The expansion of the specific trinucleotide sequence, [CTG], is the molecular pathological mechanism responsible for the clinical manifestations of DM1.
The mutation frequency for a given trinucleotide sequence is therefore proportional to e(−VSSE/ kT ).
The disorder is caused by dynamic mutation of a single trinucleotide sequence, CGG, on the X chromosome.
The origin of DM is an expansion of the trinucleotide sequence CTG in the 3'-untranslated region (UTR) of the DMPK gene.
A3G preferentially edits the third cytidine in a 5'-CCC-3' trinucleotide sequence context on single stranded DNA, whereas it is unable to edit double stranded DNA or DNA/RNA hybrids [6], [23], [24].
A number of trinucleotide sequences in DNA can form compact and stable hairpin loops that may have significance for DNA replication and transcription.
Thus, our findings suggest that fungi in the Pucciniomycotina exhibit RIP-like hypermutation of specific trinucleotides in repeated sequences or that there exists a characteristic of regulatory cytosine methylation in these fungi that is previously unseen among Eukaryotes.
The zinc-finger domains are composed of a series of four to six 30 amino acid domains that can bind to trinucleotide sequences giving the entire DNA-binding domain specificity to 12 18 nucleotides.
For a DNA region, the sequence is divided into overlapping di- or trinucleotide sequences.
Song, X. & Cao, X. Context and complexity: analyzing methylation in trinucleotide sequences.
