Most Things Biology

4.5 The Cell Cycle and Mitosis

Case home  ·  Start at the beginning  ·  The Reveal

Time To Read

27–40 minutes

Date Last Modified

Making Cells & Proteins · Chapter 5 of 7

Seventeen, senior year: the October-to-February season — strep, teardrops, shingles — which Integumentary 5.2 follows through the skin and Immunity 22.5 through the virus. Each got its own name, its own cream and its own doctor. This chapter steps back from the molecule to the whole cell and its timetable — grow, copy, grow, divide, or step off the cycle entirely — to show how one zygote’s genome reached every cell she has, and why only some of those cells ever read MEFV.

The question you will answer

Three diagnoses in one winter, in three different tissues — a throat, the skin, one nerve. Every one of the cells involved descends from the same single cell and carries the same genome, yet a skin cell races through its cycle, a nerve cell hasn’t divided in years, and a neutrophil never divides at all. The question for the chapter: if every cell carries the same instructions, what decides which cells divide, which cells read a gene — and why can’t any checkpoint catch an inherited letter?

Opener · October to February · about 2¼ minutes

The opener is the same narrated animation you will watch in Scene 1.

Watch it in Scene 1 ↓

Watch the opener first. It sets the question; the chapter answers it.

1

Read the chart

Patient chart · Stina

October 1992 – February 1993 · age 17 · strep, then teardrops, then shingles

1990–91 · 15–16
This module’s earlier chapters: “The cycle” — the fever on day one of her period, then the vomiting, then the legs, every four weeks; the appendix out at fifteen and “unremarkable,” with the same pain back three weeks later (Module 3’s); at sixteen a knife under the right ribs called “anxiety.” From then on she stops telling people when things hurt.

Oct 1992 – Feb 1993 · 17
Senior year: the October-to-February season — strep, teardrops, shingles (Integumentary 5.2 follows the skin; Immunity 22.5 the virus).

Told
“Guttate psoriasis, from the strep.” Shingles “unusual for my age,” and “whether I’d been under a lot of stress.” The chart: “Three diagnoses, three creams, three different doctors.”

Chart clues this module: 4 · this module (the Chart Reveal, logged in Chapter 7) — no lab values exist for 1992–93

Before you go on · your prediction

Strep in October, teardrop spots six weeks later, shingles in January — three diagnoses, three tissues, one winter. Before you learn how cells divide and what they read, what most likely ties the three together?

Open the one you lean toward. Nothing is recorded and nothing is revealed — you come back to it at the end.

Nothing — “Three diagnoses, three creams, three different doctors”

Watch which cells each illness involved, where those cells came from, and whether they share anything at all.

One genome, run and read differently by three kinds of cell

Watch which of the three populations divides fast, which never divides, and which one reads MEFV.

Stress — “whether I’d been under a lot of stress”

Watch what actually tells a cell to divide or to stay put, and whether worry is one of the signals a cell-cycle checkpoint reads.

From Stina’s diary

Age 17 · “October to February”

2

The story

Three short movements: the case, the anatomy and physiology, then the tie back to Stina. Each links to the scene where you’ll see it move.

I · October to February

Senior year, and Stina was seventeen. “It started with strep in October, the real kind, white patches and a fever of 104 that for once everybody believed, because they could swab it.” Between that October and the next February came the spots — guttate psoriasis, the clinic said, from the strep — and then the shingles. “Then in January the left side of my back caught fire, a burning stripe from my spine around to under my ribs, and three days later a band of blisters came up along it.” Module 5 will follow her skin through that winter (Integumentary 5.2), and Module 22 will follow the virus (Immunity 22.5), so this chapter doesn’t retell them. Hold on to the shape of the season instead. Three things arrived in a row, in three different tissues — a throat, the skin, one nerve on the left side — and each was handed to a different doctor with its own name and its own cream. Her chart would sum it up as three diagnoses, three creams, three different doctors. Nobody laid the three side by side, and nobody asked what they had in common. That question is the one this module has been building toward, and Chapter 7 takes it up in her own words. Here it gets a narrower, cellular answer: what each of those three cell populations was doing that winter, and what all of them shared.

See it move: Scene 1 · October to February

II · Grow, copy, grow, divide

Every cell comes from a pre-existing cell. You are the current end of a line that has never once stopped dividing — and the cell cycle is that line’s timetable. G1 is growth: the cell makes proteins and does its job, its DNA loose as chromatin so it can be read, because you can’t read a book that’s slammed shut and shrink-wrapped. S is synthesis: all 6.2 billion base pairs copied, each chromosome growing a sister chromatid joined at the centromere — same chromosome, two chromatids. G2 grows again and checks the copy. Together those three are interphase, most of a cell’s life; in a fast-dividing human cell in a dish a full lap takes about a day, and M takes about an hour. Some cells step off the merry-go-round into G0: most neurons for life — they really, genuinely dislike mitosis, which is a big reason nervous tissue heals so poorly — and a liver cell until the liver is injured. Gates stand between the steps. Checkpoint proteins (cyclins and their kinases, and p53) ask at G1/S whether the cell is big enough, fed and undamaged, at G2/M whether the DNA was copied completely and correctly, and at the spindle whether every chromosome is attached; a failure halts the cycle until it’s fixed, and the unfixable go to apoptosis. The system would rather lose a soldier than let a saboteur reproduce. Then mitosis, four phases I’ll hold you to: prophase, metaphase (metaphase, middle), anaphase — a surprisingly energy-hungry tug of war — and telophase, prophase in reverse; cytokinesis splits the rest. From one zygote, about 37 trillion cells, and then a lifetime of repair: my pizza burn, healed overnight by mitosis.

See it move: Scene 2 · An Ordered Sequence · Scene 3 · Metaphase, Middle · Scene 5 · Thirty-Seven Trillion Copies · Scene 6 · Guards at Every Gate

III · Same book, different pages

Here is that winter as someone who knows what Stina carries would read it. Three cell populations were busy, and every one of them held the same two variant copies — one E148Q in MEFV, one in LPIN2 — copied faithfully from her zygote through every division since, past every checkpoint, because a correctly copied letter is not damage and no gate is built to question the original text. Her keratinocytes, pushed by an immune signal after the strep, ran their cycle far faster than normal — the belt Module 5 will time. A virus that had sat silent for years in the cell bodies of sensory neurons beside her spine — cells parked in G0 that almost never divide — woke and traveled down one nerve to the skin of her left side. And her bone marrow, which makes tens of billions of neutrophils a day, poured them out to fight the strep and drive a fever of 104. Same genome in all three. Only one of them reads MEFV much. Neutrophils, monocytes and macrophages, eosinophils and dendritic cells transcribe it constantly; the keratinocyte and the neuron keep it shut. That is gene presence versus gene expression, and it is why FMF’s attacks live where neutrophils gather — the linings of the belly and chest, the joints, patches of skin — and not in her nerves. Honesty flags: nothing in FMF causes strep; guttate psoriasis is a well-known reaction to strep in people prone to it; shingles at seventeen is unusual and has many possible explanations. Whether her variants played any part in that winter is not known. What the cell cycle answers is narrower: how one inherited letter came to be in every cell, and why only some cells ever read it.

See it move: Scene 4 · Same Book, Different Pages · Scene 1 · October to February

3

Watch · explore · think · check

6 scenes. Each one has a short animation or a slide, something to explore, a true/false spot-check of your thinking, and a quick check. Every scene gives you an evidence card for your board.

How to read the scenes

  • Animation (dark teal) — a short animated explainer, one idea each
  • Slide (dark teal) — a still to study: a micrograph, a diagram or a map
  • Explore (purple) — something to push on while you watch
  • Game (purple) — a quick challenge
  • Think (gold) — reason it out, then spot-check yourself with a few true/false questions; not graded
  • Check (gold) — a quick H5P that scores itself

Scene 1 of 6

October to February

One winter, three tissues, three diagnoses — and three cell populations sitting in three very different places on the same timetable.

Animation · in production · 2 min 10 s

October to February

A calendar strip runs across the top, October 1992 to February 1993, and three icons drop onto it in order: an open mouth with reddened tonsils and a thermometer reading 104 (October), a scatter of small red teardrops on a torso outline (six weeks later), a band of blisters wrapping the left side of a back (January). Each icon sprouts its own index card — STREP · GUTTATE PSORIASIS · SHINGLES — with its own cream and its own doctor. Then the camera pulls down into three lanes of cells. Lane 1, the skin: a column of epidermis whose basal cells spin around a small cell-cycle ring faster than normal (a tag reads SEE MODULE 5.2). Lane 2, a sensory neuron in a ganglion beside the spine: the cell sits on a G0 siding off its ring, not dividing, with a dormant virus curled in its cell body; in January the virus uncurls and travels down the axon to the skin (a tag reads SEE MODULE 22.5). Lane 3, the bone marrow: precursor cells cycle and pour out mature neutrophils, which step off the ring for good, stream into the blood and crowd the throat. In every nucleus, in every lane, the same strip of genome glows with the same two marked genes — one changed copy in MEFV, one in LPIN2. A small lamp above MEFV lights in Lane 3 only. Last frame: the three index cards slide off the calendar and stack on one body outline, under a question mark.

Prefer the full lecture? The Cell Cycle (original video on the site)

Explore · in production

Three lanes, one winter

A five-month calendar runs across the top of the screen — Oct, Nov, Dec, Jan, Feb (1992–93) — with three pinned events: strep and a fever of 104 (Oct), teardrop spots (six weeks later), shingles on the left side (Jan). Below it, three horizontal lanes, each with a cell drawing at its left end and a small cell-cycle ring (G1, S, G2, M, with a G0 siding): LANE 1 · basal keratinocytes of the epidermis; LANE 2 · a sensory neuron whose cell body sits in a ganglion beside the spine; LANE 3 · neutrophils, with their precursors in the bone marrow. For each lane and each month the student sets a state from a short menu — dividing slowly · dividing fast · parked in G0 · never divides (made fresh from dividing precursors) — and predicts before the reveal. The reveals, one card per lane: keratinocytes divide continuously in the basal layer, and after strep an immune signal pushes them much faster (a SEE MODULE 5.2 tag — the timing of the skin belt is Module 5’s, not rebuilt here); the sensory neuron sits in G0 all winter and for decades — it does not divide — yet it is alive, reading its genes and making proteins every day, and it is where varicella-zoster virus waits after a first infection, reactivating in January to travel down one nerve to the skin (SEE MODULE 22.5); mature neutrophils never divide at all — they leave the marrow finished, live hours to a few days, and are replaced by dividing precursors that make tens of billions a day, more during an infection. A fourth question appears once all three lanes are set: WHICH LANE DROVE THE FEVER OF 104? (neutrophils, sending fever messengers — Module 1’s thermostat). Then a locked card: WHICH LANES READ MEFV? — opens in Scene 4. Every lane’s nucleus shows the same genome strip with two marked genes (MEFV, LPIN2), so the student sees from the first scene that cycle state and genome are separate questions. Keyboard path: Tab moves lane by lane, arrow keys move month by month, Enter opens the state menu; reveals are announced in a polite live region. A <details> text version gives the lane-by-month answers as a table and the three reveal cards in full.

Think · not graded

The neuron that hid the shingles virus hadn’t divided in years; a keratinocyte in her skin was dividing every few days; a neutrophil in her throat would never divide at all. All three carried the same genome. What does a cell parked in G0 still do with its DNA every day — and why does it matter, for an inherited variant, that a cell has stopped dividing?

The true/false spot-check for this prompt is in production.

Check · Fill in the Blanks

M phase divides; G0 opts out. Fill in each blank.

This self-scoring check is in production.

Evidence card 1

Add it to your evidence board

One winter, three tissues struck in a row — a throat, the skin, one nerve on the left side — each given its own diagnosis and its own doctor.

Scene 2 of 6

An Ordered Sequence

Grow, copy, grow, divide — or step off the cycle and just do your job.

Slide · in production

An Ordered Sequence

The cell-cycle wheel, labeled in Amy’s order: G1 (growth — the cell makes proteins and does its job; DNA loose as chromatin so it can be read) → S (synthesis — every chromosome copied, each growing a sister chromatid joined at the centromere) → G2 (growth again, and a check of the copy) → M (mitosis, or meiosis in gamete-making cells). An inner arc labels G1 + S + G2 as interphase. A siding off G1 is labeled G0 — parked off the cycle: most neurons for life, a liver cell until injury calls it back. Time labels for a fast-dividing human cell in a dish (about 24 hours a lap): G1 about 11 h, S about 8 h, G2 about 4 h, M about 1 h. Two banners: “Every cell comes from a pre-existing cell” and “Same chromosome, two chromatids.” Alt text: “Cell-cycle wheel: G1, S, G2 and M in order, with interphase spanning G1 to G2 and a G0 side branch for cells that stop dividing.”

Explore · in production

Size the pie

A round 24-hour clock face divided into four colored wedges — G1, S, G2, M — whose three inside boundaries the student can drag. Task 1: before any reveal, drag the boundaries to show how a fast-dividing human cell in a dish splits its day; a readout shows each wedge in hours and as a percentage. Reveal: G1 about 11 h, S about 8 h, G2 about 4 h, M about 1 h — interphase is about 95% of the lap, “the long, unglamorous stretch”; M is the brief, showy finale. A follow-up question: if you photographed 100 such cells at random, how many would you expect to catch in mitosis? (about 4) — with a link out to Amy’s existing Mitotic Index lab (page 36419) for students who want to count real-looking cells. Task 2: six cell cards slide in one at a time — a cell in the lining of the gut (divides about daily; the lining renews every few days), a basal keratinocyte in the epidermis (divides steadily; the epidermis renews in about four weeks — after strep in psoriasis-prone skin it speeds up, SEE MODULE 5.2), a hepatocyte (parked in G0, but re-enters the cycle when the liver is injured — a liver can regrow lost tissue), a mature neuron (G0 for life), a mature red blood cell (no nucleus — it can never divide; new ones come from marrow precursors at about two million a second), a mature neutrophil (finished, never divides; precursors in the marrow do the dividing). For each card the student drags the cell onto the ring, onto the G0 siding, or into a NEVER DIVIDES tray, and predicts before the reveal. Task 3, the counting rule: a chromosome icon shows up at G1, S, G2, prophase and metaphase and the student says ONE CHROMOSOME or TWO — the answer is one at each of those, single (G1) or duplicated (G2 onward, two chromatids at a centromere); “same chromosome, two chromatids.” Then one anaphase card: “Now two — the sisters have parted and each has its own centromere. Count the centromeres.” Keyboard path: each boundary is a slider with step buttons (1 hour); cards are placed with arrow keys and Enter. A <details> text version gives the 24-hour split, the six cell answers and the counting rule.

Prefer the full lecture? The Cell Cycle (original video on the site)

Think · not graded

In a typical 24-hour cycle, mitosis takes about an hour. If you photographed a field of actively dividing cells, roughly what share would you catch in mitosis — and why would that share tell you something about how long each phase lasts? Then name one cell in Stina’s body that would never show up in mitosis at all, and say why.

The true/false spot-check for this prompt is in production.

Check · Single Choice

What is the correct order of the cell cycle?

This self-scoring check is in production.

Evidence card 2

Add it to your evidence board

Three illnesses on three timetables: a throat infection over in ten days, spots that took six weeks to appear, a nerve that flared months later.

Scene 3 of 6

Metaphase, Middle

Four phases, three things to watch — and the one counting mistake mitosis can make, which is not the kind of mistake Stina carries.

Animation · in production · 2 min 15 s

Metaphase, Middle

An interphase cell with loose red and blue chromatin (red from Mom, blue from Dad) and a centrosome beside the nucleus. A label floats in: THREE THINGS TO WATCH — the cell’s shape, the spindle, where the chromosomes sit. Prophase: the chromatin coils into X-shaped duplicated chromosomes (a tag: SAME CHROMOSOME, TWO CHROMATIDS); the nuclear envelope turns to a dotted line and vanishes; the two centrosomes slide to opposite sides and spin out spindle fibers that hook onto the kinetochores at each centromere. Metaphase: the chromosomes shuffle into a single line across the middle — METAPHASE, MIDDLE — and a small stopwatch waits until the very last kinetochore is attached (the spindle checkpoint). A pair of scissors labeled SEPARASE snips the cohesin rings holding each pair of sisters together. Anaphase: the sisters are hauled to opposite poles in a tug of war while an energy meter in the corner drains. Telophase: two nuclear envelopes re-form and the chromosomes loosen — PROPHASE IN REVERSE. Cytokinesis: a cleavage furrow pinches the cell into two, under the banner TELOPHASE ≠ CYTOKINESIS. Two daughter cells, each with 46 chromosomes. A side panel replays the lineup with one chromosome whose two sister chromatids fail to separate: one daughter gets 47, the other 45 — A COUNTING MISTAKE (nondisjunction). The last frame zooms into one chromosome 16 in both normal daughters: the same single marked letter in MEFV, copied perfectly — A SPELLING DIFFERENCE, COPIED FAITHFULLY.

Prefer the full lecture? Mitosis (original video on the site)

Explore · in production

Count as you scrub

A continuous mitosis movie built from the same BioRender phase set, with a scrub bar along the bottom and eight stop marks on it (late G1, late G2, prophase, prometaphase, metaphase, anaphase, telophase, two daughter cells). The cell is a teaching cell with 2n = 4 (two pairs — red from Mom, blue from Dad) so every chromosome can be counted on screen. The student can scrub freely, but at each stop mark the movie locks until three counts are entered: CHROMOSOMES (count the centromeres — Amy’s rule), CHROMATIDS, and DNA AMOUNT compared with G1 (1× or 2×). A “what just changed” callout then names the one event that happened since the last stop (the envelope dissolved; the spindle attached at the kinetochores; separase cut the cohesin; the envelopes re-formed; the furrow pinched). The trap stops are built in: in G2 there are still 4 chromosomes but 8 chromatids and 2× the DNA; in anaphase, the moment the sisters part, the count jumps to 8 chromosomes (each chromatid now has its own centromere) until cytokinesis splits them 4 and 4. A switch at the end swaps the teaching cell for a human one: 46 chromosomes → 92 chromatids at metaphase → two daughters of 46. Final branch, WHEN SORTING FAILS: the student replays metaphase with one chromosome whose sister chromatids stay stuck together and predicts the daughters’ counts (one gets an extra chromosome, one is short); the card names nondisjunction as a counting mistake — and adds the contrast that frames the module: a correct count with one changed letter inside one chromosome is copied into both daughters, perfectly, every time. This explore counts; the animation above choreographs; Amy’s lab 36418 builds — three different jobs. Keyboard path: arrow keys scrub frame by frame, Tab moves to the three number fields at a stop mark, Enter checks the counts; each frame has a text description in a live region. A <details> text version gives every stop mark’s counts and the “what just changed” lines as a table.

Think · not graded

Telophase and cytokinesis get confused every year. Say what each one separates, and describe a cell that has finished telophase but is still one cell. Then explain why nondisjunction is a counting mistake, and why a single changed letter inside one chromosome is not a mistake mitosis can make or catch.

The true/false spot-check for this prompt is in production.

Check · Drag the Words

Watch three things — the cell’s shape, the spindle, where the chromosomes sit. Drag each event to its phase. Two distractors are on the bank.

This self-scoring check is in production.

Evidence card 3

Add it to your evidence board

Six weeks after the strep, spots across her chest, back and arms at once — a skin whose dividing cells had changed pace.

Scene 4 of 6

Same Book, Different Pages

Every cell in her body carries the same MEFV copy. Only a few kinds of cell ever open that page.

Animation · in production · 2 min 15 s

Same Book, Different Pages

One thick book labeled GENOME — about 20,000 genes — sits on a shelf; one page is tabbed MEFV, another LPIN2, and on the MEFV page one letter is circled. The book is copied into four cells that line up side by side: a keratinocyte, a neuron, a red-cell precursor in the marrow, a neutrophil. In each, small hands labeled TRANSCRIPTION FACTORS open a few pages and leave the rest clasped shut: keratin pages wide open in the keratinocyte, neurotransmitter-enzyme pages in the neuron, hemoglobin pages in the red-cell precursor — and in the neutrophil the MEFV page lies flat open, its message copied to mRNA and read on free ribosomes into pyrin. A banner: PRESENCE ≠ EXPRESSION. An inflammatory signal arrives as a red pulse; the MEFV page opens wider in a monocyte and a neutrophil and stays clasped in the skin and the nerve. Eosinophils and dendritic cells join the reading line; a tissue macrophage reads the LPIN2 page too, tagged “lipin-2 matters here (one study)”. The camera pulls out to a body outline: lights come on where neutrophils gather — the lining of the belly, the lining of the chest, the joints, a patch of skin on the shins — and stay dark over the brain. Last frame: EVERY CELL CARRIES IT. FEW CELLS READ IT.

Prefer the full lecture? DNA to RNA (original video on the site)

Explore · in production

Light the lamps

Eight cells stand in a row, each drawn from the Asset catalog and labeled: neutrophil · monocyte/macrophage · eosinophil · dendritic cell · keratinocyte (skin) · neuron · hepatocyte (liver) · red-cell precursor (bone marrow). Inside each nucleus the same genome strip scrolls by, with Stina’s two changed copies marked (MEFV E148Q, LPIN2) — identical in all eight, which a counter confirms: SAME GENOME 8/8. Above each cell sit five gene lamps: MEFV · KRT (keratin) · HBB (β-globin) · ALB (albumin) · ACTB (β-actin, a housekeeping gene). Round 1: the student predicts which lamps are lit in each cell by switching them on, then presses READ and the true pattern lights — ACTB in all eight (every cell needs a skeleton of actin); KRT in the keratinocyte; ALB in the hepatocyte; HBB in the red-cell precursor; MEFV bright in the neutrophil, monocyte/macrophage, eosinophil and dendritic cell, and dark in the keratinocyte, neuron, hepatocyte and red-cell precursor. A score shows how many lamps the student called. A card explains the rule: every nucleated cell carries every gene; transcription factors decide which genes are transcribed (“only selected genes are transcribed,” Chapter 3) — differentiation is identical DNA running different programs. Round 2: an INFLAMMATORY SIGNAL switch; the student predicts which MEFV lamps change, then sees them brighten in the white cells (MEFV transcription is reported to rise with inflammatory signals) while the skin, nerve and liver stay dark — the signal can’t open a page a cell keeps shut. Round 3, PREDICT THE ATTACKS: a small body map with eight tissue buttons (lining of the belly, lining of the chest, joints, skin of the shins, brain, skeletal muscle, liver, lens of the eye); the student marks where a gain-of-function pyrin should cause trouble, then the reveal lights the places neutrophils gather in an attack — the serous linings, the synovial joints, skin — and reveals skeletal muscle as SOMETIMES: FMF can cause muscle pain (her own cycle ended with “Then the legs”), though the muscle cells themselves don’t read MEFV — the white cells that reach them do — with a note that FMF’s classic attacks are exactly those (Module 1.4’s membranes). A closing line: the variant’s presence is everywhere; its expression decides where the disease lives. Keyboard path: Tab moves cell to cell, arrow keys move between lamps, Space toggles a lamp, Enter reads; every lamp state is announced (“Neutrophil, MEFV: on”). A <details> text version gives the full lamp table, the signal result and the attack map.

Think · not graded

A keratinocyte and a neutrophil from Stina’s body carry exactly the same E148Q copy of MEFV. Using what you know about transcription, explain why only one of them could ever make a changed pyrin. Then predict which tissues a trigger-happy pyrin should inflame — and which it should leave alone — and say what your prediction rests on.

The true/false spot-check for this prompt is in production.

Check · Single Choice

Every nucleated cell carries MEFV. Why do FMF attacks show up in the lining of the belly, the lining of the chest and the joints rather than in the brain?

This self-scoring check is in production.

Evidence card 4

Add it to your evidence board

A fever of 104 with the strep — the one sign that winter made by white blood cells, alongside a skin rash and a nerve’s blisters.

Scene 5 of 6

Thirty-Seven Trillion Copies

One zygote, about forty-five doublings’ worth of mitosis, and a lifetime of repair — every copy carrying the same two changed genes.

Animation · in production · 2 min 10 s

Thirty-Seven Trillion Copies

A single zygote, two pronuclei merging, and in its new nucleus a genome strip with two marked genes (MEFV, LPIN2). A counter in the corner reads 1. The cell divides: 2 (two-cell embryo), 4 (four-cell embryo), 8, 16 — a morula — then a hollow blastocyst of a hundred-odd cells, the counter climbing 2, 4, 8, 16, 32… Each daughter cell’s nucleus carries the same two marked genes. The counter speeds up and stops near the 45th doubling at about 35 trillion, beside a number card that reads ABOUT 37 TRILLION CELLS (an old card reading 60 TRILLION is crossed out). Branches fan out as cells take jobs — skin, gut lining, bone, marrow, nerve — under the line SAME INSTRUCTION, DIFFERENT ASSIGNMENTS. A second counter appears, LIFETIME DIVISIONS, and keeps running after the first one stops: red cells replaced at about two million a second, the gut lining every few days, the epidermis every few weeks. Then a close-up of the roof of a mouth with a small burn — the pizza — and neighboring cells dividing overnight to close it. Last frame: the body outline with every cell glowing the same two marked genes, and the line FIDELITY BUILT HER.

Prefer the full lecture? Mitosis (original video on the site)

Explore · in production

Double it

A single zygote sits on the left of a long log-scale ruler marked 1 · 10 · 1,000 · 1 million · 1 billion · 1 trillion · 37 trillion. Task 1, predict: before touching anything, the student guesses how many rounds of doubling it would take for one cell to reach about 37 trillion if no cell ever died (choices 23 · 45 · 100 · 1,000). Then a DOUBLE button: each press doubles the count, moves a marker along the ruler and fills a small grid of cells; milestone flags pop up — 16–32 cells (morula, about day 3–4), about 100–200 cells (blastocyst, about day 5) — and after 45 presses the counter reads about 35 trillion, within shouting distance of the real figure (Bianconi et al. 2013); the reveal card: about 45 doublings, because 2 multiplied by itself 45 times is about 35 trillion. A REAL BODY toggle then changes the game: cells die and are replaced (red cells at about two million a second, the gut lining every few days, the epidermis every few weeks, mature neutrophils after hours to days), so a second counter of LIFETIME DIVISIONS races past the body’s size — a body makes far more cells in a lifetime than it ever holds at once. Task 2, branches: at four forks the student assigns a job card (skin, gut lining, marrow → neutrophil, nerve) and watches that branch’s cells take a shape; each branch’s nucleus shows the same genome strip with the same two marked genes. A question card asks: CAN A BRANCH LOSE THE VARIANT? Options: yes, if it stops dividing · yes, if it differentiates · no — every branch inherits the zygote’s copy (with a footnote linking Chapter 2’s somatic changes, which add new letters in one lineage but never remove the inherited one). Final screen: a body outline built from the student’s branches, every cell lit, and the line “one inherited letter, every cell.” Keyboard path: Space doubles, T toggles REAL BODY, Tab moves to the forks and Enter assigns a job; the count is announced in words. A <details> text version gives the doubling table (1 to 45), the milestones and the answers.

Think · not graded

If no cell ever died, about 45 rounds of doubling would turn one zygote into roughly 37 trillion cells. Why does a real body need vastly more divisions than that over a lifetime? And why does every one of those divisions — in the gut, the marrow, the skin of a healing burn — still hand on the zygote’s two variant copies?

The true/false spot-check for this prompt is in production.

Check · Single Choice

What are the two main jobs of mitosis in the body?

This self-scoring check is in production.

Evidence card 5

Add it to your evidence board

Seventeen years old and three different tissues involved in four months — every one of them grown from the same fertilized egg.

Scene 6 of 6

Guards at Every Gate

Checkpoints are negative feedback for a dividing cell — and they are built to catch damage, not to proofread the original text.

Slide · in production

Guards at Every Gate

The checkpoint wheel with three gates and what each asks. G1/S: is the cell big enough, fed, signaled to grow, and is its DNA undamaged? (p53 can hold the cycle here.) G2/M: was the whole genome copied, completely and correctly? Spindle (M) checkpoint: is every chromosome attached to the spindle before anaphase starts? An overlay redraws one gate as Module 1’s negative-feedback loop: checkpoint proteins sense a problem, cyclin–kinase signals act as the control center, and the response halts the cycle until the problem is fixed — or, if it can’t be fixed, sends the cell to apoptosis (A5057). A side panel, THE CYCLE OUT OF CONTROL: cancer is many mutations in several genes accumulated over years, until the gates are ignored and the saboteurs reproduce (A5055). A case box: an inherited variant like E148Q isn’t damage — it is a correctly copied letter in the original text, so every gate reads it as normal and waves it through. A footnote: colchicine, the drug used for FMF, was the original spindle poison — it binds tubulin — but at FMF doses it works on neutrophils’ microtubules (Module 3) and does not stop the body’s mitosis. Alt text: “Cell-cycle wheel with three checkpoints — G1/S, G2/M and the spindle checkpoint in M — each with its pass criteria, and an apoptosis branch for cells that fail.”

Explore · in production

The inspection line

A factory-style conveyor carries cells past three gates labeled G1/S, G2/M and SPINDLE. The student is the checkpoint. Each cell arrives with a status card the student can read before deciding PASS · HOLD FOR REPAIR · APOPTOSIS: (1) a healthy G1 cell, big enough, growth signal present — pass; (2) a G1 cell with a double-strand break in chromosome 9 — hold (p53 halts the cycle while repair works); (3) the same cell, break unrepairable — apoptosis (the cell fragments into tidy apoptotic bodies; “the system would rather lose a soldier than let a saboteur reproduce”); (4) a G2 cell with one stretch of chromosome 3 not yet copied — hold; (5) a metaphase cell with one kinetochore unattached — hold at the spindle gate until it attaches; (6) a cell with an extra centriole and three spindle poles — apoptosis; (7) a cell whose card reads: all checks pass; carries one E148Q copy in MEFV and one LPIN2 variant, both copied correctly from the zygote — the student decides, and the reveal shows every gate reading it as normal, because a gate checks for damage and miscopying, not for whether the original text is a common or an uncommon spelling. A score shows the student’s calls against the gates’. Then a second lane, YEARS LATER: one cell collects hits one at a time — a growth-signal gene stuck ON, a brake gene lost, p53 lost — and with each hit one gate goes dark, until a clump of cells piles up past the line (cancer: many mutations in several genes over years). The two lanes end side by side under Amy’s line: cancer is control lost over time; an inherited variant is a letter that never trips the controls at all — same machinery, two utterly different failures. A final card about colchicine: the original spindle poison, but at FMF doses it acts on neutrophils’ microtubules and leaves the body’s mitosis running (Module 3 owns the mechanism). Keyboard path: Tab to the status card, then arrow keys and Enter choose a decision; each gate’s verdict is announced. A <details> text version lists all seven cells with the correct calls and the years-later sequence.

Prefer the full lecture? The Cell Cycle (original video on the site)

Think · not graded

A checkpoint senses a problem and stops the cycle until the problem is gone. Explain why that makes it negative feedback, naming the sensor, the control and the response. Then explain why an inherited, correctly copied variant like E148Q gives every checkpoint nothing to sense — and how that differs from what goes wrong in cancer.

The true/false spot-check for this prompt is in production.

Check · Single Choice

Why is a cell-cycle checkpoint an example of negative feedback?

This self-scoring check is in production.

Evidence card 6

Add it to your evidence board

The shingles was called “unusual for my age” — the chart named the rarity and stopped there.

4

Your evidence board

Every scene gave you an evidence card, and the chart adds more. Sort each card into the column it supports: One genome, read differently by different cells, Neither on its own, or “Unusual for my age”. Some cards can honestly go in more than one place — that’s allowed, and the feedback tells you which cards decide the case.

Evidence board · drag and drop · in production

The sorting board for this chapter’s cards is being built. Until it arrives, sort your evidence cards on paper into the three columns above.

5

Your verdict

Time to decide. Look back at your bet, then build your verdict from statements that hold up — no writing needed.

Look back at your prediction

Strep, then teardrop spots, then shingles, October to February — read through the cell cycle and gene expression, the reading that fits best is…

Find the one you chose at the top. Does the evidence support it, refute it, or revise it?

  • Nothing — “Three diagnoses, three creams, three different doctors”
  • One genome, run and read differently by three kinds of cell
  • Stress — “whether I’d been under a lot of stress”

Build your verdict · no writing

Choose the statement that holds in each set. The ones you keep become your argument.

This activity is in production.

6

The finding

Finding · the cell cycle

Every Cell Carries It; Few Cells Read It

October 1992 to February 1993, age seventeen: the October-to-February season — strep, teardrops, shingles (Integumentary 5.2, Immunity 22.5) — filed as three diagnoses, three creams, three different doctors, and the question whether she’d been under a lot of stress. Chart entry: every cell in her body descends by mitosis from one zygote and carries the same genome, including one MEFV E148Q copy and one LPIN2 copy, waved through every checkpoint because a correctly copied letter is not damage; but cells differ in what they read — neutrophils, monocytes, eosinophils and dendritic cells transcribe MEFV, while keratinocytes and neurons keep it shut. Gene presence is not gene expression, and expression decides where an FMF attack can live. Held open: how two parents’ copies came together in that zygote (Chapter 6), and what kind of person gets all three in a row (Chapter 7).

Next · Chapter 6

Meiosis and the Family Tree

Seventeen, and the withdrawal paper: “Mom signed under me and didn’t say anything, and Dad said I could get a GED.” Two parents on one page — and one copy of every chromosome from each of them.

Continue to Chapter 6 →

Reliable information on rare diseases

NORD · NIH GARD · Orphanet · MedlinePlus Genetics: FMF · FMF & AID Global Association · Autoinflammatory Alliance · Global Genes · Amyloidosis Foundation

Stina has one rare disease. In the United States, about 1 in 10 people live with one of the more than 7,000 known rare diseases. These organizations are where patients, families and clinicians go for trustworthy information.

Hop to:

← Familial Mediterranean Fever — case home

All pages for Module 4 — Making Cells & Proteins

4.0 Module Overview
4.1 The Code
4.2 Copying the Code
4.3 Transcription
4.4 Translation — and Then Break It
4.5 The Cell Cycle and Mitosis
4.6 Meiosis and the Family Tree
4.7 One Typo, Every Cell — the Chart Reveal
4.8 Conclusion and Assessment
4.9 Evidence Behind the Case

All Modules
  1. Anatomical Language, Membranes & Homeostasis
  2. Just Enough Chemistry
  3. The Cell & Its Transport
  4. Making Cells & Proteins
  5. The Integumentary System
  6. The Skeletal System
  7. The Muscular System
  8. Nervous Tissue & the Senses
  9. The Spinal Cord
  10. The Brain & the Blood–Brain Barrier
  11. The Autonomic Nervous System
  12. Special Senses (in development)
  13. The Endocrine System
  14. Blood
  15. The Heart
  16. Blood Vessels
  17. The Digestive System
  18. The Respiratory System
  19. The Urinary System
  20. Fluids, Electrolytes & Acid–Base Balance
  21. The Reproductive System
  22. The Immune System

List of terms