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Neuro Development and Disease > Neuronal Polarity > Flashcards

Neuronal Polarity Flashcards

1
Q

How does asymmetry exist in cells?

A

as cell polarity, the non-uniformed distribution of specific molecules and structures

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2
Q

Give examples of where cell polarity is seen

A
  • cytoskeletal components
  • intracellular membrane system and lipids
  • organelles
  • proteins
  • mRNA
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3
Q

What is cell polarity important for?

A

cellular function as it allows cellular activities to be segregated and compartmentalised which in turn allows energetic efficiency

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4
Q

Give examples of polarity in action

A
  • migrating fibroblasts
  • cytotoxic T cell
  • epithelial cell
  • polarised dividing cell
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5
Q

What type of symmetry do neurons exhibit?

A

morphological and functional

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6
Q

What do the presynaptic and postsynaptic vesicles each have respectively?

A
  • pre = synaptic vesicles (axon)
  • post = receptors for these vesicles (dendrite)
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7
Q

What is the main reason for a neurons existence?

A

to mediate intracellular communication

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8
Q

Where is intracellular communication achieved in neurons?

A

the bipartite synapse

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9
Q

What happens between stage 2 and 3 of synapse formation?

A

the immature exon is formed from 1 minor neurite and polarity is initiated; the rest of the neurites become dendrites

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10
Q

What does selective elongation of a designated neurite do?

A

initiate axon specification which is then followed by dendritic specification

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11
Q

What is dendritic specification established via?

A
  • cytoskeleton dynamics
  • polarity signalling molecules
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12
Q

What are the 2 types of cytoskeletal tracks?

A

short range actin (LRT) and long range MTs (MRT)

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13
Q

What is meant by cytoskeletal tracks being polar?

A
  • plus end points to the outside of the cell
  • minus end points to the inside of the cell
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14
Q

What do dendrites show?

A

reverse polarisation and bidirectionality after stage 4 i.e. ~50% of the tracks become inverted

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15
Q

What do dynamic mitochondria do?

A

follow wherever cytoskeletal tracks polymerise

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16
Q

What do dynamic polymerising MTs do?

A

extend neurites

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17
Q

What do growth cones do?

A

guide neurite elongation i.e. they tell neurons where to go

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18
Q

What are the 3 zones of growth cones?

A
  • central (C) domain
  • transition (T) zone
  • peripheral (P) domain
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19
Q

What does the C domain contain?

A
  • stable bundles of MTs
  • numerous organelles, vesicles and central actin bundles
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20
Q

What is the T zone?

A

interface between the P and C domains that regulates growth cone shape and movement

21
Q

What does the T zone contain?

A

actomyosin contractile structures (actin arcs) perpendicular to F-actin bundles

22
Q

What is the P domain made up of?

A
  • long, bundled actin filaments (F-actin bundles) that form the filopodia
  • mesh-like branched F-actin networks that give structure to lamellipodia-like veils
23
Q

What must happen for growth cones to move forward?

A

they must encounter a stimulus (substrate)

24
Q

What are the 4 steps of growth cones in axon outgrowth?

A
  1. encounter
  2. protrusion
  3. engorgement
  4. consolidation
25
Q

What happens during the encounter stage of axon outgrowth?

A
  • binding of growth cone receptors at distal end of the growth cone to adhesive substrate activates intracellular signalling cascades
  • formation of a molecular ‘clutch’ (grip) that links the substrate to the actin cytoskeleton
26
Q

What happens during the protrusion stage of axon outgrowth?

A
  • the clutch strengthens and prevents backward flow of F-actin
  • F-actin polymerisation continues in front of the clutch site, the lamellipodia-like veils and filopodia of the P domain move forward to extend the leading edge
27
Q

What happens during the engorgement stage of axon outgrowth?

A
  • F-actin arcs reorientate from the C domain towards the site of new growth
  • MTs in the C domain move towards the site of new growth
28
Q

What happens during the consolidation stage of axon outgrowth?

A
  • the proximal part of the growth cone compacts at the growth cone neck to from a new segment of axon shaft
  • the myosin II-containing actin arcs compress the MTs into the newly localised C domain (followed by MT-associated protein stabilisation)
29
Q

How do axons and dendrites not collapse or retract?

A

MAPs stabilise MT tracks

30
Q

What are the main MAPs?

A

MAP-2 and Tau

31
Q

Where are the 2 MAPs once polarity is established?

A
  • MAP-2 = dendrites
  • Tau = axons
32
Q

What kind of MAP exhibits selective localisation?

A

Tau protein

33
Q

What is the negative regulation in stage 2 of axon formation?

A
  • membrane elimination
  • degradation of proteins
  • decrease in dynamics of F-actin
  • MT catastrophe
34
Q

What is responsible for retraction to extension?

A
  • Rho GTPases and GEF
  • PI3K
  • centrosome
35
Q

What is responsible for extension to retraction?

A
  • phosphatase
  • Rho GAP
36
Q

What is the positive regulation in stage 3 of axon formation?

A
  • membrane recruitment
  • protein transport
  • increase in dynamics of F-actin
  • MT assembly
37
Q

Why does the neuron become an axon at stage 3?

A

the net congregation of signalling pathways is overwhelmed by positive regulation

38
Q

What is a prerequisite for axon formation?

A

MT stabilisation

39
Q

When does MT stabilisation occur?

A

when MAPs bind to MTs to prevent them from dissociating regulated by phosphorylation

40
Q

What does MARK2 do?

A

destabilise MT tracks

41
Q

What does PAR-3/PAR-6/atypical PKC complex do?

A

regulate axon formation through MARK2

42
Q

What does a reduction in MARK2 do?

A

decrease the phosphorylation of Tau which stabilises MT tracks to increase the number of mature exons and cause development of multi-axon neurons

43
Q

What does aPKC lambda in complex with PAR-3/PAR-6 do?

A

negatively regulate MARK2

44
Q

Where is aPKCλ + PAR-3 localised?

A

the presumptive axon

45
Q

Where are PKM-ζ and PAR-3 localised?

A

non-axon-forming neurites

46
Q

What does PKM-ζ do?

A

compete with aPKC-λ for binding to PAR-3 and disrupt the aPKC-λ–PAR-3 complex

47
Q

What does silencing of PKM-ζ or overexpression of aPKC-λ in hippocampal neurons do?

A

alter neuronal polarity, resulting in neurons with supernumerary axons

48
Q

What does over expression of PKM-ζ do?

A

prevent axon specification

Neuro Development and Disease (9 decks)

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