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34 Cards in this Set

  • Front
  • Back
Neurulation
1) notochord -- > overlying ectoderm -- > neuroectoderm -- > neural plate
2) neural plate folds -- > neural tubes (neuralpores at both ends connect tube to amniotic cavity), some cells form neural crest cells
Notochord
Solid cylinder of mesoderm extending in midline of trilaminar disk from primitive node to prochordal plate
Functions:
1) induction of ectoderm to form neruoectoderm which forms neural plate
2) induces formation of vertebral body
3) forms nucleus pulposus of intervertebral disk
Anterior Neuropore
Anterior opening of neural tube
Closes day 25
Becomes Lamina Terminalis
Failure to close: upper neural tube defects ex. anencephaly
Posterior Neuropore
Posterior opening of neural tube
Closes day 27
Failure to close: spina bifida, myeloschisis
Neural Crest Cells
From lateral border of neural plate
Mediated by BMP-4 and BMP-7
Differentiation by expression of slug (zinc-finger transcription factor)
Break away from neuroepithelium migrate to ECM -- > mesenchymal cells
Prolific migration throughout embryo
Promoters of cell migration
Fibronectin
Laminin
Type IV collagen
Proteins that restrict cell migration
Chondroitin sulfate rich proteoglycans
Cells derived from Neural Crest
1) Ganglia
2) Schwann Cells
3) Odontoblasts (dentin of teeth)
4) Pia & Arachnoid Mater
5) Chromaffin cells of adrenal medulla
6) parafollicular (C ) cells of thyroid
7) melanocytes
8) aorticopulmonary septum
9) pharyngeal arch skeletal components
10) bones of neurocranium
Cells derived from Neuroectoderm
1) neurons of CNS
2) Eye cells (retina, iris epithelium, cilliary body epithelium, optic nerve, optic chiasm, optic tract, dilator and sphincter pupillae muscles
3) astrocytes, oligodendrocytes, ependymocytes, tancytes, choroid plexus cells
4) neurohypophysis
5) pineal gland
Neural Tube Lumen
Ventricular system of brain
Central Canal of spinal cord
BMP-4
Bone morphogenic Protein-4
Inhibited by noggin, chordin, follistatin --> induction of neural plate, formation of notochord, and paraxial mesoderm
In mesoderm and ectoderm of gastrula
Ectoderm --> epidermis
Mesoderm  intermediate and lateral plate mesoderm
Present in: organizer (primitive node) notochord, prechordal mesoderm
Placodes
- Localized thickenings of surface ectoderm
- Give rise to cells that migrate into mesoderm -- > sensory receptive organs of CN1 and CN 8 and lens of eye
- lens placode from optic vesicles
- olfactory placode -- > neurosensory cells -- > Olfactory nerve (CN1) -- > olfactory bulbs
- otic placodes -- > otic vesicle
1) utricle, semicircular ducts and vestibular ganglion of CN 8
2) Saccule, cochlear duct (organ of Corti), spiral ganglion of CN8
3) vestibulocochlear nerve (abducens)
Brain vesicles
primary vesicles
1) proencephelon (forebrain)
Telencephelon -- > cerebral hemispheres, caudate, putamen, amygdalaoid claustrum, lamina terminalis, olfactory bulbs, hippocampus
Diencephalon -- > epithalamus, subthalamus, thalamus, hypothalamus, mamillary bodies, neurohypophysis, pineal gland, globus pallidus, retina, iris, cilliary body, optic nerve, optic chiasm, optic tract
2) mesencephelon
midbrain
3) rhombencephelon (hindbrain)
Metencephalon -- > pons, cerebellum
Mylencephalon -- > medulla
Flexures
1) cephalic Flexure between proencephelon and rhombencephelon
2) cervical Flexure between rhomencephelon and future spinal cord

Primary at 4 weeks, secondary at 6 weeks
Glioblasts
formed afer neuroblasts
exception: radial glial cells
form: astroglia, radial glial cells, oligodendroctyes, ependymocytes, tancytes, choroid plexus cells, microglia (hortega cells)
astrocytes
project foot processes to capillaries contribute to BBB
metabolism of NT
buffer teh K+ of CNS
form glial scars in damaged areas
glial fibrillary acidic protein (GFGAP)
glutamine synthease
Pluripotent
Cells not have a fixed development, can develop into any type, but not sufficient to generate a whole organism on their own
Totipotent
Cell capable of generating a whole organism
Problems with Cloning from stem cells
Genome wide demethylation doesn’t occur as efficiently in somatic cell nucleus as it does in germ cells
Cord Blood stem cells
Advantages
-their harvesting is not ethically controversial
-cord blood stem cells trigger little immune response in the recipient
-they have much less of a tendency to form tumors when injected into animals compared to embryonic stem cell

Disadvantages
-they cannot become every cell type (however they are particularly good at forming blood cells; a very good alternative to bone marrow transplants)
-small number in cord blood
Cell differentiation
Once committed, stays that way (arm doesn’t turn into a leg later)
Cells retain “memory” of ancestral signals
Once gene is turned on or off, it says on or off
How is a gene turned on?
Activate the transcription factor of desired gene, and it will actively transcribe for life of cell, also keeps everything else the transcription factor affects downstream turned “on”
How is a gene turned off?
Methylation of DNA
At fertilization, genome-wide wave of demethylation which allows transcription of every gene
Why embryos from artificially induced from somatic cells have severe developmental defects (Dolly the sheep)
Signals and Receptors “off “ and “on” signals
1) transmembrane molecules used for cell adhesion and cell signaling
2) gene regulatory proteins
Point of sperm entry
May determine which cells form embryoblast vs trophoblast in later cell divisions
The (x) cell divides slightly ahead of the other cell,
(fact) most often, descendents of the (x) cell form the embryoblast, descendents of the other cell form the trophoblast
Response of cell to particular signaling molecule
Dependent of combination of signals cell receiving at the time
Previous history of cell, what’s already turned on or off (time)
Amount of signal the cell is receiving (distance from origin of signal)
Sonic Hedgehog (SHH)
Dependent of combination of signals cell receiving at the time
Previous history of cell, what’s already turned on or off (time)
Amount of signal the cell is receiving (distance from origin of signal)
Sonic Hedgehog (SHH)
Secreted protein, modified by cholesterol moiety (trafficking and signalling)
Defects in cholesterol metabolism -- > Autosomal recessive Smith-Lemli-Opitz syndrome
Receptor
Patched, multipass transmembrane protein
Intracell: SHH/Patched/ 3 Gli family of TF
SHH patterning found
-somite development
-formation of anterior-posterior body axis
- developing limb bud
- developing brain
-hair follicle development
-tooth development
TGF-β
BMP, nodal and TFG-β in same family
Chordin (Sog) and Noggin inhibit.modulate extracellularly
Receptors: single pass R with Serine/Threonine kinase domain
2nd messenger: SMAD associate with other gene regulatory proteins and bind to DNA
Activities:
L- R symmetry
BMP-4 ventralization of mesoderm
Nodal- establishment of primitive streak
Factors controlling Axis formation
FGF proximal - distal
Wnt7a dorsal – ventral
SHH anterior – posterior
Homeobox Gene
Code for transcription factors involved in embryo development
Homeodomain binds sequence specific DNA motifs
Can activate or repress down stream effectors
Hox Genes
Helix turn helix TF
Clustered on chromosomes
Anterior – posterior patterning
Turn on in sequence
Highly conserved
Control segment identity
Retinoic acid -- > expression -- > defects
How do hox genes work?
Each one switched on in particular place along body
Get different combination of signals
Within segment get integrated at enhancer of target genes -- > localized activation
Regulate morphogenesis of specifc organs by activating networks of TF and s
signalling molecules
once developmental pathway is turned on by hox, never turned off
polycomb and Trithorax -- > DNA binding proteins stamp the chromatin of Hox complex with the record of embryonic signals
continuously synthesized and continuously bound to off or on position
Cadherins
Single-pass transmembrane glycoprotein
Need Ca++ to bind to another cadherins
Link by homophillic binding (desmosomes)
Keep like cells stuck together,
compaction of 8 cell embryo (e-cadherin)
condensation of mesoderm
formation of neural tube
Metastasis in tumor cells occurs with loss of cadherin
Integrins
Transmembrane R for ECM molecules
Can recognize many different ECM
Cell migration and sending signals