Quorum sensing lets bacteria coordinate gene expression when secreted signalling molecules indicate that population density has reached a threshold, linking signal detection to a specific target-cell response.
Coverage 2019–2025 · Updated 15 Jul 2026
Quorum sensing allows bacteria to coordinate gene expression by releasing and detecting signalling molecules whose concentration indicates local population density.
Each cell releases an autoinducer. At low density it diffuses away, but as population density rises its local concentration increases; once a threshold is reached, receptor activation switches on coordinated genes.
Sequence: autoinducer release → concentration rises with cell density → threshold detection → coordinated gene expression across the bacterial population.
The marine bacterium Vibrio fischeri produces bioluminescence only when a dense population in its host's light organ accumulates enough autoinducer to cross the quorum threshold.
Quorum sensing estimates local density through chemical concentration; it is not nervous communication. Dilution or flow can prevent threshold activation even when bacteria are present.
This objective is assessed through structured response, multiple choice, commonly using State / Determine / Compare.
State / Determine / Compare / Deduce / Explain / Define / Outline
Build the answer around this relationship: Quorum sensing is triggered when bacterial signal concentration reflects sufficient population density.
Representative question
B. subtilis colonies form biofilms through quorum sensing.
(i) Define quorum sensing.
(ii) State three possible advantages to B. subtilis of forming a biofilm.
1.
2.
3.
A ligand only affects target cells with the matching receptor. Quorum sensing uses autoinducers and thresholds for group behaviour. Animal signals differ by source, distance, speed, target-cell response, and chemical class. Hydrophilic ligands use transmembrane receptors and relays; steroid and thyroid hormones use intracellular receptors that affect transcription. Named pathways then show the logic: acetylcholine opens sodium channels, GPCRs switch G proteins through GDP-GTP exchange, epinephrine uses cAMP and kinase cascades, insulin RTKs use dimerisation/autophosphorylation to move GLUT4 and promote glycogenesis, steroid hormones change gene expression, and feedback either amplifies or restores stability.
