Secretory and transport vesicles
Also known as: secretory granule, transport vesicle, zymogen granule, dense-core granule, exocytosis, SNARE
Small membrane-bounded carriers that shuttle cargo between compartments and to the cell surface, where they fuse with the plasma membrane to release their contents (exocytosis).
Overview
Vesicles bud from a donor membrane with the help of coat proteins that bend the membrane and select cargo: COPII (ER → Golgi), COPI (Golgi → ER and between cisternae) and clathrin with adaptor proteins (trans-Golgi network → endosomes; plasma membrane → endosomes), the GTPase dynamin pinching clathrin-coated vesicles off. Coats are shed after budding. Rab GTPases and tethering proteins guide vesicles to the correct target, and SNARE proteins — a v-SNARE on the vesicle (VAMP/synaptobrevin) zippering with t-SNAREs on the target (syntaxin and SNAP-25) — drive membrane fusion.
Vesicles leaving the trans-Golgi network follow two secretory routes. Constitutive secretion operates continuously in all cells, delivering membrane lipids and proteins to the surface and releasing products such as collagen, albumin and antibodies as they are made. Regulated secretion occurs in specialised cells: products are concentrated and stored in secretory granules (dense-core granules of endocrine cells, zymogen granules of pancreatic acinar cells, mucinogen granules of goblet cells, synaptic vesicles of neurons) and released only after a signal, usually a rise in cytosolic Ca²⁺ sensed by synaptotagmin.
During exocytosis the vesicle membrane fuses with and becomes part of the plasma membrane, so secretion also adds membrane; this is balanced by endocytic retrieval. Vesicles are carried toward the cell periphery along microtubules by kinesin motors.
Function
- Transport of proteins and lipids between ER, Golgi, endosomes and plasma membrane.
- Storage and Ca²⁺-triggered release of hormones, enzymes, mucus and neurotransmitters.
- Delivery of new membrane and membrane proteins (receptors, channels, transporters) to the cell surface.
Clinical significance
Botulinum and tetanus toxins
Both are zinc proteases that cleave SNAREs. Botulinum toxin blocks ACh release at the neuromuscular junction → descending flaccid paralysis (used therapeutically for dystonia, spasticity, hyperhidrosis). Tetanus toxin travels retrogradely to the spinal cord and blocks release of GABA and glycine from inhibitory interneurons → spastic paralysis, trismus, opisthotonos.
Insulin-stimulated GLUT4 translocation
In skeletal muscle and adipocytes insulin triggers fusion of intracellular GLUT4-containing vesicles with the plasma membrane, increasing glucose uptake — impaired in insulin resistance.
Compiled from standard anatomy and physiology references — see the Cells & Tissues sources. For education only; not medical advice.