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vertebrate development > neural tube and crest formation > Flashcards

neural tube and crest formation Flashcards

1
Q

what is the default fate of the ectoderm

A

to become neural tissue

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2
Q

how does the neural ectoderm get specified

A

as the organiser develops in the dorsal mesoderm (beta catenin) the mesodermal cells of the organiser release chordin noggin and follistatin to act dorsally and block BMPs interactions with their receptors - this specifies the dorsal part to neural ectoderm

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3
Q

how does TGF-beta (a BMP) signal via its two receptors

A

TGF-beta binds to a TGF-β type II receptor (serine/threonine receptor kinase) which forms a dimer with the type 1 receptors and the kinase phosphorylates the type 1 receptor. This allows downstream phosphorylation of cytoplasmic SMAD proteins after which the complex can enter the nucleus and regulate transcription of target genes

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4
Q

when does neural tube formation happen in an amphibian embryo

A

Happens at the end of gastrulation – it is a dynamic process so it initiates even before gastrulation.

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5
Q

briefly describe how the neural tube forms

A

Thickening and elongation of neural plate. See formation of neural folds. During primary neuralation the neural plate will bend to help bring together the neural folds which elevate and converse towards each other to close the neural tube and separate it from the neural ectoderm

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6
Q

what does the notochord become in humans

A

the vertebral column

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7
Q

what happens when you apply morpholinos against the three BMP inhibitors chordin noggin and follistatin in an embryo

A

lack of neural tube and sox2 expression

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8
Q

what happens when embryos are treated with antisense morpholinos that destroy BMPs 2, 4, and 7

A

the neural tube is greatly enlarged

if inactivate you get complete transformation of entire ectoderm into neural ectoderm

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9
Q

BMP at high, moderate and low levels in the ectoderm become what three tissues

A

BMP levels high - surface ectoderm
BMP levels moderate - neural crest
BMP levels low - neural plate/tube

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10
Q

at gastrulation where does noggin mRNA accumulate and what does it do

A

accumulates in the dorsal marginal zone.

then as cells involute it is in the dorsal blastopore lip

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11
Q

what does noggin primarily do in the amphibian embryo

A

dorsalises it

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12
Q

in a chick embryo when does neurulation occur

A 
at about 24 hours -a long with gastrulation
The cephalic (head) region has undergone neurulation
The caudal (tail) region is still undergoing gastrulation
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13
Q

what direction does neurulation proceed in

A

Proceeds in anterior to posterior

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14
Q

where do the neural folds form

A

at the medial hinge points

apical constriction of these cells

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15
Q

how can cells of the neural plate be distinguished from other cells in the dorsal region of the ectoderm

A

they are elongated

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16
Q

describe the process of neural tube formation

A

Folding begins as the medial hinge point (MHP) cells anchor to the notochord and change their shape while the presumptive epidermal cells move toward the dorsal midline.
The neural folds are elevated as the presumptive epidermis continues to move toward the dorsal midline. Asymmetric constriction of actin on the apical side changes cell shapes to promote MHP bending.
Convergence of the neural folds occurs as the cells at the dorsolateral hinge point (DLHP) become wedge-shaped and the epidermal cells push toward the center. Similar apical constriction occurs at both DLHP.
The neural folds are brought into contact with one another. The neural crest cells disperse, leaving the neural tube separate from the epidermis

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17
Q

what leads to neural tube defects (eg failure to close neural tube)

A

activated BMP signalling (eg loss of noggin)

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18
Q

what stops formation of more hinge points

A

SHH inhibitory effect on noggin

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19
Q

what allows formation of the apical constriction at dorsal lateral hinge points (DLHP)

A

the shh inhibitory gradient ascending from the floor plate controls the expression of noggin so that its action is not as effective at the dorsal end and noggin can inhibit BMPs and cause apical constriction of the cells forming the two DLHP

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20
Q

apical constriction only occurs in cells experiencing….

A

… low enough concentrations of both BMP (MHP and DLHP) and Shh (DLHP)

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21
Q

what induces medial hinge point morphology

A

lack of BMPs and additional signals form the notochord

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22
Q

describe how dosage of BMP signalling is important for hinge point formation

A

High levels of BMP signalling inhibit MHP formation while low levels (inhibition) promotes excessive folding at the midline

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23
Q

fusion of the neural fold zips in what direction

A

posterior to anterior

24
Q

what drives the fusion of the neural folds

A

driven by actomyosin signalling which affects constriction and behaviour of cells

25
Q

how do nonneuronal ectodermal cells contribute to fusion of the neural folds

A

they establish a filopodia bridge that connects the juxtaposed neural folds

26
Q

the differential pattern of N and E cadherins during neurulation allows for what

A

for separation of the neural tube from the skin ectoderm

27
Q

what are two disorders cause by failure of neural tube closure in mammalian embryos

A

Exencephaly: spina bifida, a large amount of protruding brain tissue and absence of calvarium. facial structures and base of the brain are intact
Anencephaly - Anencephaly results when a failure to close the neural tube allows the forebrain to remain in contact with amniotic fluid and subsequently degenerate

28
Q

what is the outcome at the end of neural tube formation

A

3 brain vesicles that will specify into 5 brain vesicles helping formation of the central nervous system and leading to peripheral nervous system formation

29
Q

what are the three primary brain vesicles that form

A

prosencephalon (forebrain)
mesencephalon (midbrain)
rhombencephalon (hindbrain)

30
Q

what secondary vesicles does the hindbrain develop into

A

metencephalon and myelencephalon

31
Q

what two secondary vesicles does the prosencephalon develop into

A

telencephalon and diencephalon

32
Q

what are the secondary vesicles

A 
telencephalon
diencephalon
mesencephalon
metencephalon
myelencephalon
33
Q

what do each of the secondary vesicles develop into

A

telencephalon (olfactory lobe, hippocampus, cerebrum)
diencephalon (optic vesicle, epithalamus, thalamus, hypothalamus)
mesencephalon (midbrain)
metencephalon (cerebellum and pons)
myelencephalon (medulla)

34
Q

what are neural crest cells

A

a multipotent and migratory cell population in the developing embryo that contribute to the formation of a wide range of tissues - they have a different shape (cuboidal with apical/basal
polarity) allowing them to leave the neural ectoderm surface to migrate

35
Q

what are neurocristopathies

A

a group of diseases caused by defects in the development, differentiation and migration of neural crest cells

36
Q

what causes the population of neural crest cells to develop from the neural tube

A

they go through a epithelial-mesenchymal transition (EMT) and lose E cadherin making them more mesenchymal (more invasive) and able to lose contact with neighbouring cells

37
Q

what types of cells do the neural crest cells give rise to

A

cartilage/ bone
schwann cells
neurons
melanocytes

38
Q

what are the two modes of neural crest cell migration

A

dorsolateral or ventral

39
Q

what do the two modes of NCC migration result in contribution to

A

Ventral between the neural tube and the sclerotome contribute to: Sympathetic and parasympathetic ganglia, Adrenomedullary cells, Dorsal root ganglia.

Dorsolateral between the dermis and epidermis become pigment-producing melanocytes

40
Q

briefly describe the development to migration of neural crest cells

A

The neural crest specifies at the border of the neural plate and subsequently localizes at the apex of neural folds, then neural crest cells delaminate at the point of neural tube closure, and finally migrate out of ectodermal tissues

41
Q

what are the main four domains that neural crest cell originate from

A 
cranial neural crest 
trunk neural crest, 
vagal and sacral neural crest, 
and 
cardiac neural crest.
42
Q

where do cranial neural crest cells originate and what do they become

A

• From the pharyngeal endomesoderm
they migrate into the pharyngeal arches and the face to from the bones and cartilage of the face and neck and contribute to some of the cranial nerves

43
Q

where do vagal and sacral neural crest cells originate and what do they become

A

vagal originate near somites 1-7
sacral originate posterior to somite 28
both work together to form parasympathetic nerves of the gut

44
Q

where do cardiac neural crest cells originate from and what do they become

A

arise near somites 1 through 3
critical in making the division between the aorta and pulmonary artery
overlap between cardiac and vagal neural crest cells gives rise to the septum of the heart

45
Q

where do trunk neural crest cells originate and what do they become

A

from about somite 6 through the tail (28)
make sympathetic neurons and pigment cells (melanocytes), and a subset of them (at the level of somites 18-24) forms the medulla portion of the adrenal gland

46
Q

what is neural crest delamination and when does it occur

A

the splitting of a tissue into separate populations of neural crest cells and their surrounding tissues
delamination coincides with the separation of neural and surface ectoderms and their fusion at the midline

47
Q

what unique adhesion proteins are expressed in a each tissue during neural crest delamination

A

surface ectoderm (E-cadherin), neural tube (N-cadherin), and the premigratory neural crest (cadherin-6B)

48
Q

what changes in gene expression occur in the premigratory neural crest cells prior to delamination
(snail 2 and cadherin 6B)

A

• High levels of BMP, and intermediate amounts of Wnt (both epidermal) upregulate expression of Snail-2 (and Zeb-2)
Snail-2 proteins repress N-cadherin and E-cadherin in this domain
• Cadherin-6B is upregulated only in the apical half of premigratory neural crest cells, and activates RhoA and actomyosin contractile fibers for apical constriction and the initiation of delamination

49
Q

what proteins are localised in the apical and basal regions of premigratory neural crest cells

A

RhoA in apical part (of transition cells)

Rac1 in basal part

50
Q

what is the kiss and run (contact inhibtion) process of neural crest cells

A

When two migrating neural crest cells meet, they stop, collapse their protrusions and change direction by sending protrusions away from the location of contact - proper migration

51
Q

what control retraction of neural crest cells

A

RhoA expression activating actomyosin stress fibres

52
Q

what control the directed growth of neural crest cells

A

Rac1 expression and lamellipodia/filopodia focal adhesions

53
Q

what is the attractive signal secreted by migrating neural crest cells that ensures the neural crest cells continually grow towards each other

A

complement 3a

54
Q

why does the pattern of migration by the group of neural crest cells have a collective direction

A

due to ongoing contact inhibition at the leading edge

55
Q

collective migration of neural crest cells is mediated by what 3 things

A

low levels of N-cadherin expression
attractive C3a signals
ongoing contact inhibition (represented by differential activation of Rho GTPases)

56
Q

how is the chemotactic cell migration of neural crest cells along with the cranial placode mediated (chase and run)

A

the placode releases a chemoattractant SDF1 which binds to the CXCR4 receptor on the neural crest cell. (chase)
this attracts the leading edge of the cranial neural crest stream.
The cranial neural crest contacts the placode (Rac1), triggering contact inhibition that pushes the placode forward (run)

intermolecular events and resulting cellular behaviours yield a forward migratory movement of both the placode and cranial neural crest cells

vertebrate development (10 decks)

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