[LE 02] Ectodermal Derivatives Flashcards

Neurulation, Neural Tube Development

1
Q

ectoderm fates

A
  • epidermal cells of the skin
  • neuron of the brain
  • pigment cell
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2
Q

mesoderm fates

A
  • notochord
  • bone tissue
  • tubule of the kidney
  • RBCs
  • facial muscle
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3
Q

endoderm fates

A
  • stomach cell
  • thyroid cell
  • lung cell
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4
Q

t or f: differential signaling contributes to specification of germ layer fates

A

t

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5
Q

in the specification of the germ layer fates, these are inhibitors in the early stage of the pathway that will induce endoderm formation

A
  • wnt
  • bmp
  • activin
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6
Q

wnt, BMP, and activin inhibits

A

FGF

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7
Q

t or f: inhibition of FGF in the specification of the germ layers forms the endoderm

A

t

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8
Q

in the specification of the germ layer fates, what signal/s is/are found anteriorly?

A

activin and nodal

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9
Q

induces the formation of ectoderm cells

A

FGF

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10
Q

t or f: BMP4 induces the formation of neural cells

A

f; epidermal cells

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11
Q

t or f: high BMP4 induces the formation of posterior populations and the mesoderm in the germ layer fates

A

t

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12
Q

t or f: high activin/ nodal induces the formation of anterior populations in germ layer fates

A

t

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13
Q

t or f: presence of FGF in the specification of germ layer fates induces the formation of ectoderm cells

A

t

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14
Q

t or f: endoderm will undergo neurulation to form the neural tube

A

f; ectoderm

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15
Q

t or f: neurulation has one mechanism

A

f

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16
Q

different neurulation mechanisms

A
  • primary neurulation
  • secondary neurulation
  • junctional neurulation
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17
Q

it is the intermediate step in neurulation

A

junctional neurulation

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18
Q

how is the neural tube formed in primary neurulation?

A

forms from neural folds

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19
Q

how is the neural tube formed during secondary neurulation?

A

it is formed from mesenchyme

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20
Q

it is the transition between the primary and secondary neurulation

A

junctional neurulation

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21
Q

t or f: dissociated cells of the ectoderm become epidermal cells

A

f; neural cells

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22
Q

t or f: dissociated ectoderm cells with BMPs become epidermal cells

A

t

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23
Q

t or f: intact ectodermal cells become epidermal cells

A

t

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24
Q

t or f: intact ectoderm cells become neural cells in the presence of BMP inhibitors

A

t

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25
Q

BMP inhibitors

A
  • chordin
  • noggin
  • follistatin
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26
Q

t or f: presence of BMP inhibitors induce the formation of the epidermal cells

A

f; neural cells

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27
Q

t or f: neural tissue is specified prior to gastrulation by the primary organizer

A

t

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28
Q

t or f: absence of signals from the primary organizer supress neural differentiation

A

t

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29
Q

BMP inhibitors that induce neural cell formation is from what structure?

A

primary organizer

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30
Q

structure that acts as an inducer for neurulation

A

notochord

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31
Q

t or f: presence of BMP induces formation of epidermal cells

A

t

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32
Q

it induces the neural plate formation

A

notochord

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33
Q

it secretes the BMP inhibitors wo induce the formation of neural plate

A

notochord

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34
Q

steps of primary neurulation

A
  • elongation and folding of neural plate
  • bending of neural plate
  • convergence of neural folds
  • closure of neural tubes
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35
Q

t or f: BMP is present during neurulation

A

f; it is inhibited

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36
Q

the median hinge point can form different shapes because of

A

PCP pathway and apical constriction

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37
Q

t or f: there are cells that undergo MET during neural tube closure

A

f; EMT

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38
Q

transmembrane protein present in the Shh signaling pathway

A

PTCH and SMO

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39
Q

relationship between PTCH and SMO in the Shh pathway

A

PTCH inhibits SMO

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40
Q

steps if Shh pathway is inactive

A
  • PTCH inhibits SMO
  • SUFU sequesters GLI1
  • there is no transcription
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41
Q

steps if Shh pathway is active

A
  • Shh binds to PTCH
  • SMO is active
  • SMO inhibits SUFU
  • GLI1 accumulates
  • there is active transcription
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42
Q

result of the Shh pathway

A
  • proliferation
  • apoptosis suppression
  • stem cell self-renewal
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43
Q

interplay between these signals establishes the dorsal-ventral axis of the neural tube

A

Shh and BMP

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44
Q

t or f: interplay between Shh and BMP establishes the anterior-posterior axis of the neural tube

A

f; dorsal-ventral axis

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45
Q

antagonism between these signals contributes to neural tube dorsal-ventral patterning

A

Shh and Wnt/ beta-catenin

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46
Q

t or f: Shh and wnt/ beta-catenin are protagonists during the neural tube dorsal-ventral patterning

A

f; antagonists

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47
Q

highest signal present in the ventral side of the neural tube

A

Shh

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48
Q

highest signal present in the dorsal side of the neural tube

A

Wnt/ beta-catenin

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49
Q

t or f: Shh increases from dorsal to ventral neural tube

A

f; decreases

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50
Q

signal that promotes dorsal identities of the neural tube

A

wnt/ beta-catenin

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51
Q

wnt expresses this signal to inhibit Shh in the dorsal side of the neural tube

A

Gli3

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52
Q

signal expressed by Shh in the ventral side of the neural tube

A

Gli1

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53
Q

t or f: Shh gradient across the dorsal-ventral axis determines neural cell fates

A

t

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54
Q

t or f: the activator form of Gli is promoted by wnt/ beta-catenin

A

f; shh

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55
Q

how does wnt/ beta-catenin restrict Shh activity on the dorsal side of the neural tube?

A

it induces Gli3 expression

56
Q

t or f: the presence of Gli1 promotes ventral neural tube determination

A

t

57
Q

t or f: presence of Gli3 promotes the ventral determination of the neural tube

A

f; dorsal

58
Q

signal interactions which determine the location of the hinge points

A

Shh-noggin-BMP

59
Q

t or f: BMP gradient across the dorsal-ventral axis determines the neural cell fates

A

f; Shh gradient

60
Q

signal which inhibits hinge point formation

A

BMP

61
Q

hinge points that do not form when BMP is present

A

median hinge point and dorsolateral hinge points

62
Q

what happens if noggin is reduced during hinge point formation?

A

BMPs initiate wnt and activate EMT in the neural crest cells

63
Q

t or f: low BMP = no hinge point formed

A

f; there is hinge point formed

64
Q

it inhibits BMP during hinge point formation

A

noggin

65
Q

t or f: there is hinge point formation when noggin is present

A

t

66
Q

regulates the fusion of the neural folds

A

differential expression of cadherins

67
Q

cadherin present in the presumptive epidermis

A

e-cad

68
Q

cadherin present in the neural plate

A

n-cad

69
Q

signal which specifies the neural crest cells

A

wnt

70
Q

signal that is concentrated in the neural plate

A

FGF

71
Q

signal that is concentrated in the neural crest

A

wnt

72
Q

cell movement involved in the formation of the neural crest

A

delamination

73
Q

gene expressed and activated by BMP and wnt for neural crest to undergo EMT

A

Snail2

74
Q

signals activated for neural crest to undergo EMT

A

wnt genes

75
Q

during EMT of neural crests, wnt genes are activated by

A

BMP

76
Q

steps in neural crest EMT

A
  • start with differential cadherins
  • EMT via activation of wnt genes by BMP
  • Pre-migratory NCs have high BMP and intermediate wnt
  • increased snail2 and RhoA and Rac activation
77
Q

role of snail2 in neural crest EMT

A

represses N-cad, E-cad, Sox2 to promote delamination

78
Q

repression of these signals promotes delamination

A
  • n-cad
  • e-cad
  • sox2
79
Q

t or f: pre-migratory NCs must have low BMP and intermediate wnt

A

f; high BMP

80
Q

where does secondary neurulation occur in mammals and birds?

A

caudal region

81
Q

steps in primary neurulation

A
  • initial epithelium
  • columnarization
  • rolling/ folding
  • closure
  • neural tube complete
82
Q

steps in secondary neurulation

A
  • dispersed mesenchyme
  • mesenchymal condensation
  • medullary cord/ neural rod
  • epithelial transition/ cavitation
  • neural tube complete
83
Q

forms when the mesenchyme condenses during secondary neurulation

A

medullary cord/ neural rod

84
Q

the mesenchyme during secondary neurulation undergo this process to form a rod

A

epithelial transition

85
Q

secondary vesicles from the forebrain

A

telencephalon and diencephalon

86
Q

secondary vesicle from the midbrain

A

mesencephalon

87
Q

secondary vesicles from the hindbrain

A

metencephalon and myelencephalon

88
Q

adult derivatives of the telencephalon

A
  • olfactory lobes
  • hippocampus
  • cerebrum
89
Q

adult derivatives of the diencephalon

A
  • retina
  • epithalamus
  • thalamus
  • hypothalamus
90
Q

adult derivatives of the mesencephalon

A

midbrain

91
Q

adult derivatives of the metencephalon

A
  • cerebellum
  • pons
92
Q

adult derivative of the myelencephalon

A

medulla

93
Q

anteriorizing signals in the neural plate stage

A
  • cerberus
  • dickkopf
  • Tlc
94
Q

posteriorizing signals in the neural plate stage

A
  • wnt
  • FGF
  • RA
95
Q

it is an anteriorizing signal that is secreted later the neural plate stage

A

Tlc

96
Q

why is Tlc secreted later?

A

to specify the forebrain

97
Q

t or f: signaling proteins that specify the different brain regions is time-dependent

A

t

98
Q

first signals demarcating the isthmus

A

Otx2 and Gbx2

99
Q

it acts as an organizing center to establish the midbrain and hindbrain

A

isthmus

100
Q

secondary anterior signals in specifying the different brain regions

A
  • wnt1
  • en1
  • pax2
101
Q

secondary posterior signals in specifying the different brain regions

A
  • fgf8
  • en2
  • pax2
102
Q

these are signals that are eventually expressed in the midbrain and hindbrain

A

Pax 2, 5, 8

103
Q

signals that demarcates the forebrain-midbrain

A

Pax6 vs. En1/Pax2

104
Q

demarcates midbrain-hindbrain

A

Otx2 vs Gbx2

105
Q

specifies the hindbrain and telencephalon

A

Fgf8

106
Q

signal that stabilizes expression of En1 and Pax2

A

Fgf8

107
Q

specifies the isthmus

A

Pea3

108
Q

it is the anterior-posteriorizing organizing center of the brain

A

isthmus

109
Q

signal that the “telencephalon” organizing center expresses

A

Fgf8

110
Q

dorsal-ventral axes specifying signals of the brain

A

Shh vs BMP

111
Q

signals secreted by the isthmus

A
  • wnt1
  • Fgf8
112
Q

anterior signal secreted by the isthmus

A

Wnt1

113
Q

posterior signal secreted by the isthmus

A

Fgf8

114
Q

t or f: interactions between signals may also specify neuronal populations

A

t

115
Q

birth defect that happens when a baby’s backbone does not form normally

A

spina bifida

116
Q

it is the forebrain specifying organizing center

A

“telencephalon” organizing center

117
Q

defect wherein the brain and spinal cord are completely open

A

craniorachischisis

118
Q

defect wherein brain is open and there is no skull vault

A

anencephaly

119
Q

defect wherein there is herniation of the meninges and brain

A

encephalocele

120
Q

defect wherein there are occipital skull and spine defects with extreme retroflexion of the head

A

iniencephaly

121
Q

what does the Cre-Loxp mutant mouse do?

A

allows for precise deletion of genes of interest

122
Q

new way of knocking out of gene

A

use crespar

123
Q

deletion of this protein results in encephalocele

A

Gpr161

124
Q

role of Gpr161

A

Shh inhibitor

125
Q

cre driver in encephalocele

A

wnt1

126
Q

t or f: mechanisms involved in NTDs are likely to be multi-faceted

A

t

127
Q

what happens when the neuroepithelium is removed?

A

abnormally increased cell proliferation

128
Q

neural tube defects management approaches in utero

A
  • prenatal surgery
  • stem cell therapy
129
Q

neural tube defects management approaches in infants

A

stem cell transplantation

130
Q

neural tube defects management approaches in adults

A

surgery

131
Q

etiology and pathogenesis of NTDs

A
  • nutritional risk factors
  • genetic risk factors
  • environmental risk factors
132
Q

this affects DNA methylation and histone modification

A

folic acid

133
Q

mutation in this gene in animal models induces onset of NTDs

A

Pax

134
Q

maternal exposure to teratogens

A
  • arsenic
  • pesticides
  • drugs
135
Q

teratogen that induces NTDs which is cytotoxic

A

arsenic

136
Q

teratogen that induces NTDs which accumulates in the placenta

A

pesticides