Unit 7 covers how DNA is built, how a cell copies it before dividing, and what happens when that copy has mistakes. By the end, you should be able to use base pairing rules to predict sequences, explain each step of replication, and describe how a single base change can alter a protein.
Read the big ideas first, then work through each topic note and answer its checkpoint before checking the common mistakes at the bottom.
This unit moves from DNA's structure to how it gets copied to how copies go wrong. Each topic builds on the one before it, so the base pairing rules from 7.1 show up again in replication and in mutations.
Honors Biology Unit 7 covers DNA structure, DNA replication, and DNA mutations and repair. You learn that DNA is a double helix of nucleotides with antiparallel sugar-phosphate backbones and paired bases (A-T and G-C). You learn how helicase, primase, DNA polymerase, and ligase copy DNA semiconservatively, including why the lagging strand is made in Okazaki fragments. You also learn how substitutions, insertions, and deletions affect proteins, and how proofreading, mismatch repair, and excision repair keep error rates very low. Exact content and order vary by school.
A always pairs with T, and G always pairs with C. Each pair is one two-ring purine plus one single-ring pyrimidine, which keeps the helix the same width. If you know one strand's sequence, you know the other's.
Helicase opens the helix, primase adds RNA primers, and DNA polymerase builds new strands in the 5' to 3' direction. That one-way rule is why the leading strand is continuous and the lagging strand comes in fragments. Each finished molecule keeps one original strand.
Polymerase proofreads as it builds, and mismatch repair checks the new strand afterward. Errors that slip through become mutations. A silent substitution leaves the encoded amino acid unchanged. A nonsense or frameshift mutation can produce a shortened or altered protein.
Pairing A with T and G with C gives DNA its shape, lets each strand act as a template during replication, and lets repair enzymes spot a mismatch. An unrepaired mismatch can become a mutation when DNA is copied again. Mutations can also arise from changes such as insertions and deletions.
DNA is a polymer made of nucleotides.
Eukaryotic cells copy their DNA during S phase, before division.
A mutation is any change in the DNA sequence.
DNA is a polymer made of nucleotides. Each nucleotide has a phosphate group, a five-carbon sugar called deoxyribose, and one of four nitrogenous bases (A, T, G, or C). Phosphodiester bonds link the sugar of one nucleotide to the phosphate of the next, forming the sugar-phosphate backbone.
Two strands wind into a double helix. The backbones sit on the outside like the rails of a twisted ladder, and the bases point inward as the rungs. A pairs with T using 2 hydrogen bonds, and G pairs with C using 3. Every pair is one purine (A or G, two rings) plus one pyrimidine (T or C, one ring), so the helix keeps a constant width.
The strands are antiparallel. Each strand has a 5' end (phosphate) and a 3' end (hydroxyl on the sugar), and the two strands point in opposite directions. Hydrogen bonds between bases are individually weak, which lets the strands unzip for copying, while stacking between the flat bases helps hold the helix steady.
Because pairing is complementary, one strand's sequence tells you the other's. That is how DNA stores information and how it gets copied.
Worked example. A double-stranded DNA sample is 22% guanine. Find the other bases. G pairs with C, so C = 22%. Together G + C = 44%, which leaves 100% − 44% = 56% for A + T. A and T are equal, so A = 28% and T = 28%.
Check yourself. What is the complementary strand to 5'-ATGCCA-3'? (Answer: 3'-TACGGT-5', which written 5' to 3' is 5'-TGGCAT-3'.)
Eukaryotic cells copy their DNA during S phase, before division. Bacteria also copy their DNA before dividing. Copying starts at origins of replication. A bacterial chromosome usually has one, while each eukaryotic chromosome has many so the much larger genome finishes in time.
At each origin, helicase breaks the hydrogen bonds between bases and opens two replication forks. Single-strand binding proteins keep the separated strands from snapping back together. Primase lays down a short RNA primer, because DNA polymerase can only add nucleotides to an existing 3' end.
DNA polymerase builds new DNA only in the 5' to 3' direction. On the leading strand, that direction follows the fork, so synthesis is continuous. On the lagging strand, polymerase works away from the fork and makes short Okazaki fragments, each with its own primer. The RNA primers are removed, DNA polymerase fills the resulting gaps, and DNA ligase seals the remaining nicks in the backbone.
Replication is semiconservative. Each new double helix has one original strand and one new strand, which Meselson and Stahl showed in 1958 using heavy nitrogen ().
Worked example. Bacteria with all-heavy DNA are moved to light () medium. After one round, both of the 2 molecules are hybrid. After two rounds there are 4 molecules, but only 2 original heavy strands, so 2 of 4 (50%) are hybrid and 50% are fully light. After three rounds, 2 of 8 (25%) are hybrid.
Check yourself. Why does the lagging strand need many primers while the leading strand needs only one? (Answer: Polymerase can only build 5' to 3', so on the lagging strand it must keep restarting as the fork opens new template, and every restart needs a new primer.)
| Feature | Leading strand | Lagging strand |
|---|---|---|
| Direction of synthesis vs. fork | Toward the fork | Away from the fork |
| How it's built | One continuous strand | Short Okazaki fragments |
| RNA primers needed | One at the start | One per fragment |
| Ligase needed to finish | Yes, to seal nicks after primer replacement and join replicated sections | Yes, to join every fragment |
A mutation is any change in the DNA sequence. Mutations can arise from replication errors or DNA damage that repair systems miss. Damage can occur spontaneously or be caused by mutagens such as UV light, X-rays, and chemicals in cigarette smoke.
A substitution swaps one base for another, and its effect depends on the new codon. A silent mutation still codes for the same amino acid. A missense mutation changes one amino acid, as in sickle cell disease, where GAG becomes GTG and glutamic acid becomes valine in hemoglobin. A nonsense mutation creates an early stop codon. It can produce a shortened protein or cause the mRNA to be degraded.
Insertions and deletions are usually riskier. If the number of bases added or lost isn't a multiple of 3, the reading frame shifts. This can change downstream codons and create an early stop codon. That's a frameshift mutation.
Cells catch most errors. DNA polymerase proofreads as it builds, backing up to remove a wrong base. Mismatch repair proteins scan the new strand after replication and fix what proofreading missed. Nucleotide excision repair cuts out bulky damage such as thymine dimers caused by UV light. When repair genes are themselves mutated, errors pile up, which is one path to cancer.
Worked example. Polymerase alone makes about 1 error per bases. Proofreading improves that about 100-fold to 1 in , and mismatch repair brings it near 1 in . A human diploid cell copies about base pairs, adding about new nucleotides. At the assumed rate, errors remain across both copies. Actual rates vary.
Check yourself. Which is usually more damaging, deleting 1 base or deleting 3 bases from a gene? (Answer: Deleting 1 base, because it shifts the reading frame and can change many downstream codons or create an early stop. Deleting 3 bases preserves the reading frame, though it can affect more than one amino acid if it crosses codon boundaries.)
| Mutation type | What changes in DNA | Effect on protein |
|---|---|---|
| Silent | One base, e.g. GAA to GAG | None; both codons code for glutamic acid |
| Missense | One base, e.g. GAG to GTG | One amino acid changes (glutamic acid to valine) |
| Nonsense | One base, e.g. TAC to TAG | Early stop codon; protein is cut short |
| Frameshift | 1 or 2 bases inserted or deleted | The reading frame shifts, which can change downstream codons or create an early stop |
| Term | Definition |
|---|---|
| Nucleotide | The monomer of DNA, made of a phosphate group, a deoxyribose sugar, and a nitrogenous base. |
| Complementary base pairing | The rule that A pairs with T (2 hydrogen bonds) and G pairs with C (3 hydrogen bonds). |
| Double helix | DNA's shape, two antiparallel strands twisted around each other with bases paired in the middle. |
| Semiconservative replication | Copying in which each new DNA molecule contains one original strand and one newly built strand. |
| Origin of replication | A specific DNA sequence where helicase starts unwinding and replication begins. |
| Replication fork | The Y-shaped region where the helix is being unwound and both strands are being copied. |
| Okazaki fragment | A short piece of DNA made on the lagging strand, about 100-200 nucleotides in eukaryotes and 1,000-2,000 in bacteria. |
| Proofreading | DNA polymerase's ability to detect a wrong nucleotide it just added, remove it, and replace it. |
| Mismatch repair | A repair system that finds mispaired bases left after replication and fixes them on the new strand. |
| Mutation | Any permanent change in a DNA sequence, from a single base swap to large insertions or deletions. |
Because the lagging strand looks backward, it's easy to assume polymerase builds it backward. It doesn't. Polymerase always builds 5' to 3', and the lagging strand is made in fragments precisely because it can't go the other way.
A and G are both purines, so they get lumped together. The rule follows pairing partners, so %A = %T and %G = %C. If a double-stranded DNA sample is 30% A, then T is 30%, and the remaining 40% splits into 20% G and 20% C.
The word "semi" makes it sound like mixing happens within a strand. Each strand is either fully old or fully new. What's split is the double helix, which has one complete original strand and one complete new strand.
Many substitutions are silent because several codons code for the same amino acid, and mutations outside genes often have no effect. Some mutations are even helpful in a given environment, which is the raw material for evolution.