Quadruplet expanded DNA (QED) genetic code for eukaryotic cells**

Abstract

Abstract Genetic code translates eukaryotic cell genes into proteins for maintaining a homeostatic state. However, gene variants, transcription, and splicing errors yield dysfunctional proteins causing monogenic rare, multigenic cancers and neuro-degenerate diseases. The triplet genetic code encodes a protein but lacks gene, transcription, and splicing controls. Furthermore, alternative orthogonally expanded genetic codes failed to synthesize proteins using canonical amino acids. The QED codon was developed to overcome these limitations. While verifying the triplet genetic code, 1968 Medicine Nobel laureate H.G. Khorana observed that self-complementarity forming adjacent bases, Poly r-AU, did not promote polypeptide formation, a noncoding trait. The QED noncoding codons have similar traits. Here, the QED codon model is assumed to comprise all four DNA bases (T, C, A, and G); the code is position-independent and symmetric. The self-complementarity forming adjacent bases (AU) and (C G) with any two NN (N any T, C, A, and G) bases are noncoding. Under these QED assumptions, 256 quadruplets fall into two groups: 20 independent protein-encoding codons and 35 independent noncoding codons applicable to regulating and controlling synthesis, transcription, and splicing processes. Steps to correct dysfunctional proteins are described, anticipating strategies for developing cures for monogenic rare, multigenic cancers and neurodegenerative diseases. **Patent Pending