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Terms in this set (58)
mosaic theory of epigenesis
after a few cell divisions the embryo would be like a mosaic, each cell playing its own unique part in the entire design
having the capacity to develop in one of several ways
therefore early blastomeres were able to compensate for loss of other cells
cell division results in
a hollow ball of cells made up of blastomeres
central cavity is called a blastocoel
Invagination of the blastosphere
Final result = generation of 3 layers of embryo
what cells become mesoderm?
Cells on surface of embryo
move actively into the center of the blastula
point of initiation, a small invagination on the surface of the blastula
invaginating cells themselves that form the gut and major organs
migrating cells (during gastrulation) that form muscle, skeleton and connective tissue
led by the dorsal lip of the blastopore
induces the overlying ectoderm to become neural tissue
outer layer that forms the skin and the nervous system
from animal cap
when is the fate of neural tissue determined?
Experiments with the dorsal lips of the blastopore
This became known as "Spemann's organizer"
The only self-differentiating (causes its own differentiation) region in the early gastrula
In other words, it determines it's own fate!
Remove this region - no neural ectoderm forms
what happens if you remove Spemann's organizer?
no neural ectoderm forms
the process by which one embryonic region interacts with a second to cause the latter to differentiate in a specific direction
the dorsal lip of the blastopore
this area induces the formation of neural ectoderm
what happens if you transplant Spemann organizer?
A second neural axis was induced by the transplanted tissue
New body axis had cells from host and from transplant
So it couldn't be made from only the host or only the donor
Conclusion: dorsal lip cells could "organize" the host cells to form a new body axis
Phenomenon of "self determination" - no other part of embryo can determine its fate
Was this genetically or environmentally influenced?
animal pole as a whole before gastrulation would become
animal pole before gastrulation when dissociated (low density) would become
what is the normal fate of ectoderm?
The normal fate for the ectoderm is to become neural.
During development, this is blocked in parts of the ectoderm by a cell-to-cell interaction that inhibits neural fate and promotes epidermis.
exposure to UV light
causes damage that prevents development of neural tissue - this embryo only has a ventral side
exposure to lithium
there is "extra" neural tissue formed and the dorsal part becomes very large
Secreted protein expressed in the organizer
Over-expression in ventral part of embryo causes a secondary axis to form
known to inhibit activin (member of TGF-beta family of proteins)
Had been studying the mechanism of activin action on mesoderm induction, found that interfering with signaling disrupted normal mesoderm dev AND induced cells of animal cap to develop as neurons
this is the signaling that shifts "fate" to epidermis (through complicated transcription factor signaling pathway that you don't have to know!)
what induces overlying ectoderm to form neural ectoderm?
Underlying mesodermal cells in the "organizer" region
is neural fate actively promoted?
default fate for the entire ectoderm is to be neural
what blocks the default fate?
Default is normally blocked by secretion of neural inhibitors (the BMP family of proteins)
what does the organizer release?
substances (noggin, follistatin, chordin) that neutralize the inhibitors and induce development of neural tissue
Formation of the neural plate
Primary neurulation - folding of the neural plate to produce the neural tube
Secondary neurulation - neural tube "seals" up from top (anterior) to bottom (posterior)
think of it as a "zipping down" to close the neural tube.
The neural tube will give rise to all of the neurons of the brain and spinal cord
distinct group of cells at point of fusion of the neural tube margins
failure of neural tube to close properly
also results in neurological complications which impact:
what do neural crest cells become?
what do mesenchymal cells generate?
all peripheral neurons and glia, plus some other body tissue cells
adrenal gland cells, pigment cells, cartilage, bones in head
what do somites give rise to?
body segments (vertebral bones, ribs, muscle, etc.), from mesoderm
Four distinct migratory paths for neural crest-derived mesenchymal cells:
1,2 autonomic (visceral) ganglia neurons
3 adrenal gland neurosecretory cells (chromaffin cells)
4 non-neural cells (pigment cells, cartilage, some bone)
How does each segment become different?
Homeobox (Hox) genes
Homeobox (Hox) genes
Encode Hox proteins - family of transcription factors containing a "homeodomain"
Homeodomain is a specific DNA-binding domain
Encoded by DNA sequence known as "homeobox"
for establishing A-P axis
One of first signaling molecules to be implicated as Hox regulator
Regulates gene expression by binding to "RARE" sites on DNA
RA preferentially expressed in posterior region of embryo
From the mesoderm lying immediately adjacent to neural tube
Diffuses into hindbrain to activate Hox gene expression
retinoic acid treatment - where are the defects?
Xenopus embryos treated with RA have defects in the anterior parts of the ns
Higher concentrations of RA leads to failure to develop head structures and inhibition of anterior Hox gene expression
"activator" initial signal provided by the organizer to cause ectodermal cells to develop anterior characteristics
E.g. Noggin, chordin, produce primarily anterior brain structures
"transformer" a second signal required to transform a portion of neural tissue into hindbrain and spinal cord
3 molecular pathways implicated as contributing to the "transformer" activity
RA (retinoic acid) - remember, this can posteriorize embryos and responsible for the patterning of hindbrain Hox gene expression
Dorsal - ventral polarity in the neural tube
Different types of neurons derived from specific positions of the neural tube and reside in specific positions of the adult brain and spinal cord
Motor neurons = ventral horns
Sensory neurons = dorsal horns
most dorsal part of neural tube
most ventral part of neural tube
fissure between the dorsal and ventral parts of neural tube
how does polarity arise?
from interactions with surrounding non-neural tissue
necessary and sufficient for v/d polarity
Self-renewing, multipotent cell
can divide many times, make many cell types
Self-renewing and multipotent, but can only divide a limited number of times and make certain cell types (in the brain, neurons and glia)
where are stem and progenitor cells found?
ventricular zone (VZ) (adjacent to the hollow center of neural tube - which will form the ventricles) - these will divide and differentiate to become the neurons of the brain and spinal cord
interkinetic nuclear migration
: the nuclei of the progenitor cells undergo a constant up-and-down migration through the stages of the cell cycle.
refers to how many cells are exiting the cell cycle
They are no longer making daughter cells and will differentiate into their final cell type
low Q fraction
cells reproducing and making lots of daughter cells
high Q fraction
cells leaving cell cycle and differentiating
what does Increasing the length of the expansion phase result in?
more progenitors and oversized brain!
a developmental disorder characterized by small brain size at birth
Mutations that cause progenitors to make neurogenic divisions too early, decrease the length of the expansion phase and result in too few neurons being produced.
has ataxia and tremor
In the cerebellar cortex later generated neurons fail to migrate past those generated earlier, leads to an outside-in organization of the cerebral cortex
Defective molecule is Reelin - large glycoprotein, expressed by the most superficial neurons of the cortex (Cajal-Retzius cells) and is thought to "attract" newly born neurons to migrate in that direction
When Reelin is mutated it no longer attracts newly born neurons to migrate towards the surface and they stay deep in the cortex
This disorganization in the cerebellum causes ataxia
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