Unit 06 Pt5
Overview of Cell Movement and Motility
Focus on cell crawling and motility
Importance across various cell types
Types of Cell Movement
Cell Crawling
Classical example: Amoeba
Involves chemotaxis in:
Bacteria
Yeast
Developmental processes (e.g., neural crest cells in Drosophila)
Germ cell migration
Adult mammalian cells
Key immune system cells: neutrophils, macrophages, osteoclasts, fibroblasts
Cancer cells undergo crawling referred to as metastasis
Stages of Cell Crawling
Cell crawling is a regulated, complex process divided into three stages:
Protrusion
Formation of lamellipodium (thin protrusions at the leading edge)
Actin-rich structures push outward for directional movement
Attachment
Focal adhesions secure the cell to the substratum
Attachment involves the actin cytoskeleton interacting with the plasma membrane
Traction
Contraction of the back end of the cell pulls cytoplasm forward
Facilitated by motor proteins
Characteristics of Protrusions
Filopodia: Long, thin, one-dimensional with bundled actin (e.g., growth cones of neurons)
Lamellipodia: Wider, two-dimensional sheets with a cross-linked actin mesh, found in epithelial cells and fibroblasts
Invadopodia (Podosomes): Larger, three-dimensional protrusions important in tissue crossing, relevant in cancer metastasis
Bleb: Plasma membrane detachment from the cell cortex, actin populates the extended area
Keratocytes as a Model for Lamellipodia
Derived from frog/fish epidermis, abundant in keratin
Move rapidly (30 micrometers/minute) with large lamellipodia and small trailing cell bodies
Experimental manipulation shows continued growth even if a portion is sliced off
Actin Dynamics in Cell Movement
Stationary actin network at the substrate; polymerization at the leading edge, depolymerization at the rear
Concept of treadmilling: plus ends grow and minus ends stabilize due to binding proteins such as cofilin
Actin binding proteins: ARP complexes nucleate new filament growth at the leading edge
Cofilin binds to ADP-actin, promoting depolymerization
Active filaments predominantly in T form due to delayed ATP hydrolysis
Cell Migration Mechanisms
Cell motion requires actin polymerization forces that interact with the substratum
Formation of focal adhesions mediated by integrins linking the cell to the extracellular matrix
Myosin motor proteins induce contraction and help propel cell movement
Regulation of Cell Polarity and Migration
Front to back polarity established through signaling pathways
Involvement of cell surface receptors and Rho family proteins:
Cdc42: Induces filopodia formation
Rac: Induces lamellipodia formation
Rho: Induces formation of stress fibers
These proteins act as molecular switches, regulating actin organization and dynamics
WAS Proteins and Pathologies
Wiskott-Aldrich Syndrome (WAS): Immunodeficiency associated with abnormal actin-based motility due to WASP protein mutations
Enhances actin nucleation via binding to ARP2/3 complexes
Pathological outcomes: eczema, pneumonias, infections, B cell lymphomas
Additional Types of Cell Migration
Chemotaxis: directed movement toward/away from chemical gradients (e.g., bacteria, neutrophils responding to infections)
Examples include slime mold showing directed movement toward cyclic AMP sources.