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Anticodons are three‑nucleotide sequences on transfer RNA (tRNA) that pair with complementary codons on messenger RNA (mRNA) during protein synthesis. Of the 64 theoretical codon combinations, 61 encode the 20 standard amino acids, while the remaining three serve as stop signals that terminate translation.
Nucleotides are the fundamental units of DNA and RNA. DNA is a double‑stranded helix in which adenine pairs with thymine and cytosine pairs with guanine. RNA, a single‑stranded molecule, uses uracil in place of thymine, forming complementary base pairs with adenine and cytosine.
Protein production begins when a gene’s DNA sequence is transcribed into messenger RNA. The mRNA contains codons—triplets of nucleotides—that specify amino acids. During translation, tRNA molecules carrying a specific anticodon and the corresponding amino acid bind to the mRNA codon. The ribosome then links the amino acids together, forming a polypeptide chain.
Although 64 codon combinations exist, only 61 code for amino acids. Three codons—UAA, UAG, and UGA—are stop codons. tRNAs with anticodons complementary to these stop codons lack an attached amino acid, causing the ribosome to release the newly synthesized protein and terminate translation. Every gene contains a stop codon at its 3′ end to signal the end of protein synthesis.
Point mutations—substitutions of a single nucleotide—can alter codons and the amino acids they encode, potentially disrupting protein function. A particularly detrimental type is the nonsense mutation, which converts a sense codon into a stop codon mid‑gene, truncating the protein. Such mutations can lead to loss of function or gain of harmful activity, contributing to diseases like cancer.
Understanding the precise role of anticodons and the mechanisms of translation is essential for interpreting how genetic variation translates into cellular phenotype and disease.
