Discussion Midterm #1 Flashcards
(25 cards)
How does Shh both express genes and supress genes?
Gradients of Shh signaling drive gtradients of transriptional responses
How does BMP signlaing with Organizer REgion and Dorsoventral Axis happen?
They are TWO different BMPs.
In Organizer region, we are in blasphio stage allowing epidermal cells to be generated.
Dorsoventral Axis will have Shh but also the BMP’s
For HOX gene expression, expression of what comes after is not dependent on what comes prior–> you can still get R4 expression without R2
Progressive HOX code expression supesedes previous HOX
If you move r4 caudally up the spinal cord (versus it’s initial rostral position) it will be expressed, but if you move it back it won’t, because what’s already there will supersede it.
EphA/EphrinA vs. EphB/EphrinB
A wants to avoid A and B wants to avoid B in regards to innervating the muscle
How do functional areas re-map after we disturb normal transcription factor gradients?
FGF8 gradients establish rostral-caudal patterning of the forebrain, defining Pax6 vs. Emx2 expression.
M = motor
V = visual
A = auditory
S = somatosensory
Neural proliferation relies on symmetric and asymmetric cell division?
P = neural progenitor/stem cell that can become neuronal or glial progenitor
N = neuronal progenitor
G = glial progenitor
T/F: Neurons develop mainly via asymmetric division.
True. This is when they prioritize their differentiations and their cell fate.
T/F: Glia cells develop mainly asymetric division.
FALSE. symmetric division. Glial progenitors duplicate every generation –> notice how there are no “dead ends” until the last generation. (Glia prioritize proliferation)
The number of generations that neurons and glia go through, is that a good predictor of it’s function?
Not necessarily– the classes of neurons are more dependent on that (where you originate can have a lot to do with waht your function ends up being)
T/F: Once neurons mature, proliferation stops
True
How do I become a neuronal progenitor or glial progenitor?
In the beginning, Delta/Notch levels are equal –> so signaling is equal
HOWEVER: list some imbalances or changes of fates
1) Delta signaling increases in the left cell, causing Notch signaling to increase in the right cell (may or may not go back to asymmetric division but is mostly random)
2) Cleaved intracellular Notch inhibits Delta transcription within the right cell
3) No Delta signaling from the right cell = no Notch signaling in the left cell
4) With no inhibition, Delta signaling is further enhanced in the left cell
If I’m GETTING no delta and expressing all delta: becomes neuronal precursor
Cell that is getting delta and notch is going nuclear and is no longer expressing their own delta, they’ll go glial
Fine-tuning Notch signaling levels defines oligodendrocytes vs. astrocytes (Phase 2)
Glial progenitor becomes ana strocyte –> iwht hgh notch signaling, a neural progenitor/stemm cell becoems a gliagl genitor
Notch can promote certain TF’s to give rise to astrocytes OR can inhibit certain sicnals to result in oligodendrocytes
Radial glia cells allow for the generation of neurons, and are highly involved in neuronal migration
Radial glia are scaffolding in the brain, allows fo eventual layering (move from center outward)
Neurons move from center OUTWARD
Cortical neurons climb radial glia to build the cortex from inside-out
Cortical neurons climb radial glia to build the cortex from inside-out
Layering is first on-first off– oldest cells that developed initially will be the most basal (rope climbing class analogy)
Newer neurons leapfrog” over older neurons andjump off radial glia de to extracellular matrix (ECM) proteins. So, newer neurons end up near the skull
NReelin mutation causes detatchment issues
Doublecortin mutant can lead to lissencephaly (smooth brain) phenotype (due to neuronal migration defects)
Cells of differnet ages exist in the same corticol layers– always comes back to microtubules
Nuclear migration relies on microtubules and motor proteins. Dcx stabilizes _____ (something I didn’t catch it)
Tangential migration likely evolved as a way to increase complexity in the brain – when we talk about the CNS, we often say where you can from (develop) will determine what you do in termns of neuronal development
Free migration (more in the peripheral nervous system (neural tube and stuff)
BMP signaling turns on transcription factors that express ECM proteases, enabling the cells to embark on their journey to the periphery. (Think o the proteases as machetes that cut . . . )
Final settling posiitons of neural crest cells include adrenal medulla, dorsal root ganglion, syjmpathetic gangion, melanocytes
Free migration applies much more to neural crest cells and peripheral nervous system
What are proteases? Catalytically active enzymes,
Cholinergic fate is determined by target-generated signals (cytokines)
Sympathetic neurons are initially speciied with a noradrenergic transmitter phenotye (this is the DEFAULT fate)
Signaling from muscle tarets is needed to promote motor neuron survival
Muscles initially secrete neurotrophic caftors globally, so all approaching neurons experience signaling
