Class resources from The City University of New York describe the transfer ribonucleic acid (tRNA) anticodon as the three-peptide sequence at the base of a transfer RNA molecule that determines where and how the transfer RNA attaches to a messenger ribonucleic acid (mRNA) polymerase. As tRNA is a protein building block, anticodons are vital to living things.
When a protein is created, an mRNA is formed from the cell's DNA. This mRNA is a reverse copy of the DNA's protein code sequence. The mRNA floats into the cytoplasm, where the much smaller tRNA molecules collide with it. The three-peptide anticodon is attracted to its opposite on the mRNA, attaching itself to the appropriate sequence. Science aid compares this process to the creation of a photo negative (the mRNA), which is then used to make perfect copies of the original using tRNA.
According to ACS Publications, on either end of the mRNA's protein sequence is a "stop codon," which has no tRNA match. Since no anticodons are attracted to the stop codon, the protein build stops there. Sometimes this stop codon is a mutation, causing a flaw in the proteins that can be minor or fatal, depending on what the protein does. Certain tRNA molecules carry an anticodon mutation that suppresses stop codon mutations, correcting flaws right in the cell. The study of these mutations led to the development of ataluren, a cystic fibrosis drug the Jain Foundation describes as being like a bridge that allows the completion of the truncated protein, correcting the flaw and allowing the cystic fibrosis-afflicted cell to function properly.