head/neck development Flashcards

1
Q

morphogenesis is?

A

Coordinated and Generative

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2
Q

what codes proteins

A

Genes (DNA) encode RNA and proteins

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3
Q

what defines cell ID

A

The complement of RNA & protein produced defines the identity of each cell – its appearance and how it behaves.

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4
Q

cells and their surroundings relation

A

Cells receive and process information from their surroundings – extracellular matrix, secreted molecules (growth factors) from other cells, hormones, contact with other cells (tension), nutrients, oxygen levels, etc.
•These in turn modify the genes expressed, thus allowing the cell to adapt to its situation and take on new properties / behaviors.

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5
Q

determining phenotype

A

ØGenes (genome) provide the blueprint that ensures we all have a maxilla and mandible and an integrated oronasal cavity, etc. But gene mutation and differences in these non-genetic ‘instructions’ determines everything about our phenotype.

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6
Q

Epithelia vs mesenchyme

A

epithelia: bound cells, organized
mesenchyme: non-bound/ mobile cells

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7
Q

3 germ layers names and related to?

A

Ectoderm, mesoderm, endoderm

These are terms related to the embryonic origin of cells!

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8
Q

All aspects of the craniofacial complex are defined by what axeses?

A

3 axes:
•Left-right
•Dorsal-ventral
•Anterior-posterior

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9
Q

Clinical treatments always consider:

A

•form (eg. tooth shape, spacing, number, cusp pattern), and
•symmetry
because they are critical for function and esthetics.

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10
Q

Dorsal-ventral axis apparent by what stage?

A

•apparent by blastocyst stage

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11
Q

compaction

A

occurs with the morula to form trophectoderm and blastocyst/ ICM
ICM will form embryo (embryonic stem cells)

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12
Q

implantation

A

allows blastocyst to form more distinct layers of cells

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13
Q

what has formed by week 3?

A

all three germ layers

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14
Q

The A-P and L-R Axes determined by and when?

A

Anterior-posterior (A-P) axis [head-tail] and left-right (L-R) axis determined at start of week 3, with appearance of the primitive streak

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15
Q

primitive streak beginning

A

forms on dorsal side of bilaminar discs at midline and begins on the posterior end of the embyro
epiblastic cells will converge to form this

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16
Q

streak appearance defines?

A

Appearance defines A-P and L-R axes

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17
Q

elongation of streak

A

Furrow progressively elongates along midline

•through process of convergent extension

18
Q

Formation of 2nd& 3rd Germ Layer

how can cells be mobile?

A

Cells of the epiblast (layer 1) migrate through primitive
streak to form mesoderm & embryonic (gut) endoderm, called gastrulation

Through the process of epithelial to mesenchyme transformation (EMT) to form mesoderm, mesenchymal cells are mobile

Movement of epiblast (ectoderm) to form embryonic endoderm – both are epithelia

19
Q

Disproportionate growth of the germ layers?

A

> Greater proliferation of epiblast (ectoderm) because it also generates all mesoderm and embryonic endoderm.

20
Q

migration of proliferated mesoderm

A
Generated (proliferating) mesoderm migrates 
toward anterior (head) end
21
Q

The Node, used for?

A

Anterior-most end (dorsal side) of primitive streak is unique in both appearance and function
Essential for:
•patterning and induction of mesoderm and endoderm
•establishment of the left-right symmetry

22
Q

Factors secreted by cells of the Node induce?

A

Factors secreted by cells of the Node induce anteriorly migrating mesoderm to form:
•the prechordal plate and notochord

23
Q

prechrodal plate

A
  • most anterior region of mesoderm

* provides the signals for induction of head structures

24
Q

The notochord

A
  • transient epithelial-like rod structure along the midline.

* provides the signals for induction of the neural plate

25
Q

does the node induce body aixs? how so?
creates what symmetry in emryo? how does it do this?\
what will this symmetry result in?

A

the Node induces the body axis: > Induce and specify the fate of the mesoderm as it is formed
•Creation of asymmetry in symmetrical embryo
•First establishes molecular asymmetry
•Conversion into asymmetric organogenesis

26
Q

Establishing Molecular Asymmetry

A

Asymmetric expression of morphogenetic factors around Node
> initiates cascade of gene expression to promote asymmetric specialisation / commitment of mesoderm for organs

due to the rotational beat of nodal cells cilium (only a few hrs): generates leftward flow, resulting in asymmetric distribution of morphogens / growth factors

27
Q

Organ asymmetry, mutations?

A

Reproducible morphological & functional asymmetries in
nearly all internal organs.
» Evolutionarily conserved mechanism in vertebrates
» cilia function affected; gene expression around Node changes
1 in 8500-10000 people with situs inversus (normal health)
> cf. partial situs which can be deleterious

28
Q

Neurulation [Neural Tube Formation]
steps
precursor to?
patterning of neurons?

A
  • **precursor to brain & spinal cord
    1. Factors from the mesoderm/ notochord induce thickening of overlying ectoderm&raquo_space; neural plate
    2. Signals from notochord induce a ‘hinge’ point (floor plate) to help drive folding
    3. D-V patterning of neurons begins
29
Q

Anterior (head) Specification
different regions of the brain?
morphological difference of the anterior-most region of the neural tube reflects?
where are the cues from?

A

The morphological difference of the anterior-most region of the neural tube reflects unique underlying cellular identities and thus different inductive cues (secreted factors): produce different regions of the brain
cues come from notochord, Anterior visceral endoderm (in direct contact with ectoderm), and Pre-chordal plate

30
Q

Neural Tube Closure, anterior end maturity and directionality

A

Advanced maturity of anterior end > expanded neural plate&raquo_space; future brain
Closure of neural tube proceeds anteriorly and posteriorly from mid-region

31
Q

head and neck comprise how much of embryo by wk 3?

A

1/2 (expanded nn plate)

32
Q

Defects in Neural Tube Closure

A

variety are possible, spina bifia common and viable

others may be lethal

33
Q

Cephalization (Head Formation)

hinge point?

A

The oropharyngeal membrane serves as the hinge point during cephalization, where endo and ecto are in direct contact
neural plate will fold downward/in to form the anterior neuropore, meso will give rise to heart, etc. and the mouth will begin to form (stomodeum), lateral folding is occurring as well during this
during this time the induction of head/facial structures is occurring as well

34
Q

Embryonic Folding occurs during?
concomitant formation with?
specialization of what from this?

A

Folding of whole embryo while cephalization occurs
•Concomitant with formation of pharyngeal arches (> face & neck)
•Foregut and hindgut specialization occurs

35
Q
NCC
stemness?
origin? 
migration pattern?
become what?
A

a unique population of (pluripotent) stem-like cells originating at the ‘crest’ of the enclosing neural tube between ectoderm and nn tube
•Migrate ‘ventro-laterally’ to populate the ventral side of the embryo
•Differentiate into a wide variety of cell types / tissues

36
Q

how NCC are generated with tobe folding/closure

why would this be important?

A

•NCC generated by process of epithelial-mesenchymal
transformation (EMT) that is analogous to that generating the
third germ layer (mesoderm)
ALLOWS THESE CELLS TO BE MOBILE

37
Q

Cranial Neural Crest Cells
migration of these drives?
potential?
contribute to what structures?

A
  • CNCC migration drives outgrowth of the primitive tissue masses that will form much of the head and neck (branchial arches)
  • Unique in developmental potential (distinct from other neural crest cells) “second wave” of development (vertebrate-specific)

> Major contributor to craniofacial structure, and specifically to mineralized tissues of the oral region

38
Q

CNCC Derivatives

A

conn tissue, skeleton and mm of the craniofacial region

39
Q

Rhombomeres & Cranial Patterning
how many rhomobmeres?
regions of brain involved?
rhombomeres define what?

A
  • CNCC fate determined prior to departure from neural tube, originate at rhombomeres > ie. they have “positional identities”
  • Multiple visible constrictions in neural tube=rhombomeres 1 - 8, the diencephalon and anterior mesencephalon
  • define distinct populations of CNCC and their route of migration into early facial tissue.
40
Q

Directed CNCC Migration, manipulation?
reporducable?
defined by what germ layer?

A

•Reproducible paths of migration > defined by mesoderm

if CNCC from r1 placed in another r it may move into new branchail arch but will form same structure it was meant to be

41
Q

Coordinated Morphogenesis, what allows this?

A

All layers are differentiating and forming structures at the same times in development i.e: ectoderm, meso, branchail arches all working at same time
Early molecular patterning (est. during gastrulation) enables later coordinated tissue morphogenesis.

42
Q

Changing Cell Fates/phenotypes, what factors could play a role?

A

•Embryogenesis is a ‘generative’ process (not descriptive), many factors can play a role

Malformation and normal phenotypic variation can result from:

  • single changes in gene sequence
  • combinations of ‘normal’ gene variants
  • changes in the ‘environment’ to which cells respond