Transition mutations are about an order of magnitude more common than transversions.

The transition mutation results in exon 7 being skipped during splicing.

The presence of nitrous acid can cause transition mutations, by converting cytosine to uracil.

This results in a change in one base pair of DNA, specifically a transition mutation.

Base analog, which can substitute for DNA bases during replication and cause transition mutations.

Additionally, GT mismatches can lead to C-to-T transition mutations if not repaired.

Following subsequent rounds of replication, the original G:C base pair can become an A:T pair (a transition mutation).

Ocular findings associated with rhodopsin gene codon 17 and codon 182 transition mutations in dominant retinitis pigmentosa.

Though the exact mechanism of repeat recognition and mutagenesis are poorly understood, RIP results in repeated sequences undergoing multiple transition mutations.

This conversion of a DNA base from cytosine (C) to thymine (T) can result in a transition mutation.

This results in a post-replicative transition mutation, where the original G-C base pair transforms into an A-T base pair.

RIP causes G:C to A:T transition mutations within repeats, however, the mechanism that detects the repeated sequences is unknown.

It acts by adding alkyl groups to the O of guanine and O of thymine, which can lead to transition mutations between GC and AT.

In molecular biology, repeat induced point-mutation or RIP is a process by which DNA accumulates G:C to A:T transition mutations.

NMU is an alkylating agent, and exhibits its toxicity by transferring its methyl group to nucleobases in nucleic acids, which can lead to AT:GC transition mutations.

These increased concentrations of CpGs might be associated with the decreased methylation of cytosines often observed in CpG islands — this could result in a reduced vulnerability to transition mutations and, as a consequence, a higher equilibrium density of CpGs surviving.

Since transition mutations (purine to purine or pyrimidine to pyrimidine mutations) are more likely than transversion (purine to pyrimidine or vice-versa) mutations, the equivalence of purines or that of pyrimidines at twofold degenerate sites adds a further fault-tolerance.