Tissue Architecture Flashcards
What are the functions of the cytoskeleton on the subcellular, cellular, and tissue level?
- subcellular: organization, tensile strength, chromosome segregation, cell polarity, vesicular movement
- cellular: cell morphology/shape, motility, cell adhesion, division
- tissue: muscle contraction
- type of filament
- actin filaments (F-actin)
- present in all cell types
- generally unstable
- essential for cell movements: locomotion, phagocytosis, cell division, contraction, etc.
microfilaments
What are modifications to actin proteins by other bound proteins?
- stabilization
- strengthen
- cross-linking
- organizing
What are drugs that affect actin filaments, what affect do they have?
- phalloidin: binds and stabilizes filaments (death cap mushroom, used in microscopy)
- cytochalasin: caps filament plus ends, prevents polymerization there
- latrunculin: binds actin monomers and prevents their polymerization
- type of cytoskeleton filament
- crucial role in organization in all eukaryotic cells
- long, stiff, hollow tubes
- can undergo rapid assembly and disassembly
- (+/-) sides like actin, dimers are added to (+) end
- push/pull cells a part during cell division
- shape, organize, and act are roads to move things around
- comprise flagella and cilia
microtubules
What are drugs that affect microtubules and what is their action?
- taxol: binds and stabilizes microtubules
- colchicine, colcemid: binds tubulin and prevents their polymerization
- vinblastine, vincristine: binds tubulin dimers and prevents their polymerization
(some of these meds are occasionally used in cancer tx to prevent formation of microtubules to prevent cell division)
- type of filament
- rope-like properties give these high tensile strength
- often further stabilized by accessory proteins: cross-link filaments into bundles, link to microtubules, actin filaments, and cell junctions
- form mesh-like structure called nuclear lamina
- gives strength/stability to cell/tissue
intermediate filaments
Intermediate Filaments:
- keratin
- vimentin and vimentin-related filaments
- neurofilaments
- nuclear lamins
- condition due to lack of nuclear lamins which causes cellular instability
- mutations in type A lamin
- sx: accelerated aging
Hutchinson-Gilford Progeria Syndrome (HGPS)
- components are produced intracellularly and secreted/aggregate
- matrix that interacts w/ cells/tissues via adhesion proteins
- functions: anchor/engluf cells to define boundaries, cell polarity, cell survival/proliferation, cell movement
- composition and properties controlled/vary by tissue type, location of cell, etc.
- protein groups: proteoglycans, collagens, multi-adhesive matrix proteins
extracellular matrix and basal lamina
- main structural protein in ECM/connective tissue and basal laminae
- composed of trimeric proteins
- associate as fibers, sheets, or transmembrane structures
- affected by nutrient deficiencies and genetic conditions
collagen
How is collagen made/processed in the cell in terms of locations:
Rough ER:
Lumen of ER:
Lumen of ER and Golgi:
Secretory vesicle:
Extracellular:
Rough ER: synthesis of preprocollagen; insertion of procollagen molecule into lumen of ER
Lumen of ER: hydroxylation of proline and lysine residues; glycosylation of selected hydroxylysine residues
Lumen of ER and Golgi: self-assembly of the tropocollagen molecule, initiated by disulfide bond formation in th carboxy-terminal extensions; triple helix formation
Secretory vesicle: procollagen prepared for secretion from cell
Extracellular: cleavage of the propeptides, removing the amino and carboxy-terminal extensions, and self-assembly of the collagen molecules into fibrils and then fibers
TLDR: synthesized in the ER, processed in Golgi, further processed extracellularly
What is the mechanism of action of vitamin C deficiency leading to scurvy?
- vitamin C deficiency leads to decreased hydroxylation of the proline/lysine residues comprising procollagen
- this leads to failure of the procollagen to form the triple helix, leading to tissue instability
- sx: decreased wound healing, loss of teeth, anemia, pale skin, sunken eyes
What are the 4 types of cell connections/junctions?
- anchoring junctions
- occluding junctions
- channel-forming junctions
- signal-relaying junctions
- type of cell junction
- link cells together and strengthens contact between cells and the ECM
- ex: adheren junctions, desmosomes, hemidesmosomes
anchoring junctions
- type of cell junction
- seal gaps between cells through cell to cell contact, making an impermeable barrier for diffusion
- ex: tight junctions
occluding junctions
- type of cell junction
- link cytoplasm of adjacent cells allowing transport of molecules to occur between cells
- ex: gap junctions
channel-forming junctions
- type of cell junction
- ex: synapses in the nervous system
signal-relaying junctions
What are the 4 major types of cell adhesion molecules (CAMs)?
- cadherins: cell-cell
- intergrins: cell-ECM or cell-cell
- selectins: cell-cell in circulatory system (leukocytes/endothelial)
- Ig superfamily: variable based on tissue
- type of cell adhesion molecule group
- Ca2+ dependent adhesion
- important in formation of junctions between cells (epithelial sheets), for example, desmosomes and adherens junctions
- naming is based on location
cadherins
- subgroup of cadherins
- type I (ex: E-cadherin, N-cadherin, R-cadherin): Ca2+ dependent homophilic adhesion function, cytoplasmic domains interact w/ beta-catenin, alpha-catenin, and p120
- type II (ex: VE-cadherin): linked to the actin cytoskeleton, a/w adherens junctions
class cadherins
- subgroup of cadherins
- T-cadherin and LI-cadherin
- function as homophilic adhesion proteins w/o interaction w/ catenins or link to actin cytoskeleton
atypical cadherins
- type of cell adhesion molecule group
- 15alpha and 8beta subunits form over 20 heterodimeric integrins
- couple the ECM (fibronectin, collagen lamin) to cell cytoskeleton (intracellular actin)
- cell-cell interactions via beta2 family (these molecules on leukocytes allow for adhesion and transmigration to sites of infection)
- can activate signaling pathways and initiate multiple cellular responses
integrins
- type of cell adhesion molecule group
- calcium dependent glycoproteins
- bind to extracellular carbohydrates/ligands/integrins
- important role in host defense mechanism (increased presentation during immune response, WBC has carbs and integrins (beta2) on the surface which act as ligands for these molecules)
- ex: endothelial (E), leukocyte (L), and platelet (P)
selectins
- type of cell adhesion molecule group
- family of more than 25 calcium-independent transmembrane glycoproteins
- functions: immune cell interactions; homophilic/heterophilic binding; self recognition, binding, or adhesion processes of cells; stable adherent junctions; can give a cell polarity
- ICAM, VCAM-1, PECAM-1, NCAM: contain variable number of immunoglobulin-like domains, expressed on vascular endothelial cells and bind to various integrin molecules
- MAdCAM-1: contain Ig-like and mucin-like domains, expressed on mucosal endothelium to direct lymphocyte entry into mucosa
Ig superfamily of CAMs
