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Dev Biology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Fates of ectoderm

A

Epidermis (surface), neural crest, and neural plate/tube

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2
Q

Epidermis

A

Surface ectoderm, high levels of BMP

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3
Q

Neural crest

A

Moderate levels of BMP, lead to parts of the peripheral nervous system

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4
Q

Neural plate/ tube

A

Low BMP levels and Sox transcription factor expressed, becomes CNS and retina

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5
Q

Neurulation

A

Process of forming neural tissues, through inhibition of BMPs at dorsal midline

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6
Q

Role of Sox transcription factors

A

Activating the genes that specify cells to be neural plate and inhibiting formation of epidermis and neural crest by inhibiting BMP

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7
Q

Modes of neurulation

A

Primary and secondary

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8
Q

Primary neurulation

A

Anterior neural tube formation, Cells around the neural plate signal the neural plate cells to proliferate, invaginate, and separate from the surface ectoderm to form a hollow tube

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9
Q

Secondary neurulation

A

Posterior tube formation, Neural tube arises from the clustering of mesenchymal cells that hollow to form a tube

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10
Q

Junctional neurulation

A

Combination of primary and secondary neurulation where the two ends meet, creates the transitional zone

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11
Q

Process of primary neurulation

A

Neural folds are formed by the edges of the neural plate thickening and moving upward. Thickening of the folds form the neural groove, involves 4 stages

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12
Q

Stages of neurulation

A
  1. Elongation and folding of the neural plate
  2. Formation of mediolateral hinge point
  3. Formation of dorsolateral hinge point
  4. Closure of the neural tube
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13
Q

Process of elongation and folding of neural plate

A

Cell divisions in the anterior-posterior direction

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14
Q

Mediolateral hinge points

A

Cells at the midline, anchored to the notochord so hinge is formed and neural groove forms at the midline, neural folds elevate

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15
Q

Dorsolateral hinge points

A

Two, induced by and anchored to surface (epidermal) ectoderm, pull neural folds to the midline (convergence) while the ectoderm pushes

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16
Q

Closure of neural tube

A

Neural folds meet and adhere to each other at the midline, closing the neural tube

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17
Q

Hinge point mechanisms

A

Actin and myosin complexes apically constrict, along with increased cell divisions, leading to hinge

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18
Q

what is involved in the separation of the neural tube from the epidermis

A

differential adhesion, Neural tube express N-cadherins and epidermis express E-cadherins, SHH, TGF-beta, and BMP inhibition

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19
Q

neural tube closure defects

A

spina bifida (failure to close the posterior neuropore, exencephaly), anencephaly (failure to close anterior neuropore)

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20
Q

Process of secondary neurulation

A

occurs in the most posterior region of embryo, mesenchymal cells are patterned through morphogen gradients, cells condense into medullary cord (EMT), cavitation occurs, and individual cords combine to make longer single tube along a-p axis

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21
Q

morphogen gradients that pattern secondary neurulation

A

ectoderm cells express Sox (neural) and mesoderm activate Tbx6 (paraxial tissue)

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22
Q

medullary cord

A

cells go through EMT and condense into this in secondary neurulation

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23
Q

cavitation

A

hollowing out of medullary cord to make lumens (hollow spaces)

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24
Q

anterior patterning of the CNS

A

three primary vesicles formed, prosencephalon (forebrain), mesencephalon (midbrain), and rhombencephalon (hindbrain), starts before posterior neural tube has completed closure

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25
Q

rhomobomeres

A

small blocks of tissue that promote neuron differentiation, produced by rhombencephalon

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26
Q

differential induction of dorsal-ventral axis of neural tube

A

ventral nt forms motor neurons, dorsal nt forms sensory neurons, middle nt forms interneurons, TGF-beta gradient forms roof plate (BMP, dorsalin, and activin), SHH gradient forms floor plate, and combination of both TGF-b and SHH determine type of neuron formed

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27
Q

notochord role in DV axis of neural tube

A

potent inducer of ventral identity

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28
Q

what determines neuron identity

A

concentration or length of exposure to morphogen

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29
Q

contribution of neuromesodermal cells

A

in posterior, contribute to secondary neurulation, derived through FGF and Wbt maintained posterior epiblast, RA from anterior antagonizes FGF from posterior, some NMPs (neruomesoderm progenitors) are NT cell precursor, some become paraxial mesoderm

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30
Q

interaction of NMPs and signals

A

as NMPs leave tailbud, they interact with RA and become competent to respond to SHH and or BMPs, then they condense into neural tube with fates already determined. SHH responders become ventral, BMP responders become dorsal

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31
Q

placodes

A

derived through the thickening of non-neural ectoderm, sensory or non-sensory, formed and patterned through interactions with surrounding tissue

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32
Q

which placodes do not make sensory neurons

A

adenohypophyseal (pituitary) and lens

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33
Q

which signaling pathways induce cranial placodes

A

Wnt, BMP, FGF, SHH, and RA (retinoic acid), Wnt and BMP inhibited by FGF and cerberus

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34
Q

A-P axis signaling of placodes

A

SHH and RA, lead to general Six and Eya expression, give pre-placode identity

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35
Q

otic-epibranchial placode

A

responsible for hearing and balance, form in posterior region of cranial placodes (PPA, posterial placodal area), FGF from mesoderm induce PPA and are reinforced by neural plate

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36
Q

role of notch in otic placode

A

potentiates Wnt

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37
Q

Pharyngeal endoderm role otic-epibranchial placode

A

release BMPs, that induce epibranchial

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38
Q

otic pit

A

formed through proliferation (from signaling) and invagination of the placode

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39
Q

otic cup

A

formed through basal expansion and then apical constriction

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40
Q

otic vesicle

A

formed through the fusion of otic cup, similar to neural tube closure

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41
Q

ganglia

A

sensory neurons formed through delamination, necessary for morphogenesis, and eventually form cochleovestibular ganglion (CVG)

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42
Q

Role of Neural crest cells in morphogenesis of ear placode

A

acts as a physical guide for epibranchial ganglia

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43
Q

otocyst

A

precursor to the inner ear, must be further patterend and go through morphogenesis, folds and extends to create vestibular and cochlear structures

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44
Q

organ of corti

A

ear receptor organ formed through a complex series of differentiation, contains hair cells (sense sound) and supportive/structural cells

45
Q

Signal patterning of ear placode

A

A-p axis patterned by retinoic acid (RA), d-v axis by SHH and Wnt, and Medial-lateral access by Wnt and FGF

46
Q

Eye components

A

retina and retinal epithelium (neural) and non-neural lens placode

47
Q

lens placode

A

formed through reciprocal interactions between the optic vesicle and itself

48
Q

Anterior placode bias

A

bias to form lens, which triggers Pax6. Neural crest cells inhibit lens fate, but never contact lens due to the optic cup, which allows it to stay lens

49
Q

movements of eye placode morphogenesis

A

apical constriction, basal constriction, and filapodial contact (anchors lens to optic vesicle to allow for inductive signaling)

50
Q

optic cup layers

A

outer layer is non-nerual crest derived epithelium, inner contains retina, photoreceptors, and neurons that combine to create optic nerve, lens placode on outside of optic cup

51
Q

interaction of which structures forms the eye

A

lens placode and optic cup

52
Q

Signaling of lens placode (early gastrulation)

A

complex inductive events involving Noggin, Otx2, ET, Rx1, and Pax6. Starting in gastrulation, Noggin inhibits BMP and ET(first eye field gene) transcription factors, allowing for the expression of Otx2. Otx2 induces ET. Differential expression of Otx2 across the DV axis of the forebrain leads to a differential repression of Noggins ability to inhibit ET, allowing for ET and eye field (patterning done by neurulation)

53
Q

SHH role in eye development

A

inhibits Pax6 along the midline, separating the eye field into left and right

54
Q

is optic vesicle sufficient to produce lens?

A

no! lens and retina development require reciprocal signaling (FGFs, Wnt, and BMPs)

55
Q

signaling of lens placode (late gastrulation)

A

BMP and Wnt inhibitors and FGFs induce ectoderm to be come competent to form lens. neural tissue forms optic vesicle which grows and contacts lens placode, optic vesicle cells produce BMP, FGF, and delta (notch pathway) to instruct the cells to become lens placodes. Lens placode cells secrete FGFs that induce retina formation. Optic vesicle becomes optic cup and surrounds lens placode, which induces the differentiation of lens cells

56
Q

epidermis

A

skin, derived from the non-neural ectoderm and promoted by BMP signaling, largest singular organ, creates an impenetrable barrier around entire organism, and regenerative

57
Q

parts of the epidermis

A

dermal layers, hair follicles/feathers, and sebaceous(oil) and sweat glands

58
Q

role of BMPs in epidermis formation

A

block neural pathway with transcription factors and promote epidermis specification

59
Q

2 layers of epidermis

A

come from one layer, periderm (temporary) is outer layer, basal layer/stratum germinativum is the inner layer.

60
Q

basal layer

A

contains stem cells anchored to basal lamina

61
Q

what regulates cell divisions of the epidermis

A

dermis signaling pathways, FGFs anf TGFs. As cells divide notch signaling is activated (includes jagged ligand)

62
Q

notch signaling in epidermis leads to

A

older cells being pushed outwards, redicing proliferation, and inducing keratin expression, which leads to keratinocytes

63
Q

keratinocytes

A

differentiated epidermal cells that are bound tightly together and form the stratum corneum. They also stop transcription and metabolic activity

64
Q

when does epidermal development begin

A

after neural tube closure

65
Q

ectodermal appendages

A

structures formed on the epidermis like hair or feathers formed through interaction of the mesenchymal dermis and ectodermal epidermal layers, which forms epidermal placodes

66
Q

movement of ectodermal placodes relative to mesenchyme

A

in all cases, ectodermal placodes invaginate inwards towards mesenchyme cells

67
Q

inductive abilities of dermal mesenchyme

A

will induce formation of whichever appendage it forms in other types of epidermis

68
Q

signaling pathways involved in tooth formation

A

FGFs, Wnts, Shh, BMPs, and TGFs. BMP4 inhibits tooth ability, FGF8 promotes tooth ability

69
Q

enamel knot

A

signaling center of tooth, once formed it may use multiple signals to pattern surrounding tissue

70
Q

Role of Wnt/B-catenin

A

critical for establishing placodes for epidermal appendages

71
Q

role of FGFs in epidermal appendages

A

regulate migration of mesenchyme to form condensate (condensed mesenchyme) like enamel knot

72
Q

FGFs and their appendage

A

FGF8 is dental, FGF20 are hair follicles, and FGF10 are mammary glands. Loss of each results in loss or reduction of traits

73
Q

What patterns field and structure of appendages

A

other signaling interactions that limit boundaries, shape, cell identities

74
Q

appendages that contain stem cells to regenerate

A

teeth (except mammals), hair, skin, mammary

75
Q

mammary stem cell developmental events

A

initial development, puberty, and pregnancy

76
Q

ability of stem cells

A

to differentiate into all necessary cell types

77
Q

hair stem cells

A

follicle forms as other placodes with the invagination of epidermal layers and communication between dermal and epidermal layers, contains three stem cell types

78
Q

3 hair stem cell populations

A

hair shaft, sebaceous gland, and germinal layer of epidermis (keratinocytes). There is evidence that each type can be converted to others when needed for healing

79
Q

cycles of hair growth/regeneration

A

anagen is growth, telogen is rest, and catagen is regression

80
Q

what determines hair lengths

A

time spent in anagen (growth) stage

81
Q

region responsible for regeneration of hair

A

bulge region

82
Q

stem cell populations of bulge region

A

HFSC (hair shaft and sheath) and melanocytes (pigment)

83
Q

signaling of hair cycles

A

to activate growth, fibroblasts use Wnt and dermal papilla use FGFs and BMP inhibitors. for telogen/catagen stages, adipocytes and fibroblasts use BMPs

84
Q

HFSC bulge cell types

A

outer and inner, inner is progeny of outer and represses outer proliferation using BMP and FGFs

85
Q

hair shaft formation

A

occurs during anagen by growing around dermal papilla to form the root sheath

86
Q

Neural Crest Cells

A

ectoderm derived, vertebrate specific cells along the dorsal side of the Neural tube that eventually lead to PNS, endocrine systems, and connective tissues

87
Q

transience of neural crest cells

A

once cells migrate, neural crest disappears as the cells become their specialized forms. No adult population of NCCs

88
Q

types of nerual crest cells

A

Cranial NC (anterior), cardiac NC (ear to 3rd somite), trunk NC, and vagal NC

89
Q

Cranial NC

A

become face structures like cartilage, bones, and neurons as well as pharyngeal structures like thymus, teeth, ear and jaw bones

90
Q

cardiac NC

A

become melanocytes, neurons, connective tissues, cartilage, smooth muscle and connective tissues of the aorta

91
Q

trunk NC

A

Ventral become sensory neurons of the dorsal root ganglia, adrenal and aortic nerves. Dorsal become melanocytes

92
Q

potency of NCCs

A

multipotent, can generate different cell types with restricted specificity due to location of cells

93
Q

Equivalence of trunk and cranial NCCs

A

not equivalent, can both generate neurons, melanocytes, and glia but trunk NCCs cannot form bone/skeleton due to the expression of Hox genes in the trunk region

94
Q

evolution of trunk NCCs

A

Hox expression has led to the loss of skeletal ability, no hox expression in cranial NC so skeletal ability is present

95
Q

role of Hox gene expression in NCCs

A

give regionally limited identity

96
Q

fates of NCCs come from

A

interactions with different environments along migratory journey, receive different signaling patterns that specify cell fates

97
Q

Main signals of Neural crest cell fates/migration

A

Wnt and BMPs, FGFs, TGF-beta, and Fox and Sox

98
Q

Gene regulatory network general structure

A

Wnt, BMPs, and TGF-betas induce Msx1, Gbx2, and other ectodermal signals. Msx1 and Gbx2 induce Pax3/7 and dlx5/6, which are neural plate border specifiers and give border cells the ability to form both NCCs and dorsal NT cells. Pax3/7 and dlx5/6 induce neural crest specifiers FoxD3, Sox 9, and Snail (pre-migratory) as well as the migratory Sox10

99
Q

EMT

A

cells transitioning from epithelial to mesenchymal through downregulation of cadherins. BMPs activate Wnt genes, which allow for delamination due to expression of Snail2 and Foxd3

100
Q

cadherin groups

A

N-cadherins (NT), E-cadherins (ectoderm), and Cadherin6B (pre-migratory NC)

101
Q

Signals of NCC migration

A

BMP induces Wnt, Wnt induces Rac1 and RhoA, which lead to delamination event

102
Q

Rac and RhoA activity during EMT

A

increased RhoA and apical constriction along with activation of Rac on basal side, Rac regulate cytoskeleton producers filopodia and lamellipodia (responsible for migration), RhoA keeps Snail and Foxd active as well as organizing actin for migration

103
Q

Where do delaminating NCCs leave from the NT

A

basal surface, degradation of ECM around basal surface

104
Q

contact inhibition

A

mechanism in which when NCCs come in contact with each other, they stop and redirect movement, pushing opposite of the point of contact. This makes sure that NCCs maintain their identities and do not cross paths, which would result in them receiving different signals and differentiating into different cells than intended. Only occurs when NCCs touch each other, not when they touch other cells

105
Q

morphogenetic trigger for EMT

A

convergent extension during gastrulation is the first cue, as cells compress, they create a stiff structure for NCCs to migrate along

106
Q

role of Snail2 in EMT

A

repressive, limits boundaries of cadherins so that each type of cell can express specific ones (E,N and Cadherin6B)

107
Q

collective cell migration

A

migratory pattern in which leading edge cells pull the cells behind, which activate their cytoskeleton

108
Q

role of non-cannonical Wnt/PCP pathway in NCC migration

A

regulates intracellular actin cytoskeleton activity (RhoA and actin disassembly

109
Q

requirements for collective cell migration

A

cell-cell adhesion within the cluster, after leaving the NT, NCCs express N-cadherin to maintain grouping, contact inhibition keeps cells directional, and chemoattractant C3a secreted by NCCs keep group together

Dev Biology (5 decks)

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