1. Cell adhesion Flashcards

1
Q

How is physical stress transmitted between cells in a tissue?

A
  • ECM
  • cytoskeleton and cell-cell adhesion
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2
Q

What is physical stress in cells?

A

Changes/fluctuations of environment (solutes/ pressure/toxins/light/nutrients)

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3
Q

How is physical stress managed in plant vs animal cells?

A
  • PLANT: predominantly ECM
  • ANIMAL: use both ECM and cytoskeleton + cell-cell adhesion in diff tissues
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4
Q

What are the supportive and space filling matrices in plants?

A

Supportive matrix - cell wall
Space filling matrix - pectin (cell adhesion molecule)

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5
Q

Explain the synthesis of plant cell wall

A
  • plant cells synthesise the cell wall themselves on the outside of the cell by enzyme complexes embedded in the membrane
  • enzyme complexes are directed by microtubules aligned exactly like microfibrils -> cytoskeleton controls the modelling of plant tissues
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6
Q

What is the driving force of plant cell growth?

A

Turgor pressure

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7
Q

What are microfibrils composed of?

A

Cellulose microfibrils - long, unbranched chains of glucose -> 16 cellulose molecules assemble a microfibril

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8
Q

What macromolecules compose the plant cell wall?

A
  • cellulose microfibrils
  • pectin fibers
  • lignin ligning (not all cell walls)
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9
Q

What is pectin composed of? What is the function?

A
  • pectin - long, complex polysaccharide - forms plant cell matrix
  • to resist compression
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10
Q

Compare the structures of primary and secondary plant cell walls

A

PRIMARY:
- weaker - grows into needed size
- pectin
- cellulose
- middle lamella

SECONDARY cell wall - more rigid - starts forming when primary wall reaches the size - secondary wall forms by:
(1) thickening of primary wall
(2) deposition of new layers under old layers (ex: lignin in wood)
- when plant cells become specialised - produce cell wall specific to the cell type: wax for epidermis / hard, thick, woody for xylem

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11
Q

What does the orientation of cellulose microfibrils influence?

A

Because cellulose microfibrils resist stretching - orientation influences in which direction the cell elongates - length / width

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12
Q

Explain the synthesis of plant cell wall

A
  • plant cells synthesise the cell wall themselves on the outside of the cell by enzyme complexes embedded in the membrane
  • composition of the cell wall depends on the plant (hard thick wall - wood, thin flexible wall - leaf)
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13
Q

Which animal tissue links all other animal tissues?

A

Connective tissue (+ basal lamina / basement membrane)

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14
Q

What are the examples of animal connective tissues and their characteristics?

A

All animal connective tissues are abudant in ECM
- tendons - tough and flexible
- bone - hard
- dermis - soft and flexible
- cartilage - shock absorbing
- vitreous humour - soft and transparent

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15
Q

Explain the structure formed in bones

A

Bone - connective tissue - osteoblasts secrete collagen - Ca / Mg / P ions incorporated into matrix - hard, flexible, not brittle - form osteons

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16
Q

What is an osteon?

A

Osteons - mineralised matrix deposited around central canal with a blood vessel and nerves

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17
Q

Explain the structure of cartilage

A

Large amounts of **ECM **(abudant in collagen and proteoglycan) - no mineralisation

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18
Q

Explain the structure of vitreous humour

A

Clear, viscous gel - water, collagen, hyaluronic acid

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19
Q

What is the major protein of ECM?

A

Collagen - fibrous proteins

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20
Q

What cells synthesise collagen?

A

Fibroblasts

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21
Q

What is the structure of collagen?

A

Triple stranded helical structure - rope like superhelix -> collagen fibril -> collagen fiber
MONOMER -> TRIMER -> FIBRIL -> FIBER

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22
Q

What is collagen arrangement in skin?

A

In skin collagen is arranged both longitudinally + transversally -> allows skin to resist stress in different directions

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23
Q

What is the collagen arrangement in tendons?

A

In tendons collagen fibers are aligned parallely, along the axis of extension

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24
Q

How do fibroblasts influence the alignement of collagen?

A

In collagen secretion fibroblasts pull apart and shape it - different collagen alignments based on tissue (ex: skin vs tendon) - also vice versa collagen alignment influences fibroblast distribution

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25
Q

Explain collagen secretion by fibroblasts

A
  • collagen secreted as precursor form outside the cell - procollagen
  • enzymes add peptide extensions - assembles into collagen into fibrils
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26
Q

What could be caused by faulty collagen assembly?

A

Disorders - Ehlers-Danlos syndrome (EDS)

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27
Q

How do cells attach to ECM?

A

Via integrin proteins - they attach to cytoskeleton inside the cell and collagen in ECM

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28
Q

What is the mechanism of integrin attachment inside the cell?

A

Integrin proteins (transmembrane receptor) attaches to the cytoskeleton via actin filaments (part of cytoskeleton)

29
Q

What is the mechanism of integrin attachment outside the cell?

A

Integrins attach to collagen in ECM via fibronectins

30
Q

How integrins can be activated / deactivated?

A

Activated: both subunits are extended - triggered by binding to ECM (fibronectin) or adaptor proteins to cytoskeleton inside the cell

Deactivated: both subunits are folded
REVERSIBLE

31
Q

How do integrins coordinate cell movement?

A

Integrins create new attachment points at the front - attachments at the back are released -> cell crawls

32
Q

Compare the functions of collagen and GAGs?

A

Collagen: provide tensile strength to resist stretching
GAGs: resist compression

33
Q

What are GAGs?

A

Glycosaminoglycans (GAGs)
- neg charged (draws in H2O, ions) polysaccharide chains
- usually form proteoglycans
- common brush structure GAG aggregate
- more commonly found in soft ECM (ex vitreus humour not bone - mostly collagen)

34
Q

What is epithelium and what are its functions?

A
  • epithelium - sheet of cells
  • created barriers - external and internal lining of cavities - controls movement of molecules / microbes - maintains different environments on both sides
35
Q

What are the forms of epithelium cells? Relate to their function, give organ examples

A
  • Columnar : secretion, absorption (ex: intestine)
  • Cuboidal : secretion, absorption (ex: kidney)
  • Squamous : filtration (ex: lung)
  • Stratified : protection (ex: skin)
36
Q

What is basal lamina and what is its function?

A
  • basal lamina / basement membrane - thin, tough sheet of ECM
  • separates epithelial cells and connective tissue
37
Q

What is basal lamina composed of? What is its structure?

A
  • type IV collagen <- form conn tissue
  • laminin <- from epithelial cells
38
Q

Explain the structure and function of laminin

A
  • laminin - cross-like trimer structure
  • supplies adhesive sites in basal lamina for integrins from epithelial cells (linking role)
39
Q

Explain epithelial polarity

A
  • environments on basal - apical epithelial surfaces are different (epithelium creates barriers)
    -> ‘POLES’ of different environments are formed
    => epithelial apical-basal polarity
40
Q

Why is epithelial polarity necessary?

A

Epithelial polarity maintains barriers - necessary for:
- absorption : brush-border cells (microvilli) - take up nutrients
- secretion : goblet cells - secrete mucus

41
Q

What are the main cell junctions between epithelial cells?

A
  • tight junctions
  • adherens junctions
  • desmosomes
  • hemidesmosomes
  • gap junctions
    Honestly,** T**as Adomas Geria visa Diena
42
Q

What is the role of tight junctions in epithelial cells?

A
  • barrier function - prevent leakage
  • maintain epithelial polarity
43
Q

What proteins act in tight junctions?

A

Occludin
Claudin

44
Q

How do tight junctions maintain epithelial polarity?

A
  • prevent diffusion of membrane proteins within cell membrane
  • allow glucose transport both in and out the cell
45
Q

Explain the structure and function of adherens junctions

A
  • cadherins (need Ca2+) - key components - link cytoskeletons (actin) of adjacent cells
  • homophilic binding (two same cadherins bind)
46
Q

What are adhesion belts?

A

Adhesion belts - actin filament bundles which bind neighbouring cells via adherens junctions

47
Q

How are adherens junctions involved in epithelial sheet bending?

A

Connections between adherens junctions and cytoskeleton (adhesion belts) allow sheets to change shape

48
Q

Explain the structure and function of desmosomes

A
  • join intermediate filaments (keratin) of neighbouring cells - join cells
  • contain cadherins (different to adherens junctions)
49
Q

Explain the structure and function of hemidesmosomes

A
  • join intermediate filaments (keratin) to basal lamina
  • use integrins to connect keratin
  • looks like a half desmosome - hemidesmosome
50
Q

Explain the structure and function of gap junctions

A
  • direct channels for cytosolic communication
  • tunnels of aqueous connectivity between cells - small, water-soluble molecules pass
  • connexon proteins line up to form the water-filled channel - gap junction
51
Q

How permeable are gap junctions?

A
  • gap junctions are gated - selective
  • permeability regulated by external signals (ex dopamine)
52
Q

What is the equivalent of gap junctions in plants?

A
  • plasmodesmata in cell walls
  • no other cell-cell junctions
53
Q

How do cell adhesions influence cell behaviour?

A

Assist in cell movement in tissue growth and development

54
Q

What is compaction in embryo development?

A

Compaction - the 8-cell stage in embryo development when adherens junctions (cadherin) form between adjacent cells

55
Q

What proteins are essential in embryo compaction?

A
  • E-cadherins essential for forming adherens junctions
  • E-cadherin localisation at basolateral cell-cell conatct sites
56
Q

What are the experiments which defined cadherin mediated adhesions?

A

1) when cadherin binding antibodies were introduced in embryo - cells didn’t adhere - fell apart
2) when cadherin genes were deleted in embryos - cells didn’t adhere, embryo fell apart

57
Q

What are the main types of cadherins? What cells express them?

A
  • E-cadherin (epithelial cells)
  • N-cadherin (neurons)
  • R-cadherin (nerve, muscle, lens (retina))
  • Cadherin-6 (placenta, epidermis)
    Different cells express different cadherins
    CERN
58
Q

Explain homophilic vs heterophilic binding

A

HOMOPHILIC : like-to-like (ex: same cadherins)
HETEROPHILIC : different molecule bind (ex: ligand and receptor)

59
Q

How cell adhesions help cells sort out?

A
  • cells sort out according to type - recognise similar cells by cell adhesion molecule
  • cells adhere expressing same cadherin types
  • levels of specific cadherin expression also influence cell-cell interactions
  • cells with higher cadherin levels adhere more tightly
60
Q

How do cadherins act in cell sorting during development?

A

In neural tube formation:
1) ectoderm cells express E-cadherin
2) when neural tube pinches off - turn off E-cadherin production, turn on N-cadherin expression
3) migratin neural crest cells turn off N-cadherin expression and turn on cadherin-7 expression

61
Q

Explain epithelial to mesenchymal cell transition

A

Epithelial-to-mesenchymal transition (EMT):
- cell assembly into epithelium is reversible
- EMT found in developing tissues, tissue regeneration, wound healing
- EMT involved in cancer

62
Q

Explain what are selectins and their function

A

Selectins :
- cell surface proteins that bind to carbohydrates
- expressed in WBCs and endothelial cells
- act in inflammation
- form relatively weak cell adhesion in blood

63
Q

Explain selectin and integrin function in inflammation

A

Selectins WBC movement into tissues at inflammation sites:
- selectins on endothelial cell surface recognise WBCs sugars - form weak adhesion and rolling of WBCs along endothelial cells
- rolling by selectins done - strong adhesions formed with integrins at the site of inflammation the WBCs squeeze into tissue

64
Q

What problems can arise if selectins or integrins are defective?

A

Affects WBCs recognition at inflammation sites - leukocyte adhesion deficiency (LAD)

65
Q

Why would cells degrade ECM?

A
  • cells degrade ECM to allow cells to pass between endothelial cells to the inflammation site
  • ECM remodelling (for development, wound healing)
66
Q

What are the main groups of ECM degrading enzymes?

A
  • matrix metalloproteinases (MMPs)
  • serine proteases
  • localised degradation - highly specific enzymes (ex: collagenase)
67
Q

Why does the activity of ECM degrading enzymes must be localised?

A

ECM degradation must be highly controlled by localising ECM degrading enzymes - not to destroy ECM where not needed

68
Q

How is the activity of ECM degrading enzymes is controlled?

A

1) Enzymes expressed in inactive form (localised activators)
2) Enzymes confined by cell-surface receptors
3) Enzymes are inhibited by locally secreted inhibitors