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Neuro M101B > Module 1 Lecture 3: Neurogenesis > Flashcards

Module 1 Lecture 3: Neurogenesis Flashcards

1
Q

which cells give rise to all neurons and glia in the CNS

A

neural progenitor cells (NPCs)

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2
Q

interkinetic migration in NPCs

A

soma moves up and down the thickness of the neural tube in sync with cell cycle

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3
Q

where is NPC soma during S phase (DNA synthesis)

A

toward pial/basal side

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4
Q

where is NPC soma during G2 (2nd growth) phase

A

back at ventricular/apical side

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5
Q

where is NPC soma during M-phase (mitosis)

A

at the ventricular/apical side

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6
Q

where is NPC soma at G1 (1st growth) phase

A

starts moving back to basal side

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7
Q

first step of lineage tracing for NPCs

A

make a progenitor with a lineage tracer that can only be passed down to progeny

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8
Q

second characteristic of lineage tracing for NPCs

A

tracer can produce marker to label the whole cell outline

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9
Q

third step of lineage tracing for NPCs

A

wait

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10
Q

fourth step of lineage tracing for NPCs

A

identify progeny by shape and/or co-staining w/ genetic markers

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11
Q

application of tracer for NPCs

A

replicating incompetent retrovirus
- reverse transcribed viral genome incorporates into genome of dividing host cells
- cannot spread horizontally

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12
Q

application of markers for NPCs

A

LacZ (can paint the cell) gene engineered into retrovirus
- experiment done pre-GFP

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13
Q

how is the CNS built by NPCs

A

inside out

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14
Q

first step of birthdating

A

at chosen time, mark progenitor DNA w/ labeled nucleotide
- radioactive: 3H-thymidine
- chemical: Bromodeoxyuridine (BrdU, thymidine analog)

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15
Q

second characteristic of birthdating

A

at each round of DNA synthesis, label gets diluted
- contrast with lineage tracing

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16
Q

third characteristic of birthdating

A

post-mitotic progeny born right after label injection is most heavily marked

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17
Q

what are asymmetric divisions controlled by

A

Notch signaling

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18
Q

what kind of divisions in the expansion phase

A

symmetric divisions

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19
Q

what kind of divisions in neurogenic phase

A

asymmetric divisions

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20
Q

what is a mitogen

A

factor that promotes cell division

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21
Q

examples of mitogens

A

EGF, FGF, and Shh
- drive expansion phase

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22
Q

two hypotheses for why Shh is both morphogen and mitogen

A
  1. signaling is context dependent (concentration, duration, other molecules, history of the responding cell, etc)
  2. biology doesn’t care about our labels: possible that these two effects are not separable and/or two sides of the same coin
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23
Q

first step of Notch signaling cascade in signaling cell

A

proneural genes Ascl1 and Neurog2 lead to expression of Dll1 ligand

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24
Q

second step of Notch signaling cascade in signaling cell

A

Dll1 is presented at the cell surface

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25
Q

first step of Notch signaling in the receiving cell

A

Notch binds Dll1

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26
Q

second step of Notch signaling in the receiving cell

A

Notch intracellular domain (NICD) gets cleaved and translocates to the nucleus

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27
Q

third step of Notch signaling in the receiving cell

A

NICD binds to Rbpj and Maml

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28
Q

fourth step of Notch signaling in the receiving cell

A

complex turns on transcription of Hes, Hey

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29
Q

fifth step of Notch signaling in the receiving cell

A

proneural genes Ascl1 and Neurog2 are downregulated

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30
Q

three key features of Notch signaling

A
  1. requires cell-cell contact
  2. involves feedback loop(s)
  3. biology uses it to build patterns
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31
Q

what does Ascl1 stand for

A

Achaete-Scute like 1

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32
Q

what does Maml stand for

A

Mastermind-like

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33
Q

what does Hes stand for

A

hairy/suppressor of split

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34
Q

characteristics of neurogenic region

A
  • induced at the ventral midline using similar molecules and mechanisms as vertebrate neural induction
  • segmented, arrayed along the ventral midline
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35
Q

function of delaminating neuroblasts

A

they internalize the future CNS instead of neural tube closure
- they are the NPCs of the fly

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36
Q

role of asymmetric divisions in fly neurogenesis

A

regenerate the neuroblast and make a ganglion mother cell (GMC)

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37
Q

role of ganglion mother cells (GMCs) in fly neurogenesis

A

divide once to produce post-mitotic neurons
- similar to vertebrate intermediate precursor cells

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38
Q

characteristics of neurogenic islands

A

8 per hemisegment
- 5-7 ectodermal cells in each hemisegment

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39
Q

how is the neuroblast determined out of the clusters?

A

younger embryos express Ascl1 gene in each neurogenic cluster; soon after, only one cell continues to express Ascl1 –> this will be the neuroblast

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40
Q

what happens if you kill a neuroblast?

A

another one takes its place
- all cells in the neurogenic cluster are competent to become the NB; cell-cell interactions decide which gets picked

41
Q

what happens if there are no proneural genes in the neurogenic cluster

A

no neuroblast develops

42
Q

what happens if there is no Notch or Delta

A

too many NB

43
Q

role of proneural genes in neuroblast development

A

necessary for neuroblasts

44
Q

role of Notch and Delta in neuroblast development

A

control the number of neuroblasts

45
Q

lateral inhibition meaning

A

small quantitative differences between neighboring equivalent cells are amplified through Notch-Delta positive feedback until two qualitatively different cells emerge

46
Q

how does lateral inhibition determine which cell becomes the neuroblast

A

lateral inhibition happens between the 5-7 ectodermal cells in each neurogenic cluster, and each cell either becomes a neuroblast or an epidermal cell (bifurcation)
- the signaling cell with Asc expression becomes the neuroblast
- the receiving cell without Asc expression becomes the epidermal cell

47
Q

what is the mammalian Notch component

A

hex/her

48
Q

what happens if hes/her is autoinhibited?

A

lack of bifurcation between the signaling and receiving cells; results in fluctuation between the two fates

49
Q

how do NPCs control asymmetric division

A

oscillatory circuits

50
Q

effect of inhibiting Notch in NPC asymmetric divisions

A

premature differentiation

51
Q

effect of overactivating Notch in NPC asymmetric divisions

A

remains progenitor or become glia

52
Q

what proneural genes are involved in NPC asymmetric division

A

Ascl1, Neurog2, Olig2

53
Q

what are the Notch-responsive transcription factors in NPC asymmetric divisions

A

Hes, Hey (auto-inhibitory)
- relative levels determine which daughter cells differentiation

54
Q

function of Hes1 oscillations

A

maintain NPC renewal

55
Q

what happens if Ascl1 dominates in NPC asymmetric divisions

A

differentiates as neuron

56
Q

what happens if Olig2 dominates in NPC asymmetric divisions

A

differentiate as oligodendrocyte

57
Q

what happens if Hes1 always dominates in NPC asymmetric divisions

A

differentiates as astrocyte

58
Q

what kind of molecule drives symmetric divisions

A

mitogens (EGF, FGF, Shh)

59
Q

what kind of signaling drives asymmetric divisions

A

Notch signaling

60
Q

what is the neocortex

A

6 layered derivative of telencephalon
- present in mammals, but not in other vertebrates

61
Q

main characteristic of mammalian neocortex assembly

A

depends on interplay between developmentally transient structures that are built through ongoing self-proliferation, migration, & differentiation

62
Q

lissencephalic vs gyrencephalic cell division

A

cortical progenitors undergo 11 rounds of cell division in lissencephalic brains, vs >28 in gyrencephalic

63
Q

why is radial glia a misnomer

A

they are not actually glia, but are NPCs of corticogenesis; they undergo asymmetric division to form 1 radial glia cell and 1 neuron
- appeared to act as a scaffold for migrating neurons, but play a more complex role

64
Q

which phase of corticogenesis are intermediate precursor cells (IPCs) involved in

A

indirect neurogenesis

65
Q

intermediate precursor cells (IPC) characteristics

A
  • daughters of RGCs
  • divides once to make two neurons
  • similar to ganglion mother cells (GMC) in the fly
66
Q

what phase of corticogenesis are outer Radial Glia (oRG) involved in

A

neurogenesis through oRG cells

67
Q

characteristics of outer Radial Glia (oRG)

A
  • daughter of RGCs
  • unipolar w/ one process attached to the basal membrane
  • true progenitors; can re-new, make neurons directly, or through IPCs
68
Q

ventricular zone characteristics

A

ventricle/apical side of neuroepithelium
- home to NPCs; most cortex neurons derived from here
- VZ

69
Q

preplate characteristics

A

first neurons born from VZ
- gives rise to marginal zone (MZ) and subplate (SP)
- PP

70
Q

marginal zone characteristics

A

home to Cajal-Retzius cells; will become L1
- most superficial layer
- MZ

71
Q

characteristics of sub-ventricular zone

A
  • “above” VZ
  • home to IPCs and bRGCs
  • route for incoming migratory neurons (GABAergic)
  • SVZ
72
Q

cortical plate characteristics

A

will become layers 2-6, starting with 6 (inside out)
- CP

73
Q

characteristics of intermediate zone

A

home to incoming neurons from other parts of the brain

74
Q

what do apical radial glial cell (RGC), intermediate precursor cells (IPC), and basal radial ganglion cells (bRGC) have in common

A

all neural progenitor cells

75
Q

characteristics of outer subventricular zone (oSVZ)

A

generated by massive expansion of basal radial glia
- one of the reasons we have gyrencephalic brains

76
Q

what cells are in the vertebrate marginal zone?

A

horizontal cells
- not in fish

77
Q

where are horizontal cells born

A

cortical hem (transient structure, arises next to the former roof plate)

78
Q

where do horizontal cells go after being born

A

migrate out and cover the whole cortex surface

79
Q

how long do Cajal-Retzius cells stay

A

in mice, gone by 1 week after birth; in humans, most disappear but a few persist

80
Q

when were Cajal-Retzius cells discovered

A

turn of 19th century
- still do not know how they do what they do
- express Reelin

81
Q

what are reeler mice

A

RELN-/- mice
- have ataxia (impaired balance and motor coordination)

82
Q

structural phenotype of RELN+/+ in brain

A

normal

83
Q

structural phenotype of RELN+/- in brain

A
  • no growth pathology
  • structural alterations
  • fine histological changes
  • GABAergic neurons
  • pyramidal neurons
  • dendritic spines
84
Q

structural phenotype of RELN-/- in brain

A
  • lissencephaly
  • cerebellar hypoplasia
  • structural alterations
  • loss of layered structures
  • severe histological changes
85
Q

what are mutations in Reelin linked to

A

Lissencephaly 2

86
Q

effect of Lissencephaly 2

A
  • abnormalities of the skull and face
  • severe or profound intellectual disability
  • seizures
  • abnormally increased muscle tone
  • exaggerated reflexes
  • severe growth failure
87
Q

how is cortex assembly affected by Reln-/-

A
  • new neurons cannot migrate past older ones; outside-in (and scrambled) assembly
  • disrupted organization
88
Q

what is Reelin

A

secreted glyco-protein

89
Q

what is the only source of Reelin during cortical development

A

Cajal-Retzius cells

90
Q

what receptors do migrating cortical neurons express for Reelin

A

VLDLR and ApoER2 (very low density lipoprotein receptor)

91
Q

relationship between Dab1 (adaptor protein) and Reelin

A

gets phosphorylated when Reelin binds its receptors
- Dab1 mutant mice have a reeler-like phenotype

92
Q

what is the ultimate target of Reelin signalin

A

regulation of cell migration

93
Q

characteristics of most neurons born at the ventricular zone of the developing cortex

A

pyramidal, glutamatergic, projection neurons

94
Q

where the GABAergic interneurons of the cortex migrate in from

A

the Medial Ganglionic Eminence (MGE)

95
Q

what is the medial ganglionic eminence

A

a temporary subcortical structure which disappears in humans by age 1
- contributes neurons to the basal ganglia

96
Q

role of subventricular zone in building the cortex

A

incoming neurons migrate along the sub-ventricular zone and follow the radial glia processes to find their layers

97
Q

where does neurogenesis occur in the adult mammalian brain

A
  1. subventricular zone (SVZ) of the lateral ventricle
  2. dentate gyrus of the hippocampus
98
Q
A

Neuro M101B (6 decks)

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