Bio 325 Final Exam

Front 1

Ectoderm differentiates into what three tissues?

Back 1

Surface Ectoderm-epithelial
Nueral crest-mesenchyme
Neural tube-epithelial

Front 2

Epithelial versus. Mesenchymal

Back 2

Base Membrane
Apical Polarity
Adhesion molecules

Front 3

Surface Ectoderm Derivations

Back 3

Epidermis
Hair
Nails
Sebaceous glands
Olfactory epithelium
Mouth Epithelium
Lens, Cornea

Front 4

Nueral Crest Derivations

Back 4

PNS
Adrenal Medula
Melanoyte-skin pigment cell(melanin)
Facial Cartilage
Dentine of Teeth

Front 5

Nueral Tube Derivations

Back 5

Brain
Neural Pituitary
Spinal cord
Motor Neurons
Retina

Front 6

Telon Cephalon

Back 6

This comes from the bulge at the head, it helps contribute to the retina

Front 7

Neural Folds

Back 7

Two ridges that develop form the primitive streak, these later converge to form the neural tube

Front 8

Neural Plate

Back 8

Where the primitive streak and Hensen node form during gastrulation

Front 9

Hensen Node

Back 9

Mesoderm flow through this hole and migrate to areas where they differentiate

Front 10

What are the four stages of primary Neuralation?

Back 10

Shaping
folding elevation
Convergence
Closure

Front 11

Shaping (P.N.)

Back 11

Cells in the middle of the plate begin to elongate through convergent extension, due to BMP inhibitors, like noggin, follinstatin and chordin, expressed from the mesoderm below it. Outer rims of neural Plate have small amounts of BMP Expression, less elongation

Front 12

Folding and Elevation(P.N.)

Back 12

neural groove begins to form with trapezoidal like cells on long the slanted edges . BMP inhibitors are longer expressed on elevated cells

Front 13

Convergence(P.N.)

Back 13

Nueral folds begin to come together forming the nueral tube
Note Lateral and medial hinges, these hinges have attachments which anchor them; this helps when the ectoderm pushes to fore a tube structure

Front 14

What allows the neural folds and related features to bend?

Back 14

Actin cytoskeleton

Front 15

Closure(P.N.)

Back 15

Neural tube formed, epidermis on top and nueral crest precursors

Front 16

Cadherin importance related to epidermis and neural tissue

Back 16

N-cadherin (Neural) and E-Cadherin (epidermis) are expressed due to BMP expression or lak ther of and help to differentiate the the tissues

Front 17

What cells are the precursors of neural crest cells?

Back 17

tips of neural folds, with a little BMP they can remove Cadherins and migrate

Front 18

Where does the brain start to form and how?

Back 18

Anterior part of the neural tube
fluid fills up the lumen like a water balloon. Lumen more is closed forcing the liquid to stay in the anterior region

Front 19

Failure of Nueral tube closing

Back 19

Birth defects, spina bifada and anencephaly, exposes neural tissue to amniotic fluid, which has toxins causing a lot of cell death

Front 20

Importance of folic acid in development

Back 20

folic acid reduces neural tube defects, helps with closure

Front 21

What would happen if you knocked down E-Cad or N-Cad in nueral formation

Back 21

N-cad KD neural tube doesn't raise much and the convergence doesn't happen,

Front 22

What happens when N-Cad is overexpressed in Neural Plate?

Back 22

Convergence is irregular

Front 23

What is a morpholino?

Back 23

single stranded oligo-nucelotide, prevent specific mRNA from being translated

Front 24

Mammilian Nerual Tube Closure Sequence

Back 24

1) upper back
2) Cranium(Anencephaly)
3) Front of face
4) Back of Head
5) Lower back(Spina Bifada majority)

Front 25

What happens to neural development if pax3 is knocked out? Alternatives?

Back 25

Closure does not happen in site 2.
Adding Folic acid or Thymine causes complete closure

Front 26

how does folic acid help neural tube closure?

Back 26

Biochemical pathways shows it plays a role in pyramidine(Nucletotides T and C) formation, which helps with cell Division

Front 27

Methionine

Back 27

Blocks pyramidine formation and increases chances of neural tube defects

Front 28

Wardenburg Syndrome

Back 28

white hair streaks, from dorsal neural tube defects, pax3 mutations are cause for some cases. This causes neural crest defects.

Front 29

Neural Crest is responsible for what?

Back 29

pigmentation
Peripheral Nervous System(in part)

Front 30

Hex and Goosecoid transcription factors give rise to what during gastrulation?

Back 30

DKK, Frzb, Cerberus, Lefty, Noggin, Chordin, Follistatin

These are BMP, WNT and Nodal inhibitors

Front 31

Introducing BMP, Nodal and WNt Inhibitors during gastrulation in areas where it is not normally expressed can cause what?

Back 31

Another Head to form

Front 32

BMP, Nodal and Wnt inhibitors give rise to what transcription factors in regards to nueral development?

Back 32

Hesx1, Lim1, Bf1, and Otx2

Front 33

Otx2 expression when and where?

Back 33

expressed throughout anterior neural plate long before primary neuraltion. labeling forebrain and midbrain cells

Front 34

Bf1 expression

Back 34

Brain Factor 1, expressed in most anterior region of neural plate, most anterior neural cells

Front 35

Krox20 expression

Back 35

posterior part of the brain
labeling hindbrain

Front 36

DVE and AVE, location and gene expression and derivatives

Back 36

Distal Visceral Endoderm is located posterior portion of the embryo and expresses Hex, Cer, and DKK. These cell migrate taking up an entire side of the embryo, AVE while still expressing these genes. Brain will form near here and the primitive streak begins to form on the opposite side of the embryo

Front 37

What happens when you KO Otx2, Lim1 or Hesx1?

Back 37

Lose anterior part of brain/ loss of head structures

Front 38

K.O, Chordin

Back 38

Ear is missing

Front 39

K.O. chordin and Noggin

Back 39

Cyclops deformed fetus

Front 40

posterior gastrulation signals: mesoendoderm to ectoderm

Back 40

wnt, fgf, and ra secreted by mesendoderm help activate cdx2 im ectoderm which turn activates hox genes, specifying importance in differentiation

Front 41

how does decreasing or increasing wnt signaling affect specification?

Back 41

wnt overexpressed: bf1 lost, otx2 area reduced and krox 20 remains the same, ultimately posterioirzes the embryo.
limited expression causes bf1 and otx2 the greatly increase and krx 20 is greatly reduces which ultimately anterioizes the embryo

Front 42

what happens when Ra s overexpressed?

Back 42

duplication of posterior axis,

Front 43

wnt3a k.o.

Back 43

posterior developments is changed dramatically

Front 44

What allows hinge points to change shape? how do we know?

Back 44

The cytoskeleton of the cell is responsible.
Experiments:
Colchine(Microtubule polymerization inhibitor) Addition: stops cells from elongating
Cytochalasin B(Microfilament formation inhibitor) Apical Constriction doesn't occur; ells don't go into trapezoid form but stay square

Front 45

When does AVE release BMP inhibitors? is it throughout embryo development?

Back 45

The AVE starts releasing hex before gastrulation, after gastrulation the mesendoderm starts expressing the genes, it takes the lace of the AVE in this process

Front 46

How are Hox Genes activated?

Back 46

Concentration of cdx2, high levels required

Front 47

How do HOX genes affect DNA?

Back 47

Bind to enhancers thereby activating targets in a regional and time specific manner

Front 48

What happens in Drosopoholia when there's mutation in ulrtabithorax gene?

Back 48

Two sets of wings are formed, skipping a segment known as thorax 3, which forms small buds called halteres. Ultrabithorax is responsible for distinguishing T2 and T3 cells

Front 49

Otx2, Engrailed(En) and Krox 20 determine what?

Back 49

Forebrain, (Prosencephalon), bulge
Midbrain(Mesencephalon)
Hindbrain(Rhombencephalon) Rhombomeres
Chemicals expressed prior to neural tube formation

Front 50

How does the mesoderm influence the ectoderm in nueral development?

Back 50

The mesoderm releases bmp inhibitors(Noggin, chordin, follistatin) causing the middle of the ectoderm layer to become neural tissue/neural plate. the rest of it has gradient of BMP where the ectoderm is fated to epidermis and the areas where little BMP is exrpessed become nueral crest cells. Anterior mesoderm expresses DKK and Cerb which specify brain region.
South of the brain region there is a gradient of wnt, fgf and RA which help induce the spinal cord

Front 51

Holoprosencephaly and cyclopia

Back 51

hemispheres don't divide,
K.O. of chordin and noggin can cause this
Shh mutation also causes this.
Note: nose and eye prescursors start with nose on top and eye on bottom, further in development they switch around. In this mutation, you can see the eye is below the nose. shh may be responsible for separting the two hemispheres. its turned on by bmp inhibitors

Front 52

Rx1 and Pax6

Back 52

Expressed centrally to otx2 expression and specify the eye field

Front 53

Otx2 expression in relation to eyefield: what tissues express it?

Back 53

otx2 is expressed in a horizaontal region in the ectoderm. this later splits into the nueral plate, neural crest precursors and epidermis. The eyefield which has otx2 as well the smaller region of rx1 and pax6, covers all these region prior to when they form, which is why the eye region pulls from all three tissue sources

Front 54

eye derivates of epidermis and neural plate?

Back 54

neural plate=retina
epidermis=lens and cornea

Front 55

Noggin and otx2 pathway

Back 55

Noggin suppresses ET as well as, in combination with DKK and Cerb, activate Otx2. Otx2 will then stop noggin from repressing ET which will then go on to activate rx1. rx1 actiavtes pax6 as well as repress otx2. This negative feedback loop system is in place to get the right amount of transcription factors. Pax6 is responsible for eye tissue differentiation

Front 56

What happens if rx1 is knocked out?

Back 56

eye will not form,

Front 57

What happens when pax6 is knocked out?

Back 57

eye is missing and part of face

Front 58

What happens when your heterozygous for pax6 mutation

Back 58

anridia, iris is missing

Front 59

cave dwelling and wild type differences of mexican tetra(fish?)?

Back 59

cave dwellers don't have eyes, the reason for this is that the ssh region of expression in neural plate is broader then wildtype and supresses eye development. Experiment detected ptc2 and pax2, since they are dependent on ssh expression. Optic cups don't form

Front 60

What does differentiation of the eye begin with?

Back 60

Optical vessicles begin to form in the neural tube, diencephalon

Front 61

How do the opitcal vessicles induce the ectoderm?

Back 61

They grow and come in contact with it, causing the immediate area to thicken, creating a lens placode.
Opitical vessical does notch delta signaling and releases BMP 4 to induce these changes

Front 62

Bmp4 and Delta-Notch Signaling activate which transcription factors?

Back 62

Sox2 and Lens1

Front 63

Lens 1 requires what enahcers to be transcribed?

Back 63

otx2 and Notch

Front 64

What does sox2 do in eye differentiation?

Back 64

it works in conjunction with pax6 to activate crystallin genes needed for lens differentiation

Front 65

What does lens1 do in eye differentiation?

Back 65

encodes a transcription factor needed for cell proliferation and subsequent closure of the lens vesicle

Front 66

Structurally, what is happening as the lens placode is forming?

Back 66

a Lens vesicle forms from the overlying ectoderm and invaginates towards the optical vessicle which collapses into the optic cup