- D1 ✏︎ Molecules -
D1.1 - DNA Replication (SL/HL)
LECTURE VIDEO
DESCRIPTION
Imagine copying the entire Harry Potter series by hand. Perfectly. Millions of times. Without spellcheck. That’s your DNA every time a cell divides. And honestly? It nails it.
Watch the cellular photocopier in action:
- Semiconservative Replication: The genius move. Each new DNA molecule keeps one original strand and builds one new one. It’s not reinventing the wheel—it’s just making a really good twin.
- Helicase: The Unzipper – This enzyme barges in, grabs both strands, and yanks them apart like ripping open a stubborn bag of chips. Finally, some action.
- DNA Polymerase: The Builder – Slides along the separated strands, reading the template and bringing in the matching bases. A pairs with T. C pairs with G. It’s not complicated—it’s just loyal.
Understand the simple, elegant, ridiculously reliable system that lets you grow, heal, and exist—one perfectly paired base at a time.
TIMESTAMPS
STUDY RESOURCES
00:00 – Where Is DNA?
01:19 – Why DNA Replication?
04:31 – Review Of DNA Structure
10:47 – DNA Replication Is Semi-Conservative
13:12 – DNA Replication EXPLAINED
23:48 – Summary Of DNA Replication
24:39 – IB Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!
D1.1 - DNA Profiling (SL/HL)
LECTURE VIDEO
DESCRIPTION
Forget fingerprints. Your DNA is the ultimate giveaway—and we only need a microscopic speck of it. Saliva on a coffee cup? Skin cell under a fingernail? That’s enough to build a genetic mugshot. We just need to photocopy it a billion times first.
Crack the case with these forensic tools:
- PCR (The Genetic Photocopier): Polymerase Chain Reaction takes one tiny, sad little DNA sample and turns it into “we have WAY too much now” quantities. Heat, cool, replicate. Repeat 30 times. Boom—evidence buffet.
- The PCR Cast: DNA template (the original), primers (sticky notes saying “start here”), Taq polymerase (heat-loving bacteria enzyme that doesn’t cook to death), and nucleotides (the building blocks). It’s a biochemical soup that prints genetic cash.
- Gel Electrophoresis (The DNA Race): Load your amplified DNA into a gel, hit it with electricity, and watch the fragments race. Small ones zoom ahead. Big ones lag behind like they didn’t train for this.
- The Band Pattern: Everyone’s DNA has different lengths between specific markers. When you run them on a gel, you get a barcode of black lines. That barcode is basically your genetic signature. No two people (except identical twins) have the same one.
- Crime Scene Math: Match the suspect’s bands to the evidence bands? Congratulations, you’ve got your person. No match? Back to the drawing board, detectives.
Learn how a drop of saliva becomes a courtroom slideshow—and why PCR is the most important photocopier you’ll never see.
TIMESTAMPS
STUDY RESOURCES
00:00 – What is in D1.1?
00:48 – DNA Profiling Intro & Crime Scene
06:22 – Polymerase Chain Reaction (PCR)
17:19 – Gel Electrophoresis
27:56 – Summary Of DNA Profiling [STEPS]
29:29 – Purposes Of DNA Profiling
30:34 – Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!
D1.1 - DNA Replication (HL)
LECTURE VIDEO
DESCRIPTION
Forget everything you know about photocopiers. DNA replication is a coordinated strike team of enzymes working at warp speed with zero coffee breaks. It’s happening right now in billions of your cells, and it’s honestly the most impressive thing you’ve never thought about.
Meet the all-star cast of cellular copying:
- Helicase: The ripper. Barges into the double helix and tears the hydrogen bonds apart like opening a Velcro wallet. Creates the replication fork.
- Single-Strand Binding Proteins: The babysitters. Once helicase splits the strands, these little guys rush in to keep them separated. No re-zipping allowed. We’re busy here.
- Primase: The sticky note supplier. DNA polymerase can’t start on bare DNA—it needs a primer. Primase rolls in and drops a short RNA “START HERE” tag. Humble job. Critical job.
- DNA Polymerase III: The workhorse. Reads the template strand and brings in complementary nucleotides. A to T, C to G. Loyal, fast, and surprisingly accurate. Only builds 5′ to 3′ though—it has rules.
- Leading vs. Lagging Strand: One faces the fork and gets built continuous and smooth—the favourite child. The other faces away and gets built in awkward, stuttered chunks called Okazaki fragments. It’s fine. No bitterness.
- DNA Polymerase I: The swapper. Sees those RNA primers still hanging around and replaces them with proper DNA nucleotides. “You did your job, primase. Now step aside.”
- Ligase: The finisher. Seals those Okazaki fragments into one continuous strand. Also fixes any nicks left behind. It’s the glue guy. The closer. The reason everything actually holds together.
- Proofreading: DNA polymerase III checks its own work as it goes. Catches a wrong base? Snips it out, tries again. Error rate before proofreading: 1 in 10,000. After proofreading: 1 in 10 million. Humble brag.
Understand the symphony of enzymes that turns one helix into two perfect copies—and why your cells are better at multitasking than you’ll ever be.
TIMESTAMPS
STUDY RESOURCES
00:00 – Where & What Is DNA?
01:26 – Why DNA Replication?
05:24 – Review Of DNA Structure
12:21 – DNA Replication Is Semi-Conservative
14:59 – Prokaryotic & Eukaryotic Replication
16:56 – Helicase & SSBP’s & Replication Fork
22:41 – Leading Strand Explained
32:09 – Lagging Strand Explained
40:59 – Summary Of DNA Replication
41:57 – IB Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!
D1.2 - Protein Synthesis (SL/HL)
LECTURE VIDEO
DESCRIPTION
Your DNA is a massive engineering archive filled with blueprints for every protein in your body. But the master copy never leaves the records office (nucleus). You need a blueprint copier, a courier, and a whole construction crew to actually build the thing. Bob the Builder has nothing on this operation.
Follow the build from gene to finished machine:
TRANSCRIPTION: Copying the Blueprint
- RNA Polymerase: The foreman who actually does work. Rolls into the nucleus, finds the right gene, and unzips a small section of DNA. Reads the template strand and builds a complementary mRNA blueprint—except it swaps T for U because mRNA uses its own hipster shorthand.
- mRNA: The blueprint courier. Leaves the nucleus through a nuclear pore and heads to the construction site (ribosome). Plans in hand. Doesn’t get lost. Somehow.
TRANSLATION: Assembling the Rocket
- Ribosome: The construction platform that never takes a lunch break. Reads the mRNA blueprint three letters at a time (codons). Holds everything steady while the parts arrive. Multitasking queen.
- tRNA: The parts delivery truck with excellent GPS. One end carries a specific amino acid (the building material), the other end has an anticodon that matches the mRNA codon. Finds its match? Drops off the component. Misses? Tries again. No road rage.
- Peptide Bonds: The ribosome welds amino acids together. The polypeptide chain grows. The rocket takes shape, one tiny piece at a time.
- Start & Stop Codons: AUG says “BEGIN CONSTRUCTION HERE.” UAA, UAG, UGA say “PROJECT COMPLETE. PACK UP. GO HOME.” No overtime pay, no complaints.
- The Final Product: A folded, functional protein—an enzyme wrench, a hormone communication system, an antibody defence turret, or the collagen steel beams holding your face exactly where it should be.
Understand how a four-letter code becomes a twenty-material parts list becomes the three-dimensional machines that build and run your entire biological construction site. Bob the Builder would cry. This is next level.
TIMESTAMPS
STUDY RESOURCES
00:00 – BOB The Builder [Analogy]
05:36 – Genes can be ON or OFF
08:13 – TRANSCRIPTION EXPLAINED
16:21 – Word Summary Page [Transcription]
17:36 – TRANSLATION EXPLAINED
36:11 – Word Summary Page [Translation]
38:01 – Test your understanding!
39:08 – tRNA, mRNA, rRNA Summary
39:29 – QUICK REVIEW (Transcription & Translation)
40:14 – Sickle Cell (Mutation & Protein Synthesis)
43:56 – Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!
D1.2 - Protein Synthesis (HL)
LECTURE VIDEO
DESCRIPTION
You’ve seen the basic build. Now it’s the extended edition—post-production edits, quality control, and the cellular recycling centre. Protein synthesis isn’t just construction. It’s a whole film studio. Roll camera on the cellular blockbuster:
DIRECTIONALITY: Read Left to Right, Nerds
– 5′ to 3′. No exceptions. Ribosomes start at the 5′ end and march toward 3′. No skipping ahead. No reading backwards. Thems the rules.
NON-CODING SEQUENCES: Not Useless, Just Background
– Introns: The deleted scenes. Transcribed, then ruthlessly cut out. Not in the final protein, but maybe they’re secret regulators. Sus.
CONTROL OF GENE EXPRESSION: Who Gets Cast?
– Transcriptional Control: Transcription factors are casting directors. No factors? The gene never auditions.
POST-TRANSCRIPTIONAL MODIFICATION: Polishing the Script
– 5′ Cap: VIP pass slapped on the front. “START HERE.” Also prevents mRNA assassination.
– Poly-A Tail: Hundreds of As stitched on the back. Job security. Helps mRNA exit the nucleus and not die immediately.
– Splicing: Introns out, exons glued. Alternative splicing? Same gene, different edit. One blueprint, multiple movies.
POLYPEPTIDE MODIFICATION: Post-Production Edits
– Folding: Chaperone proteins prevent misfolding disasters. No chaperones? You get protein clumps. Alzheimer’s, Parkinson’s—this is where it starts.
– Cutting & Snip-Snip: Some proteins are made long and useless. Proinsulin needs a chunk cut out before it works. Like removing training wheels.
– Protein Bling: Phosphate groups, carbs, lipids. Attached after translation. Functional decorations.
RECYCLING: The Circle of Molecular Life
– Ubiquitin: The death tag. Old or damaged protein? Slap a ubiquitin on it.
– Proteasome: The cellular woodchipper. Sees the tag, shreds the protein, spits out amino acids.
– Reuse: Those amino acids go right back to the tRNA delivery trucks. No waste. No landfill. Your body is an environmental queen.
Understand the full pipeline—from casting call to post-production to dignified protein death. Every amino acid gets an encore.
TIMESTAMPS
STUDY RESOURCES
00:00 – Outline Of This Video
01:00 – Intro to regulation of protein synthesis
04:43 – Directionality in protein synthesis
09:12 – Non-coding sequences
12:53 – Control of transcription
22:57 – Splicing [Post transcriptional modification]
29:13 – Alternative splicing [Post transcriptional modification]
35:02 – Cap & Poly A tail [Post transcriptional modification]
40:35 – Translation key points
50:31 – Polypeptide modification
55:18 – Recycling of amino acids
58:19 – Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!
D1.3 - Mutations & Gene Editing (SL/HL)
LECTURE VIDEO
DESCRIPTION
Your DNA is a 3-billion-letter instruction manual. Sometimes, your cells copy it perfectly. Sometimes, they slip. A missing/extra letter here, a swapped base there. That’s a mutation. Sometimes it’s harmless. Sometimes it’s devastating. Sometimes it gives you superpowers (okay, brown eyes).
But the real question is: does the typo die with you, or do your kids inherit your genetic oopsie? Time to embrace the typos of life:
POINT MUTATIONS: One Rogue Letter
- Substitution – One base swapped for another. Like typing “the Sad cat” instead of “the Bat cat.” Might change nothing (silent). Might swap one amino acid (missense). Might yell “STOP” mid-sentence (nonsense). Awkward either way.
- Insertion/Deletion – Add or lose a single letter. Now EVERYTHING after is gibberish. “the sad cat” becomes “ath esa dca.” Reading frame? Destroyed. Protein? Trash.
SOMATIC vs. GERM: Does It Run in the Family?
- Somatic Mutations – Happen in body cells—skin, liver, lung. The typo stays with you. Your kids won’t get it. But if enough build up? Cancer. You are a mutation retirement home.
- Germline Mutations – Happen in sperm or egg cells. The typo is now an heirloom. Passed down for generations. Thanks, grandpa.
- Same mutation, different stakes – A lung cell mutation = just you. A sperm cell mutation = your entire bloodline.
CAUSES: Who Keeps Hitting Caps Lock?
- Spontaneous – DNA polymerase just had a bad day. No external cause. Cellular oopsie.
- Mutagens – The external troublemakers. Radiation (UV, gamma) = physical violence. Chemicals (benzene, mustard gas) = molecular sabotage. Viruses = shoving foreign DNA where it doesn’t belong.
CONSEQUENCES: Good, Bad, or Meh?
- Silent – Mutation happened. Amino acid didn’t change. DNA got spicy for absolutely no reason.
- Missense – Wrong amino acid. Sometimes fine. Sometimes sickle cell anemia. Depends on the swap.
- Nonsense – Premature stop codon. Protein gets cut off mid-construction. Incomplete. Useless. Tragic.
- Frameshift – Everything after is nonsense. Protein looks like it was assembled by a toddler.
- Beneficial Mutations – Rare, but real. Lactose tolerance? Mutation. HIV resistance? Mutation. Your ancestors got lucky. You’re welcome.
Understand the typos, rearrangements, and biochemical oopsies that drive evolution, cause disease, and occasionally let adults drink milk. Mistakes aren’t always bad—sometimes they’re just edits. But maybe don’t make them in your germ cells.
TIMESTAMPS
STUDY RESOURCES
00:00 – Outline Of This Video
00:37 – Intro To Mutations
05:14 – Analogy
10:23 – Base substitution mutations
20:25 – Sickle Cell Disease
28:35 – Deletions & Insertions
30:04 – Huntingtons Disease (Insertion disease)
35:14 – Frameshift mutation
39:44 – CCR5 delta 32 (Deletion disease)
45:40 – Mutations are only BAD?
47:47 – Causes of mutations
52:59 Germ and somatic cell mutations
57:56 – Where are mutations found?
59:03 – Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!
D1.3 - Mutations & Gene Editing (HL)
LECTURE VIDEO
DESCRIPTION
For centuries, mutations were random. Now? We grab scissors and decide exactly where to snip. Welcome to rewriting the code of life.
GENE KNOCKOUT: Breaking Things on Purpose
Turn a gene off and see what breaks. Tail missing? Congrats, you found a tail-suppressor gene. Now the obvious question is…How do we do it? Short Answer = CRISPR
CRISPR:
- Cas9:Molecular scissors with an address.
- Guide RNA:The GPS that leads it there.
- The hack:Snip both strands, cell panics, gene dies. Or insert a template and fix it.
Fast. Works in everything. Labs went from “maybe someday” to “we edited 50 embryos this Tuesday.”
THE ETHICS: Just Because We Can…
Cure Huntington’s? Tempting. Designer babies? Now you’re making Gattaca.
CONSERVED SEQUENCES: Evolution Was Too Scared to Touch These
Human, mouse, zebrafish—same gene, barely a typo. Millions of years, zero changes. Why? Because messing with it means death. Not lazy evolution. Perfection.
We’re not just reading the blueprint anymore. We’re rewriting it.
TIMESTAMPS
STUDY RESOURCES
00:00 – Outline Of This Video
00:37 – Intro To Mutations
05:14 – Analogy
10:23 – Base substitution mutations
20:25 – Sickle Cell Disease
28:35 – Deletions & Insertions
30:04 – Huntingtons Disease (Insertion disease)
35:14 – Frameshift mutation
39:44 – CCR5 delta 32 (Deletion disease)
45:40 – Mutations are only BAD?
47:47 – Causes of mutations
52:59 – Germ and somatic cell mutations
57:56 – Where are mutations found?
59:03 – Questions & Answers
NOTES – All you need to know in one place!
QUESTIONS – Test your Big Brain!