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Lecture

ENDOCYTOSIS

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School
McMaster University
Department
Biology
Course
BIOLOGY 2D03
Professor
Laura Parker
Semester
Fall

Description
ENDOCYTOSIS: helps to maintain cell size/volume via cell membrane for nutrition, defense, and homeostasis bacteria/viruses take advantage of it PHAGOCYTOSIS attachment: receptor mediated not energy dependent engulfment: energy dependent actin-based rearrangement around bacteria ends in membrane fusion also involves unconventional myosin motors degradation: PHAGOSOME fuses with lysosome KILLING STRATEGIES - 1. oxygen dependent – use of hydrogen peroxide 2. oxygen independent – enzymatic (degrade bacterial walls/membranes) SUBVERSION – fusion inhibition hydolase resistance  intracellular survival escape RECEPTOR-MEDIATED / CLATHRIN DEPENDENT ENDOCYTOSIS Overview: small particle internalization binding concentrates the ligand  greater efficiency/selectivity similar machinery as used in exocytosis Steps: 1. clustering 2. internalization 3. uncoating 4. endosome fusion CLUSTERING: concentrating step LDLR defects – cytoplasmic tail mutation that prevents clustering does not affect ligand binding several kinds of endocytic signals; vary in distance from lipid bilayer TYPES: constitutive – receptors cluster w/out ligand binding induced – activated by ligand binding tethered – anchored to cytoskeleton  SLOW endocytosis INTERNALIZATION – clathrin mediated (also involved in lysosomal targeting during exocytosis) TRISKELION – CCV subunit; 3HC + 3LC various vesicle sizes (12 pentagons + various hexagons) form BASKETS spontaneously in vitro ATP, adapters, cytosolic factors ne
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