The RNA matches the coding strand, U for T, and runs antiparallel to the template.
DNA is the master copy, and it stays put. Transcription makes a short-lived RNA copy of one gene to do the work, and in eukaryotes that copy is capped, tailed, and spliced before it leaves the nucleus.
Key terms
- Template strand — the DNA strand RNA polymerase reads. The RNA is complementary to it.
- Coding strand — the other DNA strand. Its sequence matches the RNA's, with T wherever the RNA has U.
- Promoter — a DNA sequence right before a gene, where RNA polymerase binds to start transcription.
- Introns and exons — introns are cut out of the pre-mRNA. Exons are kept and joined together.
- 5' cap and poly-A tail — a modified G nucleotide at the 5' end and a long run of A's at the 3' end.
- mRNA, tRNA, rRNA — all made by transcription. mRNA carries the code, tRNA carries amino acids, rRNA forms the ribosome's core.
How it works
- In eukaryotes, proteins called transcription factors gather at the promoter first. RNA polymerase joins them, which sets it in place to start at the right base.
- RNA polymerase unwinds a short stretch of DNA and reads the template strand 3'→5'. It needs no primer.
- It builds the RNA 5'→3'. Template A → U in the RNA, T → A, G → C, C → G.
- Behind the polymerase, the RNA peels away and the DNA zips back up. One gene can be transcribed thousands of times.
- In eukaryotes, the pre-mRNA gets a 5' cap and a poly-A tail. Both protect the ends and help the ribosome attach later.
- A spliceosome cuts out the introns and joins the exons. Joining different sets of exons, called alternative splicing, lets one gene make several proteins.
Why it matters
Cells control which proteins they make largely by controlling which genes get transcribed, so the regulation topics build on this one. Keep eukaryotes and bacteria apart, too. Bacteria have no nucleus, so transcription and translation share one space: ribosomes can start on an mRNA before transcription finishes.
Exam traps
| Trap | Actually |
|---|
| The RNA has the same sequence as the template strand, with U for T. | It is complementary to the template. It matches the coding strand, the one polymerase does not read, with U in place of T. |
| The RNA's 5' end lines up with the template's 5' end. | Antiparallel: the RNA's 5' end faces the template's 3' end. If the template is written 5'→3', reverse the order of your paired bases. |
| The cap and tail supply the start and stop codons. | Start and stop codons are part of the message itself. The cap and tail protect the ends and help ribosomes attach. |
| Protein output fell, so the drug must block translation. | Compare the RNA data. If new RNA drops first and protein trails behind, transcription is blocked; existing mRNAs keep being read until they decay. |
Worked example
Researchers put two versions of a human gene into bacteria. Version 1 is copied straight from human chromosomal DNA. Version 2 is a DNA copy of the gene's finished mRNA. The bacteria make a working human protein from version 2, but an abnormal, inactive protein from version 1. What explains the difference?
- Find what differs between the versions. Version 2 was copied from finished mRNA, so it holds only what survived editing in the human nucleus. Version 1 is the raw gene.
- The edit that removes sequence from the middle of the message is splicing. Human cells cut the introns out, so version 2 has none and version 1 still has them all.
- Bacteria have no spliceosome. They transcribe version 1 with its introns in place, and their ribosomes translate the intron sequence as if it were code.
- Extra codons wreck the protein: added amino acids, a shifted reading frame, or an early stop codon.
Version 1 still contains introns. Bacteria cannot remove them, so intron sequence stays in the mRNA and gets translated.
Splicing is the difference that matters between the two inserts. The tempting pick is that bacteria read the genetic code differently. If that were true, version 2 would fail too. It works, so the code is fine, and the unremoved introns are the problem.