STEPTRACKERMICROBIOLOGY + GENETICS | BACTERIAL BASICS | HIGH-YIELD REVIEW

Bacterial Genetics

How bacteria swap DNA — and pick up resistance and toxin genes — by taking it up, mating, catching it from phages, or moving it within their own genome.

FOCUS ON

Transformation: naked DNA taken up by competent bacteria (S pneumoniae, H influenzae, Neisseria); DNase blocks it. Conjugation: F⁺ → F⁻ via sex pilus; plasmids with resistance genes. Transduction: phage carries DNA — generalized (random packaging) vs specialized (excision of a lysogenic prophage with flanking genes). Lysogenic conversion gives toxins: Shiga-like, botulinum, cholera, diphtheria, erythrogenic (scarlet fever). Transposition: "jumping genes" move within the genome (vanA in VRE).

PROCESS

HOW DNA MOVES

BLOCKED BY · REQUIRES

EXAMPLE

Transformation

Uptake of free DNA from a lysed bacterium

Blocked by DNase · needs competence

S pneumoniae, H influenzae, Neisseria, Helicobacter

Conjugation — F⁺ × F⁻

Sex pilus bridges cells; F plasmid copied to recipient

Needs cell contact

Resistance plasmids among gram-negatives

Conjugation — Hfr × F⁻

F plasmid integrated in chromosome → chromosomal genes transferred too

Cell contact

High frequency of recombination

Generalized transduction

Lytic phage accidentally packages random bacterial DNA

DNase-resistant (protected in capsid)

Any gene can move

Specialized transduction

Lysogenic prophage excises imprecisely, taking adjacent genes

—

Only genes next to the integration site

Lysogenic conversion

Integrated phage genes are expressed by the bacterium

—

Shiga-like toxin, botulinum, cholera, diphtheria, erythrogenic toxins

Transposition

Transposons move between chromosome, plasmids and phages

No homology needed

vanA (VRE), many multidrug-resistance cassettes

Integrons & gene cassettes

Collect multiple resistance genes in one array

—

Multidrug-resistant gram-negatives

Mutation

Chromosomal changes under drug pressure

—

Rifampin (rpoB), fluoroquinolone (gyrA), TB resistance

Phenotypic mixing

(Viral) coat of one virus around genome of another

Temporary; progeny revert

See viral genetics (5.01)

Picture it — three ways bacteria share genes

TransformationA competent cell takes up naked DNA from its surroundings; DNase prevents it.

ConjugationA sex pilus links an F⁺ donor to an F⁻ recipient and a plasmid copy passes across.

TransductionA bacteriophage packages host DNA by mistake and delivers it to the next cell it infects.

Schematic diagrams, not to scale.

Mechanism — four ways to move DNA

TransformationFree DNA → competent cell

ConjugationPilus contact → plasmid

TransductionPhage carries DNA

TranspositionJumps within one cell

Only transformation is stopped by DNase; only conjugation needs cell contact; only transduction needs a virus.

Phage-encoded toxins — ABCDE

LETTER

TOXIN

ORGANISM

ShigA-like (Shiga-like) toxin

EHEC

Botulinum toxin (some types)

C botulinum

Cholera toxin

V cholerae

Diphtheria toxin

C diphtheriae

Erythrogenic toxin

S pyogenes

How it's tested

COMMON CONFUSIONGeneralized transduction moves any gene (lytic packaging error); specialized moves only the genes next to the prophage.

THE TRAPA nontoxigenic C diphtheriae becomes toxigenic after infection by a β-phage — that is lysogenic conversion (specialized transduction setting), not mutation.

YOUR APPROACHDoes it need contact (conjugation), a phage (transduction), free DNA (transformation), or nothing (transposition)?

If you see… think…

Resistance transfer blocked by adding DNase → transformation

Bacteria naturally competent → S pneumoniae, H influenzae, Neisseria

Resistance spreads only with direct cell contact → conjugation (sex pilus)

Random bacterial genes packed into a phage → generalized transduction

Phage-coded toxin expressed by the host bacterium → lysogenic conversion

Vancomycin resistance gene moving between plasmids → transposon (vanA)

Chromosome genes transferred with an integrated F factor → Hfr conjugation

Toxins encoded by phages → Shiga-like, botulinum, cholera, diphtheria, erythrogenic

Rifampin resistance in TB → chromosomal rpoB mutation

Multiple resistance genes collected in one array → integron