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2B · Cells, microbes, and how they organize and divide
The structure, growth, physiology, and genetics of prokaryotes and viruses
Prokaryotes (bacteria and archaea) are single cells with no nucleus or membrane-bound organelles; viruses are not cells at all — they're packets of nucleic acid in a protein coat that can only reproduce inside a host. This category covers prokaryotic structure, growth, and gene transfer, then viral structure and life cycles.
Cell theory
Cell theory: all living things are made of cells, the cell is the basic unit of life, and all cells arise from pre-existing cells.
The modern theory adds that cells carry hereditary information (DNA) passed on during division, and that energy flow (metabolism) occurs within cells. Note the historical caveat AAMC sometimes leans on: viruses are an exception — they are not cells and don't satisfy the theory (no independent metabolism or division), which is why they sit at the edge of "living."
Prokaryotic cell structure
A prokaryote has no nucleus (its DNA sits in a nucleoid), no membrane-bound organelles, a cell wall, and 70S ribosomes. The two domains are Bacteria and Archaea.
Prokaryotes keep a single circular chromosome in the nucleoid region — not enclosed by a membrane — plus often small plasmids. They lack mitochondria, ER, Golgi, and a true nucleus; metabolic reactions happen in the cytoplasm or on the plasma membrane. Archaea resemble bacteria in size and form but differ biochemically (distinct membrane lipids and cell-wall chemistry) and include many extremophiles.
Shapes, the cell wall & Gram staining
Bacteria come in three shapes — cocci (spheres), bacilli (rods), spirilla (spirals) — and split by cell wall into Gram-positive (thick peptidoglycan, stains purple) and Gram-negative (thin peptidoglycan + an outer membrane, stains pink).
The cell wall is made of peptidoglycan and protects against osmotic lysis. Gram-positive cells have a thick peptidoglycan layer that traps the crystal-violet stain (purple). Gram-negative cells have a thin peptidoglycan layer sandwiched under an outer membrane containing lipopolysaccharide (LPS, an endotoxin); they lose the violet stain and take the pink counterstain. The outer membrane also makes Gram-negatives harder for many antibiotics and the immune system to penetrate.
Don't confuse
Gram-positive = thick wall, purple; Gram-negative = thin wall + outer membrane, pink. "Positive/thick/purple" travel together.
Flagella, pili & motility
A bacterial flagellum is a rotating protein filament driven by the proton-motive force (not microtubules); pili/fimbriae attach cells to surfaces and to each other (the sex pilus mediates conjugation). Chemotaxis steers movement toward attractants.
The bacterial flagellum spins like a rotary motor powered by H⁺ flowing across the membrane — structurally and mechanistically unrelated to the microtubule 9+2 eukaryotic flagellum (a recurring "analogous, not homologous" trap). Bacteria sense chemical gradients and bias their swimming (runs and tumbles) toward food and away from toxins — chemotaxis.
Ribosome Subunits: 70S vs. 80S
Prokaryotes have 70S ribosomes (a 30S + a 50S subunit); eukaryotes have larger 80S ribosomes (a 40S + a 60S subunit). Svedberg (S) units measure sedimentation, so they don't simply add (30 + 50 = 70, not 80).
A ribosome is built from two subunits made of rRNA + protein; the small subunit binds mRNA and the large subunit catalyzes peptide-bond formation. The numbers are the clue to the source: prokaryotic = 70S (30S + 50S), eukaryotic = 80S (40S + 60S). Note the mitochondrial and chloroplast ribosomes are 70S-like, evidence for the endosymbiotic origin of those organelles.
Don't confuse
The S (Svedberg) unit reflects how fast a particle sediments in a centrifuge — a function of size and shape — so subunit S-values are not additive (30S + 50S → 70S). Mnemonic: prokaryotes get the odd numbers (30/50/70), eukaryotes the even ones (40/60/80).
How AAMC tests it
The 70S/80S difference explains selective antibiotic toxicity: drugs like aminoglycosides and tetracyclines target the bacterial 30S subunit, while macrolides/chloramphenicol hit the 50S — bacterial ribosomes are inhibited but the host's 80S ribosomes are spared.
Exotoxins vs. Endotoxins
Exotoxins are actively secreted proteins (classically from Gram-positive bacteria) that act at low doses and are often very specific. Endotoxin is lipopolysaccharide (LPS) in the Gram-negative outer membrane, released when the cell dies/lyses, triggering a generalized fever and inflammatory (septic) response.
Exotoxins are gene-encoded proteins a living cell exports (e.g., tetanus, botulinum, diphtheria toxins); because they're proteins they can often be denatured into toxoids for vaccines, and they tend to be potent and targeted. Endotoxin is the lipid A portion of LPS built into the Gram-negative outer membrane (see Gram staining); it isn't secreted — it's liberated when the bacterium lyses, and it provokes a strong innate-immune reaction (fever, inflammation, and in excess, septic shock).
Don't confuse
Exotoxin = secreted protein, Gram-positive, heat-labile, specific, often a vaccine toxoid. Endotoxin = LPS (part of the cell), Gram-negative, released on lysis/death, heat-stable, nonspecific fever/inflammation. Memory hook: endotoxin is inside the wall and comes out only when the cell breaks; exotoxin is exported by a live cell.
Growth & physiology of prokaryotes
Prokaryotes reproduce asexually by binary fission and can grow exponentially. They are classified by oxygen use — obligate aerobes, obligate anaerobes, facultative anaerobes — and adapt fast, which is how antibiotic resistance spreads.
Binary fission copies the chromosome and splits one cell into two identical daughters — fast but, by itself, clonal (no recombination). A culture's growth curve runs lag → log (exponential) → stationary → death. Oxygen relationships matter: obligate aerobes require O₂; obligate anaerobes are poisoned by it; facultative anaerobes use O₂ when present but ferment when it's absent (the most versatile). Because populations are huge and division is fast, mutations plus horizontal gene transfer let advantageous traits (like resistance) spread quickly under selection.
Metabolic & nutritional categories
Prokaryotes are grouped by carbon source (autotroph vs. heterotroph) and energy source (phototroph vs. chemotroph) — e.g., a chemoheterotroph gets both energy and carbon from organic molecules.
Combine the two axes: energy from light = photo-, from chemicals = chemo-; carbon from CO₂ = -autotroph, from organic compounds = -heterotroph. Most bacteria of medical interest are chemoheterotrophs. Some can also live as parasites (harming the host) or symbionts/mutualists (e.g., gut flora).
Genetics of prokaryotes
Beyond fission, bacteria gain genetic diversity by horizontal gene transfer — moving DNA between cells — and they regulate genes economically with operons.
Because binary fission alone produces clones, the real engine of bacterial variation is horizontal gene transfer: acquiring new DNA from the environment, a virus, or another cell. Plasmids — small, circular, extragenomic DNA — often carry the transferred traits (including resistance genes) and replicate independently of the chromosome.
Transformation, transduction & conjugation
Three routes move DNA horizontally: transformation (uptake of free DNA from the environment), transduction (DNA carried in by a bacteriophage), and conjugation (direct transfer through a pilus, e.g., an F plasmid).
- Transformation — a cell takes up naked DNA fragments released by dead cells from its surroundings.
- Transduction — a virus (phage) accidentally packages host DNA and injects it into the next cell it infects. (See viral cycles below.)
- Conjugation — two cells join via a sex pilus and one transfers DNA (often an F/fertility plasmid, the basis of "F⁺ → F⁻") directly to the other. This is the closest bacteria get to "sex," but it's one-way transfer, not reproduction.
Don't confuse
Transformation (free environmental DNA) vs. transduction (phage-delivered) vs. conjugation (cell-to-cell pilus). Mnemonic: transFORM = pick up DNA from your environ-FORM-ent; transDUCT = a phage "ducts" it in; conjugation = cells conjugate (join).
Operons & gene regulation
Bacteria cluster related genes under one promoter as an operon, switching the whole set on/off together — the lac (inducible) and trp (repressible) operons are the canonical examples.
An operon lets a cell respond to its environment cheaply: the lac operon is normally off and is induced when lactose is present (catabolism); the trp operon is normally on and is repressed when tryptophan is abundant (biosynthesis). This is the prokaryotic side of the gene-regulation story covered under operons in 1B.
Virus structure
A virus is a genome (DNA or RNA) wrapped in a protein capsid, sometimes with a lipid envelope stolen from a host membrane. Viruses have no organelles, no ribosomes, and no metabolism, and are far smaller than cells.
The capsid (built of repeating capsomere subunits) protects the genome and helps the virus attach to host cells. Enveloped viruses (e.g., HIV, influenza) wear a host-derived lipid bilayer studded with viral glycoproteins; naked viruses have only the capsid and tend to be hardier in the environment. The genome can be DNA or RNA, single- or double-stranded, linear or circular — a diversity that shapes how each virus replicates.
Bacteriophage structure
A bacteriophage ("phage") infects bacteria; the classic T-phage has an icosahedral head holding DNA, a tail sheath, and tail fibers that recognize and latch onto the host, then inject the genome like a syringe.
The phage doesn't enter the cell — its tail fibers bind a receptor on the bacterial surface, the sheath contracts, and only the nucleic acid is injected while the empty capsid stays outside. (This injection mechanism was the basis of the Hershey–Chase experiment that confirmed DNA, not protein, is the genetic material.)
Viral life cycles
All viruses follow the same arc — attach → penetrate → replicate using host machinery → assemble → release — but differ in whether they kill the cell immediately (lytic) or hide in its genome first (lysogenic), and in how their genome is copied.
Lacking their own ribosomes and enzymes, viruses must commandeer the host's. The key variable is timing and integration: a virus can replicate and burst out right away, or integrate and lie dormant, replicating passively with the host until conditions trigger it to go active.
Lytic vs. lysogenic cycles
In the lytic cycle, the virus immediately replicates and lyses (bursts) the host. In the lysogenic cycle, the viral genome integrates into the host chromosome as a prophage and replicates silently with the cell until something triggers it to switch to lytic.
Lytic = fast and destructive: hijack, mass-produce, burst, release. Lysogenic = stealthy: the prophage is copied every time the host divides, spreading through the population without killing cells, until a stress signal (e.g., UV) induces the lytic switch. A lysogenic phage can also carry host genes between cells — the mechanism behind transduction.
Don't confuse
Lytic lyses now; lysogenic integrates and waits. The integrated, dormant viral genome is a prophage (in bacteria) or provirus (in animal cells).
Animal virus entry & release
Animal viruses enter the whole virus (by endocytosis or membrane fusion), not just the genome, and enveloped viruses often exit by budding — wrapping themselves in host membrane — rather than lysing the cell.
Naked animal viruses typically enter by endocytosis and exit by lysis; enveloped viruses fuse with or bud through host membranes, which lets them release continuously without immediately killing the cell. Budding is also how a virus acquires its envelope and glycoproteins.
Retroviruses & HIV
A retrovirus (e.g., HIV) carries RNA and the enzyme reverse transcriptase, which copies its RNA into DNA; integrase then inserts that DNA into the host genome as a provirus.
Retroviruses reverse the usual flow of information (RNA → DNA): reverse transcriptase makes a DNA copy of the viral RNA, integrase splices it into the host chromosome, and the host then transcribes and translates viral genes as if they were its own. The integrated provirus can persist for life, which is why HIV is so hard to clear — and why reverse transcriptase and integrase are prime antiretroviral drug targets.
Positive- vs. Negative-Sense RNA Viruses
A positive-sense (+) RNA genome reads like mRNA, so host ribosomes can translate it directly on entry. A negative-sense (−) RNA genome must first be copied into its complement, so the virion must carry its own RNA-dependent RNA polymerase (RdRp / RNA replicase) into the cell.
Host cells have no enzyme that copies RNA into RNA, so every RNA virus needs an RdRp at some point. A (+) sense virus (e.g., poliovirus) acts as mRNA immediately — its first job is to translate an RdRp to replicate the genome. A (−) sense virus (e.g., influenza, rabies) cannot be translated as-is; it must transcribe a complementary (+) strand first, which is impossible unless the RdRp travels packaged inside the virion. This makes the naked (−)-sense genome non-infectious on its own.
Don't confuse
This is a separate branch from retroviruses ((+) RNA that uses reverse transcriptase to make DNA). Classify by what the genome does first: translated directly (+ sense), copied to its complement by carried-in RdRp (− sense), or reverse-transcribed into DNA (retrovirus — see Retroviruses & HIV).
How AAMC tests it
Expect a stem describing an injected/extracted viral genome that is (or isn't) infectious by itself: a (−)-sense genome alone can't start an infection because the host lacks RdRp, so the virion must supply it.
Worked question
A bacterial population is exposed to a bacteriophage. Some infected cells do not lyse; instead, the phage DNA is detected integrated into the bacterial chromosome and is copied each time those cells divide. Weeks later, UV exposure causes many of these cells to suddenly produce phages and burst. The integrated phage DNA is best described as a: