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BMS > Development of the Neural Crest > Flashcards

Development of the Neural Crest Flashcards

1
Q

Levels of BMP regulate nervous system formation from the

A

Ectoderm

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2
Q

BMP near the midline is suppressed by

A

Noggin, Chordin, and FGF

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3
Q

Low levels of BMP allow the development of the

A

Nervous System

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4
Q

The first step of neural crest formation is to become distinct from both the

A

Adjacent ectoderm and neural tissue

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5
Q

The second step of neural crest formation is to begin

A

Migration

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6
Q

The third step of neural crest formation is to

A

Localize and differentiate

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7
Q

We can use quail-chick cell transplantation to create a chimeric embryo that allows us to

A

Map Neural Crest (NC)

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8
Q

The neural crest arises from the

A

Ectoderm

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9
Q

The qual-chick experiment allowed us to identify classic derivatives of the neural crest. What are the three cranial derivatives?

A
  1. ) Neurons and glia of cranial ganglia
  2. ) Cartilage and bone
  3. ) Connective tissue
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10
Q

The qual-chick experiment allowed us to identify classic derivatives of the neural crest. What are the three trunk derivatives?

A
  1. ) Pigment cells
  2. ) Sensory Neurons and glia
  3. ) Sympatho-adrenal cells
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11
Q

What are the levels of BMP for the following tissues?

  1. ) Epidermal
  2. ) Neural crest
  3. ) Neural
A
  1. ) High
  2. ) Intermediate
  3. ) Low
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12
Q

Forms at the boundary where presumptive neural plate meets the ectoderm

A

Neural crest

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13
Q

At this boundary, intermediate levels of BMPs in conjunction with FGF and other molecules induce

A

“snail” and “border specifier” genes

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14
Q

The “snail” and “border specifier” genes, in conjunction with BMPs and Wnts, then induce additional transcription factors that specify the

A

Neural crest

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15
Q

Stimulates c-Kit (pigment cells) and c-Ret (enteric neural precursors) expression on NC cells that have long migratory pathways

A

NC specifier transcription factor Sox10

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16
Q

In the initiation and pathways of trunk neural crest migration, first NC must change from epithelium to

A

Mesenchyme

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17
Q

To change from epithelium to mesenchyme, the NC loses its

A

6B class of Cadherins

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18
Q

The NC then migrates into a space filled with

A

Hyaluronic acid

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19
Q

Some disease conditions have deficiencies in several migratory cell populations such as

A

Pigment cells, hemopoetic cells, and germ cells

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20
Q

Specific ligand-receptor systems are used in

A

Neural crest migration

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21
Q

Different mutations in different strains of mice (called Dominant spotting and Steel) alter pigmentation and also lead to

A

Anemia and Sterility

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22
Q

These mutations encode either a specific receptor on the cell surface of the migratory cells or the ligand for that receptor that is produced by the cells in the

A

Migratory environment

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23
Q

Thus, for germ cells, hemopoetic cells, and NC-derived pigment cells, the tyrosine kinase C-kit receptor (mutated in dominant spotting mutation) on migratory cells binds

A

Steel factor ligan

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24
Q

Produced in migratory pathways used by germ cells, hemopoetic cells, and NC-derived pigment cells

A

Steel factor ligand

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25
Q

Production of ligand in the migratory pathway suggests that Steel peptide functions as a chemoattractant for

A

Receptor Expressing Cells

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26
Q

As in mouse, humans heterozygous for c-Kit mutation have

-as well as some deficits in hemopoetic and germ cell migration

A

Pigment migratory deficits

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27
Q

Provides progenitors for enteric nervous system

A

Migration of neural crest into the gut

28
Q

The major congenital abnormality of the gut

-characterized by megacolon

A

Hirschsprung’s Disease

29
Q

Individuals with Hirschprung’s disease have a deficiency of enteric ganglia and as a result suffer from

A

Constipation

30
Q

Two non-linked mouse genes producing megacolon when mutated were also identified and turned out to represent another ligand-receptor pair. What is the:

  1. ) Receptor
  2. ) Ligand
A
  1. ) c-Ret

2. ) GDNF

31
Q

c-Ret is expressed in

A

Neural crest cells

32
Q

GDNF is expressed in the

A

Gut

33
Q

In both c-Ret and GDNF mutant mice, NC migration is

markedly reduced and NC cells never reach the

A

Posterior gut

34
Q

The mutation that causes the distal enteric ganglia not to form and results in Hirschsprung’s disease is a mutation in

A

c-Ret

35
Q

Functions as a chemo-attractant as neural crest cells colonize the gut

A

GDNF

36
Q

Neural crest cells interact with multiple cells/matrix components during

A

Migration

37
Q

Characterized by deficits seen in the pharyngeal arches and pouches (pharynx, larynx) and also in neural crest derivatives (thymus, parathyroid, etc)

A

DiGeorge Syndrome

38
Q

Develops as the neural crest enters the structure

A

Pharyngeal system

39
Q

May be the result of initial failure of the pharynx and/or secondary failure of the neural crest

A

DiGeorge Syndrome

40
Q

Variable size deletions 1.5-3 MB of human Ch22, which contains over 30 genes, are present in >90% of

A

DiGeorge patients

41
Q

DiGeorge syndrome is the most common microdeletion in humans with an occurance of

A

1/4000

42
Q

The region corresponding to the human DiGeorge region, 22q11, was found on mouse chromosome

A

16

43
Q

Experimentation on mice showed that naturally occuring deltions indicated positive expression of

A

DiGeorge Syndrome

44
Q

The relevant regions that lead to DiGeorge Syndrome include a gene for the transcription factor

A

Tbx-1 (A T-Box TF)

45
Q

Developmentally important family of transcription factors

-Several mutations in this family are associated with human congenital abnormalities

A

T-Box gene family

46
Q

Expressed in all cell types of the pharynx at mid-gestation, but NOT in the migrating neural crest cells

A

Tbx1

47
Q

If Tbx1 is involved in Digeorge syndrome, this expression pattern suggests that deficiencies in NC-derived structures are likely secondary to failure of

A

Pharyngeal cells

48
Q

When we knock out the Tbx-1 gene in mice, the mutant mice have multiple features of

A

DiGeorge Syndrome (i.e. cleft palate, low set ears, abnormal aortic arches)

49
Q

Upstream regulators of Tbx-1 include

A

Sonic Hedgehog (Shh)

50
Q

Bind to 5’ regulatory regions in FGF family genes

A

Tbx-1

51
Q

If FGF is diminished in Tbx1 expression domain, phenotype similar to

A

Tbx-1 mutant mice

52
Q

Is Tbx1 the only gene involved in DiGeorge syndrome?

A

No

53
Q

An adaptor protein implicated in TGF-β and FGF signaling

-another contributer to DiGeorge syndrome

A

Crkl gene

54
Q

In contrast to Tbx-1, Crkl is expressed in

A

Neural crest

55
Q

Absence of Crkl (via gene KO) impairs

A

TGF/FGF signaling

56
Q

The impaired signaling caused by KO of Crkl leads to severe defects in cardio vascular patterning that are specific to the

A

Neural crest (pharyngeal derivatives = normal)

57
Q

Implicated in the initial formation of pharyngeal arches and pouches prior to neural crest migration

A

Tbx-1

58
Q

Teratogenic influence on anterior nervous system and neural crest development due to alcohol intake

A

Fetal Alcohol Syndrome

59
Q

The third leading cause of mental retardation behind fragile X syndrome and Down Syndrome

A

Fetal Alcohol Syndrome

60
Q

2-3 oz hard liquor/day and or a single binge drinking

episode during pregnancy can induce

A

Fetal Alcohol Syndrome

61
Q

What is the incidence of Fetal Alcohol Syndrome?

A

1/500 - 1/750 children

62
Q

Giving prenatal mice alcohol showed that 12 hours after a single EtOH exposure, there was cell death in the

A

Anterior neural ridge

63
Q

The mice were then exposed to alcohol at a stage when neural folds were forming and neural crest cells started to migrate. The result was that

A

NC migration was deficient (Much apoptosis)

64
Q

The alcohol exposure also led to a reduced contribution to

A

Nasal and maxillary processes

65
Q

Forms and disperses as a result of activation of a sequential cascade of transcription factor activation initially elicited primarily by specific levels of BMP

A

Neural Crest

66
Q

Migration of neural crest cells to different destinations

is controlled in large part by

A

Specific ligand receptor systems

67
Q

The ligand in the specific ligand-receptor systems functions as a

A

Chemoattractant

BMS (62 decks)

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