module 8 Flashcards
explain: 1907 wilson experiment (sponges)
- used cells of 2 sp. of sponges
- cells were separated w/ a fine mesh
- mixed back together
- cells from same sp. were able to recognize each other and reassociate back
explain: 1950’s holtfreter experiment (frog)
- cells from frog embryo
- took cells from 2 diff. developmental germ layers and separated indiv. cells
- mixed together
- cells from similar tissues associated back together
- mimicked organization seen in OG embryo
question: how are the same cells reassociating in the frog embryo exp. and the sponge exp.?
- cell adhesion molecules (CAMs)
⤷ type of transmem. prot. - after aggregating back together, cells for junctions that stabilize cell-cell interactions + facilitate comms.
name: types of cell-cell junctions in epithelial cells (5)
- tight junctions
- adherens junctions
- desmosomes
- hemidesmosomes
- gap junctions
explain: epi. struc. (junctions) + involvement of adhesion complexes
- epi. cells connect to form sheets to line body cav.
- many connections hold the lateral surfaces of the cells together
- basal surface of cell anchored to basement mem.
⤷ connected by hemidesmosomes - lateral surfaces connected by:
⤷ tight junctions
⤷ gap junctions
⤷ desmosomes
⤷ adherens junctions
explain: tight junctions (func., location)
- connect adjacent cells just below apical surface of cells
- completely seal off space between cells
- prevents fluid from moving across + restricts diffusion
⤷ good for gastrointestinal tract - have points where cells are pinched together
- linear arrays formed by prot. (occludin and claudin)
- freeze fracturing shows points of weakness
⤷ showed lateral surface between cells
⤷ showed that tight junctions = accumulation of structures (web of lines = linear arrays)
explain: role of junctional band in tight junctions
- prevents diffusion of membrane prot. from apical to basolateral regions of plasma mem.
- completely prevents diffusion of molecules in extracellular space
- ex. lanthanum hydroxide diffusing from basal surface of epithelial sheet
⤷ seen that cannot move any further towards apical surface bc tight junction doesn’t allow it
explain: gap junctions (func., struc., location)
- directly link cytosol of one cell to the cytosol of the adjacent cell
- allows integration of metabolic activities of all cells in a tissue
⤷ bc allows exchange of ions and small molecules between cells - gap junction channel = 1.5 - 2 nm in diameter
⤷ allows free diffusion of molecules - 6 connexin prot. subunits -> hexagonal connexon hemichannel
- 1 hemichannel sit in cell mem. of each of the 2 connected cells
⤷ channels line up to make gap junction - channels found in groups to form many gap junctions in one region
- pinches cell mem. + holds cells together
- molecules can diffuse around the junctions
question: how do gap junctions work (in action)?
- ions, cAMP, calcium can diffuse through gap junctions
- ex. allows fast coordination of cardiac musc. contraction and uterine musc. contraction
- stim. of one cell -> resp. of many cells bc mvt. of secondary messengers through the cyto. of diff. cells
- ex. exp. w/ fluorescent molecule
⤷ fluorescent is seen to diffuse into neighboring cells when connected by gap junctions
explain: gap junctions in plants
- plasmodesmata
- important to struc. and func. of phloem
- phloem = system of elongated tubes formed from linear arrays of connected cells
⤷ carries nutrients - phloem = connected by plasmodesmata that form sieve tube plate
- companion cells = closely assoc. to sieve tube plate
⤷ provide ATP, prot.
⤷ also get connected to phloem - plasmodesmata spans both cell mem. but also cell walls of plant cells
question: how do plasmodesmata work (in action)?
- phloem = circulatory system
- prot. made in companion cells -> transported to and w/in phloem
- plasmodesmata also does trafficking of informational macromolecules
⤷ transcription factors
⤷ gene transcripts
⤷ small RNs
question: how could gap junctions be harmful?
- important for cell function
- but also help pathogens spread more quickly
⤷ use gap junction channels to spread intercellularly
explain: anchoring junctions (func., struc., location)
- adherens junctions, desmosomes, hemidesmosomes
- assoc. w/ cytoskeleton
⤷ actin - desmosomes link two cells together
- hemidesmosomes attach cells to extracellular matrix
- end result = adherens junction indirectly connecting actin between neighbouring cells
name: families of adherens junctions (4)
- cadherins
- members of the Ig-superfamily
- integrins
- selectins
- some connect similar cells (homophilic), some connect diff. cells (heterophilic)
- cadherins, Ig-superfamily = homo.
- integrins, selectins = hetero.
explain: cadherins (types, func., location)
- 3 major classes
1. E (epithelial)
2. N (neural)
3. P (placental) - calcium dep.
- homophilic interactions
- mediate near apical surface, just below tight junctions
question: what is adhesion mediated by?
-multiprot. complexes
- involves transmem cadherins, cytosolic cofactors, catenins
⤷ catenins anchor cadherin to actin cytoskeleton)
explain: epi. cells and E-cadherin (explain exp. results w. and w/out calcium)
- do not normally aggregate
- introduce E-cad. -> aggregation
- E-cad mediates calcium dep. adhesion cells in epi. cells
⤷ so won’t aggregate w/out calcium
RESULTS
- no E-cad. = no aggregation
- yes E-cad. w/ calcium = aggregation
- yes E-cad. w/out calcium = no aggregation
explain: exp. testing cadherins and cell differentiation (E-cad)
- labeled E-cad. w/ GFP
- put cells w/ E-cad. into medium w/ calcium
- over time, saw aggregation of E-cad. expressing cells
- maintenance of adhesion + formation of junctions = shown by aggregation of GFP:E-cad. at surfaces of cells
explain: examples where cell needs temporary associations (established and broken)
ex. allowing cells to migrate across extracellular surface + migration of cells during embryogenesis
ex. mvt. of leukocytes (WBC) in resp. to infection or injury
- req. mvt. of blood cells in and out fo vessels
- leukocytes dep. of sequence of adhesive interactions to facilitate process of extravasation
⤷ mvt. of WBC to surrounding tissue
- adhesion between cells of blood vessels usually prevent leakage
- when WBC need to get to injury site = need to establish temporary connections w/ cells of blood vessels
name + explain: types of leukocytes (3)
- granulocytes
- target pathogens
- ex. neutrophils, eosinophils, basophils
- neutrophils = most common, target bac. infections, first cells to resp.
- neutrophils go through extravasation - monocytes
- differentiate into macrophages
- engulf bac./dead/damaged cells through phagocytosis - lymphocytes
- ex. natural killer cells (NK), T and B cells
- T and B prod. antibodies as part of immune resp.
- also do extravasation
name: steps of extravasation (5)
- capture
- rolling
- slow rolling
- firm adhesion
- transmigration
explain: capture step in extravasation
- 1st step
- temporary association between neutrophil and apical surface of endothelial cell in blood vessel
- neutrophils still pushed by flow of blood but mvt. = slower
- sig. from site of infection trigger capture of neutrophil
⤷ site releases cytokines to change beha. of endo. cells - cytokine ex. = TNF-alpha
- receptor on basal surface of endo. cell receives sig. + triggers release of selectins
- P-selectins of endo. cells = held in regulated secretory vesicles
- cytokine sig. -> secretory vesicles transport P-selectins to surface of endothelial cells
- P-selectins can now interact w/ ligand on surface of leukocyte
explain: rolling step in extravasation
- 2nd step
- cells roll along surface of endo. cells
- rolling = neutrophils establishing and losing connections w/ the endo. cells
explain: slow rolling step in extravasation
- 3rd step
- more assoc. between neutrophils and endo. cells -> rolls slower
- density of selectins on endo. surface increases as neutrophil gets closer to infection
⤷ bc more endo. at site of infection are showing P-selectin and E-selectin - more assoc. between selectins and ligands makes rolling even slower
explain: firm adhesion/tight binding step in extravasation
- 4th step
- stronger attachment of neutrophil w/ endo. cells
- WBC to break connections between endo. and migrate along surface of cells into space outside vessel
- membrane anchored sig./cytokine on endo. = PAF (platelet activating factor)
- PAF can interact w/ recep. on neutrophil
- ex. of recep. = CXCR2 and VCVR2
⤷ both GPCR - binding to recep. can only happen if slow rolling
- Paf binding -> initiates STP in neutrophil
⤷ ex. changing gene exp., activating another CAM - activates integrin adhesion molecule on neutrophil
⤷ integrin can interacts w/ ligand, ICAMs
⤷ makes mvt. even slower
question: how are integrins activated in extravasation (during firm adhesion)?
- propeller and beta-A domains of dimeric integrin prot. = ligand binding domain
- folded down = can’t recog. ligand
- PAF signaling activates domain -> ligand binding domain straightens up into active state
- allows integrin to bind to ICAMs on endo.
- ligands = stronger than selectin interactions
- makes neutrophil mvt. even slower + establishes firm adhesion
- activating integrins -> signals more changes in beha. of neutrophil -> reorg. actin cytoskeleton to allow cell migration
explain: transmigration step of extravasation
- 5th step
- swelling happens at site of infection
⤷ bc blood plasma escapes into surrounding areas - transmigration of leukocytes also contributes to swelling
- neutrophil no longer in blood flow
- stopped at site of infection
- migrates by crawling between endo. cells
- connections between endo. cells break bc enx. prod. by transmigrating neutrophil
- neutrophil changes shape to leave blood vessel
