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# RNA processing (cap, poly-A tail and splicing)

Newly made RNA matures in the nucleus: it gets a cap and a poly-A tail and loses its introns by splicing before it leaves for the cytoplasm.

Updated 2026-11-01

## Key facts

- 5' cap: 7-methylguanosine joined by a 5'–5' triphosphate bond; it protects the mRNA and helps the ribosome find it.
- 3' poly-A tail: about 200 adenylates added after a cut about 10–30 nt past the AAUAAA signal.
- Splicing: the spliceosome removes introns (GU at the start, AG at the end, a branch point with an A) and joins the exons.
- Alternative splicing lets one gene make several different proteins.
- A mutation at a splice site can skip an exon or keep an intron (e.g. β-thalassemia).

## In detail

- All three changes happen while Pol II is still transcribing, coordinated by the phosphorylated CTD.
- Splicing chemistry: two transesterifications. The branch-point A attacks the 5' site and forms a lariat; then exon 1 attacks the 3' site and the exons are joined.
- The U1, U2, U4, U5 and U6 snRNPs form the spliceosome; U1 recognises the 5' site and U2 the branch point.
- RNA editing: in the intestine, deamination of a C to U in ApoB mRNA creates a stop codon and gives ApoB-48 instead of ApoB-100.
- mRNAs with a premature stop codon are degraded by NMD (nonsense-mediated decay).
- rRNAs and tRNAs are processed too: long precursors are cut, bases are modified (pseudouridine, methylation) and tRNAs get CCA added at the 3' end.

**Also called**
mRNA maturation, Splicing

## Clinical notes

- Anti-Smith (anti-Sm) antibodies against snRNP proteins are highly specific for lupus; anti-U1 RNP marks mixed connective tissue disease.
- In β-thalassemia, many HBB mutations disturb splicing and reduce or abolish β-globin.
- Splice-switching antisense oligonucleotides (for example to skip an exon in Duchenne dystrophy, or to include SMN2 exon 7 in spinal muscular atrophy) are approved therapies.

## Related conditions

- [Thalassemias (α and β)](https://durgical.com/en/conditions/thalassemias/)
- [Systemic lupus erythematosus](https://durgical.com/en/conditions/systemic-lupus-erythematosus/)

## Related

- [Transcription](https://durgical.com/en/biochemistry/topics/transcription/)
- [Spliceosome](https://durgical.com/en/biochemistry/enzymes/spliceosome/)
- [Translation and the genetic code](https://durgical.com/en/biochemistry/topics/translation-and-the-genetic-code/)
- [Types of mutations](https://durgical.com/en/biochemistry/topics/types-of-mutations/)
- [Central dogma of molecular biology](https://durgical.com/en/biochemistry/topics/central-dogma-of-molecular-biology/)

## Test yourself

Think of the answer, then tap the question to see it.

## Which sequences mark the start and the end of an intron?

GU at the 5' end and AG at the 3' end (the GU–AG rule), with an A at the branch point.

## How are ApoB-48 and ApoB-100 made from the same gene?

By mRNA editing in the intestine: a C becomes U, a stop codon appears and the protein is cut short (ApoB-48).

## Which autoantibodies against the spliceosome are typical of lupus?

Anti-Smith (anti-Sm) antibodies, directed at snRNP proteins.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: [Processing of Capped Intron-Containing Pre-mRNA](https://reactome.org/PathwayBrowser/#/R-HSA-72203) (Reactome, 2026); [mRNA Splicing](https://reactome.org/PathwayBrowser/#/R-HSA-72172) (Reactome, 2026); [Beta thalassemia: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/beta-thalassemia/) (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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