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Uni year 1 > Cell biology - adhesion and movement > Flashcards

Cell biology - adhesion and movement Flashcards

1
Q

Features of epithelial cells

A
  • apical surface is free
  • basal surface is attached to basement membrane
  • lateral surfaces adhere to neighbouring cells
  • presence of specialised cell-cell junctions
  • polarised morphology
  • tight junctions prevent proteins moving
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2
Q

Give 2 examples of cell-cell junctions

A

adherens

desmosomes

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3
Q

Give an example of a cell-matrix junction

A

hemidesmosome

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4
Q

Which junctions interact with intermediate filaments

A

desmosomes and hemidesmosomes

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5
Q

Which junctions interact with actin microfilaments?

A

adherens junctions and focal adhesions

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6
Q

Which junctions are for adhesion?

A

adherens
desmosomes
hemidesmosomes
focal adhesions

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7
Q

Which junctions are for communication?

A

Gap junctions

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8
Q

What are tight junctions for?

A

barrier and fence functions

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9
Q

What are the layers of the skin?

A

Epidermis
Dermis
Hypodermis
Epidermal appendages

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10
Q

What is the epidermis composed of?

A
  • stratified squamous keratinised epithelium

- kertinocytes, melanocytes, langerhans cells

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11
Q

What is the dermis composed of?

A

Dense fibro-elastic connective tissue

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12
Q

What is the hypodermis composed of?

A

Loose fibro-fatty connective tissue

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13
Q

What is the epidermal appendages made of?

A

hair follicles
sebaceous glands
sweat glands

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14
Q

From stem cells to skin surface…

A
  • stem cells are only found in the basal layer
  • stem cells divide to produce new cells
  • cells stop dividing and leave cell cycle
  • cells migrate towards surface as they differentiate
  • surface cells are dead, flat and anuclear
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15
Q

desmosomes

A
  • cell-cell adhesions
  • anchor keratin intermediate filaments to membrane
  • found on lateral (on basal surfaces they are hemidesmosomes)
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16
Q

What is pemphigus?

A

An autoimmune disease that causes blistering of the skin due to defective cell-cell adhesion

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17
Q

What is pemphigus foliaceus ?

A

Autoanitbodies recognise desmoglein 1

Blistering occurs in the upper epidermis

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18
Q

What is pemphigus vulgaris?

A

Autoantibodies recognise desmoglein 3

Blistering occurs in lower epidermis

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19
Q

Hemidesmosomes

A
  • mediate cell-extracellular matrix adhesion
  • found in simple and stratified epithelia at the basal surface of basal layer cells
  • anchor keratin intermediate filaments to membrane
20
Q

Adherens junctions

A
  • mediate cell-cell adhesion
  • found in simple and stratified epithelia
  • anchor actin filaments to the membrane
21
Q

What are components of the basement membrane?

A

laminin - contains collagen and cell-binding domains, helps cells attach to organising matrix
collage IV - 3 collagen a-chains wound to form triple helical structure, resist stretching forces

22
Q

Hemidesmosome composition

A

Integrins - adhesion molecules
membrane spanning protein BPAG2
cytoplasmic protein BPAG1 and plectin

23
Q

Epidermolysis bullosa

A

Family of genetic blistering diseases of the skin that are caused by defective cell-ECM adhesion

24
Q

What are the 3 types of epidermolysis bullosa?

A

EB simplex - localised to hands and feet, mild
Juncitonal EB - large areas of skin covered by blistered skin at birth
Dystrophic EB - repeated blistering and scarring throughout life, increased risk of squamous cell carcinomas

25
Q

What are adherens juncitons made of?

A 
classical cadherin 
beta-catenin or plakoglobin (cytoplasmic protein)
alpha catenin (cytoplasmic protein)
26
Q

What are the 4 types of classical cadherins and where are they found?

A

E-cadherin - epithelia
N-cadherin - neurons, heart muscle, fibroblasts
P-cadherin - placenta, epidermis, breast
VE-cadherin - endothelial cells

27
Q

Which cadherins can be lethal in embryogenesis?

A

E-cadherin (blastocyst implantation)
N-cadherin (heart defects)
VE-cadherin (vascular defects)

28
Q

Formation of neural tube during embryogenesis

A
  1. Epithelial cells of the embryonic ectoderm lose expression of E-cadherin and acquire N-cadherin. As this happens ectoderm invaginates to form a tube because E-cadherin is more adhesive than N-cadherin
  2. Cells that are part of the neural tube lose N-cadherin and gain cadherin-7. This allows cells to break away to form the neural crest which migrate away from neural tube. Cadherin-7 holds migrating cells in clusters.
  3. Two groups of migrating cells re-express N-cadherin which allows them to differentiate to form peripheral ganglia
29
Q

What is the epithelial-mesenchymal transition?

A

Process where neural crest cells break awat from the neural tube and migrate
epithelial cells gain different characteristics
Can be induced by alteration in adhesion between cells

30
Q

What can cause an EMT?

A

expression of E-cadherin and reduced cell adhesion

31
Q

What does loss of E-cadherin promote?

A

Invasion and metastasis
Allows invasion of underlying connective tissue
Tumour cells able to enter bloodstream

32
Q

How can loss of expression of E-cadherin be caused?

A

Mutation - inherited in CDH1
promoter hypermethylation
transcriptional silencing

33
Q

What do focal adhesions do?

A

Mediate cell-matrix adhesions

Anchor actin microfilaments to the membrane

34
Q

What are focal adhesions composed of?

A

Integrins - link signalling proteins
Structural proteins
Signalling proteins - focal adhesion kinase

35
Q

How is integrin activated?

A

Binding to ligand (outside in signalling)

Binding to talin (inside out signalling)

36
Q

Focal adhesions and cell migration

A

During cell migration focal adhesions form at the leading edge of the cell (lamellipodium)
Incorporates actin microfilaments of the actin cortex

37
Q

Steps of cell migration

A

Protrusion - actin polymerisation at leading edge pushes out a lamellipodium
Attachment - integrins engage ECM proteins, lamellipodium attached to substratum
Traction - stretches actin cortex creating tension, contraction relieves tension and pushes cell forward
Cell cycle is then repeating moving cell forward

38
Q

Outside in signalling

A

cells come into contact with ECM proteins, integrins bind and switch to active conformations
Other focal adhesion proteins recruited to form focal adhesion complex
Important for cell migration and cell growth

39
Q

inside out signalling

A

platelets express inactive integrin
When platelets come into contact with thrombin talin is activated so it turns into activated integrin
Increases affinity of integrin for fibrinogen leads to platelet formation at site of injury

40
Q

Glanzmann’s disease

A

mutations in integrin chains prevents interaction of platelets with fibrinogen
Causes defective clotting and excessive bleeding

41
Q

Minimum requirements for actin based motility

A

Nucleation of new actin filaments
Capping of older filaments
Recycling of monomers from older filaments

42
Q

What is the Arp2/3 complex and where does it localise?

A

7 protein complex containing 2 actin related proteins
Can form a trimer allowing polymerisation of new filaments
Localises towards the leading edge of a cell

43
Q

What are the different types of capping proteins?

A

Gelsolin - binds to plus end, severs actin filaments
gCap39 - non-muscle capping protein, doesn’t sever
All bind to barbed end near cell membrane

44
Q

Why do cells need capping proteins?

A

To allow cells to switch polymerisation on/off

Prevents disassembly

45
Q

What is used to recycle actin monomers and how do they work?

A

ADF/cofilin - Bind to actin monomers in ADP form and destabilises them
Profilin - promotes exchange of ADP for ATP, adds to barbed ends of filaments

46
Q

What are lamellipodia formed from?

A

Nucleation of new filaments and prevention of capping/removal of caps

Uni year 1 (19 decks)

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