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).

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.

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.

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.

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

Sources: Processing of Capped Intron-Containing Pre-mRNA (Reactome, 2026); mRNA Splicing (Reactome, 2026); Beta thalassemia: MedlinePlus Genetics (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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Representative model, for educational purposes only.