Intron

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An intron is a non-coding sequence in a gene.

It is any nucleotide sequence within a gene that is removed by RNA splicing to get the final RNA product of a gene.[1][2] The term intron refers to both the DNA sequence within a gene, and the corresponding sequence in RNA transcripts.[3]

A spliceosome removes introns from a transcribed pre-mRNA segment (top). This is called 'splicing'. After the introns have been removed (bottom), the mature mRNA sequence is ready for translation.

Sequences of coding DNA which are joined together in the final RNA after RNA splicing are exons. They code for amino acids in the final polypeptide.

Introns are in the genes of most organisms and many viruses. They can be in a wide range of genes, including those that generate proteins, ribosomal RNA (rRNA), and transfer RNA (tRNA). RNA splicing takes place after transcription and before translation.

  • Introns: parts of a gene which are discarded: non-working bits.
  • Exons: parts of a gene which are expressed: bits of a gene which code for amino-acid sequences in a protein.

The discovery of introns led to the Nobel Prize in Physiology or Medicine in 1993 for Phillip Sharp and Richard Roberts. The term intron was introduced by American biochemist Walter Gilbert.[4]

Biological meaning[change | change source]

There are many unanswered questions about introns. It is unclear whether introns serve some specific function, or whether they are selfish DNA which reproduces itself as a parasite.[5]

Recent studies of entire eukaryotic genomes have now shown that the lengths and density (introns/gene) of introns varies considerably between related species. There are four or five different kinds of intron. Some introns represent mobile genetic elements (transposons).

Alternative splicing of introns within a gene allows a variety of protein isoforms from a single gene. Thus multiple related proteins can be generated from a single gene and a single precursor mRNA transcript. The control of alternative RNA splicing is performed by complex network of signalling molecules. In humans, ~95% of genes with more than one exon are alternatively spliced.[6]

References[change | change source]

  1. Alberts, Bruce (2008). Molecular biology of the cell. New York: Garland Science. ISBN 0-8153-4105-9.
  2. Stryer, Lubert; Berg, Jeremy Mark; Tymoczko, John L. (2007). Biochemistry. San Francisco: W.H. Freeman. ISBN 0-7167-6766-X.
  3. Kinniburgh, Alan; Mertz J. and Ross J. (July 1978). "the Precursor of mouse β-globin messenger RNA contains two intervening RNA sequences". Cell 14 (3): 681-693. http://www.cell.com/abstract/0092-8674(78)90251-9#.
  4. Gilbert, Walter (1978). "Why genes in pieces". Nature 271 (5645): 501. doi:10.1038/271501a0. PMID 622185.
  5. Orgel L.E. & Crick, F.H.C. 1980. Selfish DNA: the ultimate parasite. Nature, 284, 604-607.
  6. Pan, Q; Shai O, Lee LJ, Frey BJ, Blencowe BJ 2008. Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing. Nature Genetics 40 (12): 1413–1415. doi:10.1038/ng.259. PMID 18978789.