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Cells to Organisms 2 > Cell Adhesion 4 - Adhesion on behaviour > Flashcards

Cell Adhesion 4 - Adhesion on behaviour Flashcards

1
Q

What is compaction?

A
  • hallmark event of 8 cell stage in mouse embryo developement
  • when you can no longer see the intercellular boundaries as adhering junctions form
  • E-cadherin is essential for formation of adhering here
  • found mainly on basolateral cell-cell contact sites
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2
Q

Where is E-cadherin mainly found during compaction?

A

Basolateral cell-cell contact sites

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3
Q

Describe 2 experiments defining cadherin-mediated adhesion

A
  • adhesion-blocking antibodies - exposure to anti-cadherin antibodies causes embryo to fall apart
  • expression and deletion of cadherin - mutant embryos lacking E-cadherin fall apart
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4
Q

Explain loss and gain of function mutations

A
  • if you remove what you think is causing the effect, does the effect still happen?
  • when the feature is back does it function again?
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5
Q

name 3 different types of cadherins?

A
  • E-cadherin
  • R-cadherin
  • Cadherin-6
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6
Q

Where is E-cadherin expressed in the embryo?

A
  • mainly in epithelial cells
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7
Q

Where is R-cadherin and N-cadherin mainly expressed?

A

nerve, muscle and lens cells

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8
Q

Where is P-cadherin expressed in the embryo?

A
  • placenta
  • epidermis
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9
Q

Where is Cadherin-6 expressed?

A

kidney

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10
Q

What is homopihilic binding?

A
  • 2 molecules that are identical on different cells bind
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11
Q

What is heterophilic binding?

A

two molecules that are different on different cells bind

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12
Q

Explain homophobic binding in cadherin

A
  • happens at the N-terminus - furthest point from the membrane
  • Ca2+ is required or hinge would be floppy
  • Changes conformation of the N-terminus
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13
Q

Explain overall connections of cadherins

A
  • individual interactions are relatively weak
  • combination is strong
  • important as cell-cell interactions commonly break and re-from during embryonic development
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14
Q

What allows cells to sort according to origin

A
  • homophilic binding - cadherins bind well to the same type of cells
  • suggests that tissues are maintained by differential affinities of cells for each other
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15
Q

What causes tissue maintenance

A
  • cadherins bind well to the same type of cell
  • cells have differential affinities for each other
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16
Q

What is an L-cell?

A

cells in the GI tracts that secreted hormones regulating appetite

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17
Q

Explain L-cells and cadherins

A
  • they do not normally express cadherins
  • can be cultured to express L-cells
18
Q

What does a higher level of catherine expression mean?

A
  • stronger interaction - more tightly packed in the centre
19
Q

What does a lower level of expression of cadherin mean?

A
  • weaker interactions - around the outskirts
20
Q

Explain overall sorting of cells based on their catherine expression

A
  • express different cadherins - will group together into completely different groups
  • express different levels of the same cadherin
    - more cadherin in the centre, less catherine in outskirts
21
Q

Explain the expression of cadherins in neural tube development

A
  • ectoderm expressed E-cadherin
  • as neural tube starts to form - stop making E-cadherin - start making N-cadherin
  • cadherin 6B expressed increases at join between E-cadherin and N-cadherin
  • some cells stop making N-cadherin and start making cadherin-7
  • neural crest is then formed and more cadherin-7 is made

DRAW IT OUT

22
Q

What is the effect of over expression of N-cadherin in neural tube formation?

A
  • failure to leave the neural tube
23
Q

Name 6 epithelial features

A
  • regular columnar morphology
  • high degree of cell adhesion
  • cell-cell junctions
  • specialised apical membrane (eg brush border)
  • underlying basement membrane
  • cells relatively static
24
Q

Name 6 mesenchymal features

A
  • irregular rounded or elongate morphology
  • loss of apico-basal polarity
  • front-back polarity
  • dynamic adhesions
  • lamellipodia and filopodia
  • cells highly motile
25
Q

What are lamellipodia?

A
  • protrusion from migrating cells
  • lots of actin
26
Q

what are filopodia?

A
  • extensions in migrating cells
  • made of membrane
  • sensory function
27
Q

Explain the epithelial-mesenchymal transition (EMT)

A
  • formation of epithelium is reversible
  • cells can transition from epithelium so mesenchymal cells
28
Q

Explain epithelial-mesenchymal transition in cancer progression

A
  • cancer happens due to an accumulation of mutations in different genes
  • allows for metastasis
  • carcinomas are around 80% of all cancer cases
  • metastasis accounts fro 90% of cancer deaths
29
Q

What is carcinoma?

A
  • cancers arising from epithelial cells
30
Q

What are selections?

A
  • proteins on the cell surface that bind carbohydrates
  • expressed by white blood cells and epithelial cells (these line the blood vessels)
  • linked to actin through transmembrane proteins
  • mediate cell-cell adhesions in the bloodstream
31
Q

Explain the role of selectins in inflammation

A
  • weak binding and rolling of white blood cells along blood vessels
  • leukocytes activate integrins, which recognise epithelial membrane proteins
  • stronger adhesion
  • lymphocyte will escape into the tissues
32
Q

Explain defects in leukocyte adhesion

A

LAD-I - absent or decreased integrins - defective tight adhesion and invasion

LAD-II - glycosylation defect causing selectin defects - defective initial binding and rolling

LAD-III - activation defect of integrin - defective tight adhesion and invasion

33
Q

What does LAD stand for?

A

leukocyte adhesion deficiency

34
Q

What is LAD-I?

A

absent or decreased integrins - defective tight adhesion and invasion

35
Q

What is LAD-II?

A

glycosylation defect causing selectin defects - defective initial binding and rolling

36
Q

What is LAD-III?

A

activation defect of integrin - defective tight adhesion and invasion

37
Q

What is the role of remodelling of the ECM in inflammation?

A

allows white blood cells tp pass between cells

38
Q

Name the 2 main groups of ECM degrading enzymes

A
  • matrix metalloproteinases (MMPs) -> need Ca2+ or Zn2+ to work
  • serine proteases -> conserved serine residue on the active site

Very specific enzymes

39
Q

Explain localised ECM degradation

A
  • overall ECM structure stays the same
  • but there is enough room for cells to migrate through
40
Q

Explain localisation of ECM degradation

A
  • some proteases secreted in inactive forms
  • localised activator converts to be active
    • tissue plasminogen activator activates plasminogen to dissolve blood clots
  • some proteases confined by cell-surface receptors
    • urokinase-type plasminogen activator (uPA) found at the growing tip of migrating cells
  • some proteases are inhibited by locally secreted inhibitors
    • tissue inhibitors of metalloproteinases (TIMPs)
41
Q

Explain ECM remodelling in cancer

A
  • carcinoma in situ
  • basement membrane breakage
    • proteolytic ECM degradation happens
  • invasive tumor
    • tumor spreads

Cells to Organisms 2 (26 decks)

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