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2C · Cells, microbes, and how they organize and divide
Processes of cell division, differentiation, and specialization
One cell becomes many through the cell cycle and mitosis, and those identical cells become different through differentiation — guided by signals, regulated gene expression, and programmed cell death (apoptosis). This category covers the cell cycle and its control, mitosis, how cells specialize, and the stages of early development.
The cell cycle
The cell cycle is interphase (G1 → S → G2, where the cell grows and copies its DNA) followed by M phase (mitosis + cytokinesis). Non-dividing cells rest in G0.
Interphase is most of the cycle: G1 (growth, normal metabolism), S (DNA synthesis — each chromosome is copied into two sister chromatids), and G2 (growth, prep for division, error-checking). M phase then splits the nucleus (mitosis) and the cell (cytokinesis). Cells that have exited the cycle — neurons, mature muscle — sit in G0, alive but not dividing.
Checkpoints, cyclins & CDKs
Checkpoints verify the cell is ready before it proceeds. They're driven by cyclins binding cyclin-dependent kinases (CDKs); p53 guards the G1/S checkpoint, halting a damaged cell.
The major checkpoints are G1/S (the "restriction point" — is the DNA undamaged and are conditions favorable to commit to division?), G2/M (was DNA replicated correctly?), and the spindle (M) checkpoint (are all chromosomes attached to the spindle before separation?). Cyclin levels rise and fall through the cycle; a cyclin activates its CDK partner, and the cyclin–CDK complex phosphorylates targets that push the cell into the next phase. p53 is the central guardian: on sensing DNA damage at G1/S, it arrests the cycle for repair or, if damage is severe, triggers apoptosis.
Cancer: oncogenes vs. tumor suppressors
Cancer is loss of cell-cycle control. Oncogenes are overactive accelerators (a gain-of-function mutation in a proto-oncogene, e.g., ras); tumor suppressors are failed brakes (a loss-of-function mutation, e.g., p53, Rb).
Think of two pedal types. A proto-oncogene normally promotes division; mutate it to be hyperactive and it becomes an oncogene — a stuck accelerator. A single activating mutation is enough, so oncogenes act dominantly at the cell level. A tumor suppressor normally restrains division or triggers apoptosis; you must knock out both copies to lose the brake, so tumor suppressors act recessively (the "two-hit" idea). Cancer cells also evade apoptosis, divide without limit, and lose contact inhibition.
Don't confuse
Oncogene = gain of function, accelerator on, one hit; tumor suppressor = loss of function, brake off, two hits. p53 is a tumor suppressor (the most commonly mutated gene in cancer), not an oncogene.
Mitosis
Mitosis divides one nucleus into two genetically identical nuclei. Its phases are prophase → metaphase → anaphase → telophase (PMAT), followed by cytokinesis.
Mitosis is the engine of growth, repair, and asexual reproduction — equal division producing two diploid daughters identical to the parent. The chromosomes (already duplicated in S phase into joined sister chromatids) are lined up, split, and parceled out evenly by the spindle.
The phases & cytokinesis
Prophase — chromatin condenses, spindle forms, nuclear envelope breaks down. Metaphase — chromosomes align at the metaphase plate. Anaphase — sister chromatids separate to opposite poles. Telophase — nuclear envelopes re-form. Cytokinesis splits the cytoplasm.
Each phase has a signature you can be tested on: condensation + spindle assembly (prophase), single-file alignment in the middle (metaphase), the moment of chromatid separation that makes each pole's set complete (anaphase), and re-forming two nuclei (telophase). Cytokinesis differs by kingdom: animal cells pinch in with an actin cleavage furrow; plant cells build a cell plate down the middle because a rigid wall can't pinch.
Spindle, centrosomes & kinetochores
The mitotic spindle is built from microtubules organized by centrosomes (containing centrioles) at the poles; spindle fibers attach to each chromatid at its kinetochore (on the centromere).
Centrosomes migrate to opposite poles and nucleate the spindle; kinetochore microtubules bind the kinetochore protein complex at each sister chromatid's centromere, while motor proteins shorten them in anaphase to haul the chromatids apart. This is why microtubule poisons (taxol, vinca alkaloids) arrest cells in mitosis — they jam the spindle.
Mitosis vs. meiosis
Mitosis = one division → two identical diploid cells (growth/repair). Meiosis = two divisions → four genetically unique haploid cells (gametes), with crossing over and independent assortment.
The defining differences: mitosis has no synapsis and no crossing over, keeps the chromosome number (2n → 2n), and yields clones; meiosis pairs homologs (synapsis/tetrads), recombines them, and halves the chromosome number (2n → n) across two rounds, yielding variation. The reductional step is meiosis I (homologs separate); meiosis II resembles mitosis (sister chromatids separate). (Full meiosis detail lives in 1C.)
Don't confuse
Sister chromatids separate in mitosis and meiosis II; homologous chromosomes separate in meiosis I. Crossing over happens only in meiosis I.
Apoptosis
Apoptosis is programmed, controlled cell death — the cell neatly dismantles itself (via caspases) without spilling its contents, so there's no inflammation. It contrasts with necrosis, the messy, injury-driven death that does inflame.
Apoptosis sculpts the body: it removes the webbing between fingers, prunes excess neurons, and deletes self-reactive immune cells. The cell shrinks, fragments its DNA, and packages itself into "apoptotic bodies" that neighbors clean up. Because it's deliberate, it requires energy and signaling — and failure of apoptosis (e.g., a broken p53 pathway) lets damaged cells survive and contributes to cancer.
Don't confuse
Apoptosis = programmed, tidy, no inflammation; necrosis = unplanned, cell bursts, causes inflammation.
Differentiation & stem cells
Differentiation is how identical cells become specialized — by turning different subsets of the same genome on and off. The less differentiated a cell, the more cell types it can still become (its potency).
Every somatic cell has the full genome; what differs is which genes are expressed (the eukaryotic gene regulation of 1B). As cells commit to fates, they progressively lose options — and the cells that retain options are stem cells, the body's reservoir for growth and repair.
Determination vs. differentiation
Determination is the commitment to a fate (set internally, often before any visible change); differentiation is the visible specialization that follows — the cell actually expressing its fate.
A determined cell looks unchanged but is already locked onto a path; differentiation is the cash-out, when it builds the proteins and structures of its specialized type. Determination can be driven by cytoplasmic determinants (molecules unevenly distributed in the egg) or by induction from neighboring cells.
Stem-cell potency
Totipotent cells can become any cell including the placenta (the zygote and very early cells); pluripotent cells can become any of the three germ layers but not the placenta (embryonic stem cells); multipotent cells make a limited family (adult stem cells, e.g., blood-forming).
Potency is a ladder of narrowing options:
- Totipotent — can form a complete organism and extra-embryonic tissue (placenta). Only the zygote and earliest cleavage cells.
- Pluripotent — can form any cell of the body (all three germ layers) but not the placenta. The inner cell mass of the blastocyst; embryonic stem cells.
- Multipotent — can form several related cell types within a lineage. Most adult/somatic stem cells (e.g., hematopoietic stem cells → all blood cells).
Don't confuse
Toti = total, includes placenta; pluri = all body cells, no placenta; multi = one lineage only. The jump people miss is that pluripotent cells cannot form the placenta.
Induction & cell communication
Induction is one group of cells secreting signals (morphogens) that direct the fate of nearby cells; concentration gradients of these signals give cells their positional information.
Development is choreographed by cells talking to neighbors. A classic example: the notochord induces the overlying ectoderm to become the neural plate (the start of the nervous system). Morphogens diffuse to form gradients, and a cell reads its concentration to "know" where it is and what to become — high vs. low signal triggers different gene programs.
Early embryonic development
After fertilization, the embryo runs an ordered program: cleavage → blastula → gastrulation → neurulation, establishing the three germ layers that give rise to every tissue.
The sequence is the thing to memorize cold (AAMC loves "what comes next" and "which layer makes X"). Rapid cell divisions partition the egg, a cavity forms, cells rearrange into layers, and the nervous system is laid down — each step setting up the next.
Fertilization, cleavage & the blastula
Fertilization forms the diploid zygote; cleavage is a series of rapid mitotic divisions with no growth (cells get smaller), producing a solid morula that hollows into a fluid-filled blastula (a blastocyst in mammals).
Cleavage divides the large egg into many small cells without increasing total size, raising the cell-to-cytoplasm ratio. The blastula is a hollow ball around a cavity (blastocoel); in mammals, the blastocyst's inner cell mass (pluripotent) becomes the embryo while the outer trophoblast becomes placental tissue. Implantation follows in mammals.
Gastrulation & the three germ layers
Gastrulation rearranges the blastula into three germ layers — ectoderm (outer), mesoderm (middle), endoderm (inner) — each the source of specific tissues.
Cell movements form a gastrula with a primitive gut (archenteron) opening at the blastopore. The derivatives are high-yield:
- Ectoderm ("attract-o-derm," the outer + nervous): epidermis, hair, nails, and the entire nervous system (brain, spinal cord, neurons), plus lens of the eye.
- Mesoderm (the "middle/muscle" layer): muscle, bone, connective tissue, blood and heart, kidneys, and gonads.
- Endoderm (the inner linings): epithelial lining of the gut and respiratory tract, and the liver, pancreas, and other gut-derived glands.
Don't confuse
The nervous system is ectoderm, not mesoderm — the single most-tested germ-layer fact. Muscle, bone, blood, and gonads are mesoderm; the gut/lung/liver linings are endoderm.
Neurulation
Neurulation builds the nervous system: the notochord (mesoderm) induces the overlying ectoderm to fold into a neural tube, which becomes the brain and spinal cord.
The neural plate folds up, its edges meet, and it pinches off as the neural tube below the surface; neural crest cells break away from it and migrate widely (forming peripheral neurons, some skull and facial structures, and pigment cells). The notochord itself later regresses, leaving remnants in the spinal discs. This is the textbook case of induction driving differentiation.
Worked question
A gene's protein normally halts the cell cycle when DNA is damaged. Researchers find that cancer develops in this tissue only when both copies of the gene are inactivated, while inactivating just one copy has little effect. This gene is best classified as a: