synthesis; thus ending up with a new genetic code with six nucleotides and three pairs of
purine-pyrmidine nucleotides (A-T, G-C, I-U)
C. Introns and non-protein coding extrons are recessive nucleotides which code for the three other
macromolecular groups ie. lipds, carbohydrates, and nucleic acids
III. Atomic Molecular Evolution with The Missing Genetic Code
A. Sulfur
B. Pyrmidines
C. Metabolic Disorders
1. Opportunistic Internal & External "selfish" DNA based organisms
D. Genetic Diseases
1. Inosine, Xanthosine, Guanosine ammonia, uric acid diseases
2. Adenosine Deaminase A to I - SCIDS, Heart Disease, Serotonin depletion
3. IMPDH 1 and 2 - DNA synthesis malfunctioning; guanosine triphosphate and
deoxytriphosphate synthesis is blocked and destroys delicate checks and balances positive
and negative feedback mechanisms engineered into purine and pyrmidine metabolism
E. Enzyme Dysfunctionality
1. Catalying Conditions Unsuitable
2. Usual Protein Sizes Very Different
3. Amino Acids Mutations change Protein Functionality
F. Gene Suppression
1. Switching Signals Inverted
2. Cell Cycle Phase Shifts
3. Cell apotosis
G. Cellular Organelle Weakening
1. Mitochondria
2. Ribosomes
3. Cell Semi-Permeable Membranes
H. Protein Synthesis Disruption
 1. Replication
2. Transcription
3. Translation
IV. RNA Editing
A. Transcription
1. Post Transcriptional mRNA Editing
2. Post Translational Protein Modifications