[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
2
Q
mesoderm fates
A
- notochord
- bone tissue
- tubule of the kidney
- RBCs
- facial muscle
3
Q
endoderm fates
A
- stomach cell
- thyroid cell
- lung cell
4
Q
t or f: differential signaling contributes to specification of germ layer fates
A
t
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
6
Q
wnt, BMP, and activin inhibits
A
FGF
7
Q
t or f: inhibition of FGF in the specification of the germ layers forms the endoderm
A
t
8
Q
in the specification of the germ layer fates, what signal/s is/are found anteriorly?
A
activin and nodal
9
Q
induces the formation of ectoderm cells
A
FGF
10
Q
t or f: BMP4 induces the formation of neural cells
A
f; epidermal cells
11
Q
t or f: high BMP4 induces the formation of posterior populations and the mesoderm in the germ layer fates
A
t
12
Q
t or f: high activin/ nodal induces the formation of anterior populations in germ layer fates
A
t
13
Q
t or f: presence of FGF in the specification of germ layer fates induces the formation of ectoderm cells
A
t
14
Q
t or f: endoderm will undergo neurulation to form the neural tube
A
f; ectoderm
15
Q
t or f: neurulation has one mechanism
A
f
16
Q
different neurulation mechanisms
A
- primary neurulation
- secondary neurulation
- junctional neurulation
17
Q
it is the intermediate step in neurulation
A
junctional neurulation
18
Q
how is the neural tube formed in primary neurulation?
A
forms from neural folds
19
Q
how is the neural tube formed during secondary neurulation?
A
it is formed from mesenchyme
20
Q
it is the transition between the primary and secondary neurulation
A
junctional neurulation
21
Q
t or f: dissociated cells of the ectoderm become epidermal cells
A
f; neural cells
22
Q
t or f: dissociated ectoderm cells with BMPs become epidermal cells
A
t
23
Q
t or f: intact ectodermal cells become epidermal cells
A
t
24
Q
t or f: intact ectoderm cells become neural cells in the presence of BMP inhibitors
A
t
25
BMP inhibitors
- chordin
- noggin
- follistatin
26
t or f: presence of BMP inhibitors induce the formation of the epidermal cells
f; neural cells
27
t or f: neural tissue is specified prior to gastrulation by the primary organizer
t
28
t or f: absence of signals from the primary organizer supress neural differentiation
t
29
BMP inhibitors that induce neural cell formation is from what structure?
primary organizer
30
structure that acts as an inducer for neurulation
notochord
31
t or f: presence of BMP induces formation of epidermal cells
t
32
it induces the neural plate formation
notochord
33
it secretes the BMP inhibitors wo induce the formation of neural plate
notochord
34
steps of primary neurulation
- elongation and folding of neural plate
- bending of neural plate
- convergence of neural folds
- closure of neural tubes
35
t or f: BMP is present during neurulation
f; it is inhibited
36
the median hinge point can form different shapes because of
PCP pathway and apical constriction
37
t or f: there are cells that undergo MET during neural tube closure
f; EMT
38
transmembrane protein present in the Shh signaling pathway
PTCH and SMO
39
relationship between PTCH and SMO in the Shh pathway
PTCH inhibits SMO
40
steps if Shh pathway is inactive
- PTCH inhibits SMO
- SUFU sequesters GLI1
- there is no transcription
41
steps if Shh pathway is active
- Shh binds to PTCH
- SMO is active
- SMO inhibits SUFU
- GLI1 accumulates
- there is active transcription
42
result of the Shh pathway
- proliferation
- apoptosis suppression
- stem cell self-renewal
43
interplay between these signals establishes the dorsal-ventral axis of the neural tube
Shh and BMP
44
t or f: interplay between Shh and BMP establishes the anterior-posterior axis of the neural tube
f; dorsal-ventral axis
45
antagonism between these signals contributes to neural tube dorsal-ventral patterning
Shh and Wnt/ beta-catenin
46
t or f: Shh and wnt/ beta-catenin are protagonists during the neural tube dorsal-ventral patterning
f; antagonists
47
highest signal present in the ventral side of the neural tube
Shh
48
highest signal present in the dorsal side of the neural tube
Wnt/ beta-catenin
49
t or f: Shh increases from dorsal to ventral neural tube
f; decreases
50
signal that promotes dorsal identities of the neural tube
wnt/ beta-catenin
51
wnt expresses this signal to inhibit Shh in the dorsal side of the neural tube
Gli3
52
signal expressed by Shh in the ventral side of the neural tube
Gli1
53
t or f: Shh gradient across the dorsal-ventral axis determines neural cell fates
t
54
t or f: the activator form of Gli is promoted by wnt/ beta-catenin
f; shh
55
how does wnt/ beta-catenin restrict Shh activity on the dorsal side of the neural tube?
it induces Gli3 expression
56
t or f: the presence of Gli1 promotes ventral neural tube determination
t
57
t or f: presence of Gli3 promotes the ventral determination of the neural tube
f; dorsal
58
signal interactions which determine the location of the hinge points
Shh-noggin-BMP
59
t or f: BMP gradient across the dorsal-ventral axis determines the neural cell fates
f; Shh gradient
60
signal which inhibits hinge point formation
BMP
61
hinge points that do not form when BMP is present
median hinge point and dorsolateral hinge points
62
what happens if noggin is reduced during hinge point formation?
BMPs initiate wnt and activate EMT in the neural crest cells
63
t or f: low BMP = no hinge point formed
f; there is hinge point formed
64
it inhibits BMP during hinge point formation
noggin
65
t or f: there is hinge point formation when noggin is present
t
66
regulates the fusion of the neural folds
differential expression of cadherins
67
cadherin present in the presumptive epidermis
e-cad
68
cadherin present in the neural plate
n-cad
69
signal which specifies the neural crest cells
wnt
70
signal that is concentrated in the neural plate
FGF
71
signal that is concentrated in the neural crest
wnt
72
cell movement involved in the formation of the neural crest
delamination
73
gene expressed and activated by BMP and wnt for neural crest to undergo EMT
Snail2
74
signals activated for neural crest to undergo EMT
wnt genes
75
during EMT of neural crests, wnt genes are activated by
BMP
76
steps in neural crest EMT
- 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
role of snail2 in neural crest EMT
represses N-cad, E-cad, Sox2 to promote delamination
78
repression of these signals promotes delamination
- n-cad
- e-cad
- sox2
79
t or f: pre-migratory NCs must have low BMP and intermediate wnt
f; high BMP
80
where does secondary neurulation occur in mammals and birds?
caudal region
81
steps in primary neurulation
- initial epithelium
- columnarization
- rolling/ folding
- closure
- neural tube complete
82
steps in secondary neurulation
- dispersed mesenchyme
- mesenchymal condensation
- medullary cord/ neural rod
- epithelial transition/ cavitation
- neural tube complete
83
forms when the mesenchyme condenses during secondary neurulation
medullary cord/ neural rod
84
the mesenchyme during secondary neurulation undergo this process to form a rod
epithelial transition
85
secondary vesicles from the forebrain
telencephalon and diencephalon
86
secondary vesicle from the midbrain
mesencephalon
87
secondary vesicles from the hindbrain
metencephalon and myelencephalon
88
adult derivatives of the telencephalon
- olfactory lobes
- hippocampus
- cerebrum
89
adult derivatives of the diencephalon
- retina
- epithalamus
- thalamus
- hypothalamus
90
adult derivatives of the mesencephalon
midbrain
91
adult derivatives of the metencephalon
- cerebellum
- pons
92
adult derivative of the myelencephalon
medulla
93
anteriorizing signals in the neural plate stage
- cerberus
- dickkopf
- Tlc
94
posteriorizing signals in the neural plate stage
- wnt
- FGF
- RA
95
it is an anteriorizing signal that is secreted later the neural plate stage
Tlc
96
why is Tlc secreted later?
to specify the forebrain
97
t or f: signaling proteins that specify the different brain regions is time-dependent
t
98
first signals demarcating the isthmus
Otx2 and Gbx2
99
it acts as an organizing center to establish the midbrain and hindbrain
isthmus
100
secondary anterior signals in specifying the different brain regions
- wnt1
- en1
- pax2
101
secondary posterior signals in specifying the different brain regions
- fgf8
- en2
- pax2
102
these are signals that are eventually expressed in the midbrain and hindbrain
Pax 2, 5, 8
103
signals that demarcates the forebrain-midbrain
Pax6 vs. En1/Pax2
104
demarcates midbrain-hindbrain
Otx2 vs Gbx2
105
specifies the hindbrain and telencephalon
Fgf8
106
signal that stabilizes expression of En1 and Pax2
Fgf8
107
specifies the isthmus
Pea3
108
it is the anterior-posteriorizing organizing center of the brain
isthmus
109
signal that the "telencephalon" organizing center expresses
Fgf8
110
dorsal-ventral axes specifying signals of the brain
Shh vs BMP
111
signals secreted by the isthmus
- wnt1
- Fgf8
112
anterior signal secreted by the isthmus
Wnt1
113
posterior signal secreted by the isthmus
Fgf8
114
t or f: interactions between signals may also specify neuronal populations
t
115
birth defect that happens when a baby's backbone does not form normally
spina bifida
116
it is the forebrain specifying organizing center
"telencephalon" organizing center
117
defect wherein the brain and spinal cord are completely open
craniorachischisis
118
defect wherein brain is open and there is no skull vault
anencephaly
119
defect wherein there is herniation of the meninges and brain
encephalocele
120
defect wherein there are occipital skull and spine defects with extreme retroflexion of the head
iniencephaly
121
what does the Cre-Loxp mutant mouse do?
allows for precise deletion of genes of interest
122
new way of knocking out of gene
use crespar
123
deletion of this protein results in encephalocele
Gpr161
124
role of Gpr161
Shh inhibitor
125
cre driver in encephalocele
wnt1
126
t or f: mechanisms involved in NTDs are likely to be multi-faceted
t
127
what happens when the neuroepithelium is removed?
abnormally increased cell proliferation
128
neural tube defects management approaches in utero
- prenatal surgery
- stem cell therapy
129
neural tube defects management approaches in infants
stem cell transplantation
130
neural tube defects management approaches in adults
surgery
131
etiology and pathogenesis of NTDs
- nutritional risk factors
- genetic risk factors
- environmental risk factors
132
this affects DNA methylation and histone modification
folic acid
133
mutation in this gene in animal models induces onset of NTDs
Pax
134
maternal exposure to teratogens
- arsenic
- pesticides
- drugs
135
teratogen that induces NTDs which is cytotoxic
arsenic
136
teratogen that induces NTDs which accumulates in the placenta
pesticides
