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BMS 249 - Developmental Neurobiology > Anterior vs posterior > Flashcards

Anterior vs posterior Flashcards

1
Q

What are the anterior fates of the embryo?

A

The forebrain

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2
Q

What are the posterior fates of the embryo?

A

The hindbrain and spinal chord

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3
Q

What 3 components is the nervous system made of?

A

1) CNS
2) PNS
3) Enteric nervous system

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4
Q

What is the CNS comprised of?

A
  • Brain
  • Spinal chord
  • Specialised sensory derivatives derived from forebrain tissue (eg. retina, olfactory, taste receptors)
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5
Q

Where are all the components of the nervous system derived from?

A

From the neural plate of the line of cells which lie on the boundary between the neural plate and the surface ectoderm (the neural plate border)

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6
Q

When does the neural plate form in embryogenesis in humans?

A

Week 3-5

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7
Q

How do we know that all the main different parts begin to be established early on in embryogenesis?

A

Can ‘tag’ specific molecules using antibodies, complimentary to proteins expressed:

Reveals organisation/regionalisation/development of specific regions

Not all the cells are the same - different transcriptional profile and therefore different proteins

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8
Q

What does convergent extension cause?

A
  • Anterior endoderm and prechordal mesoderm to lie underneath one end of the neural plate
  • Notochord to lie underneath the other end
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9
Q

How are the signals secreted from the anterior endoderm and axial mesoderm different?

A

TFs from the anterior endoderm and prechordal mesoderm induce ANTERIOR-TYPE transcription factors in the overlying neural plate cells

TFs from the notochord induce POSTERIOR-TYPE transcription factors in the overlying neural plate cells

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10
Q

What is sox2?

A

A highly conserved transcription factor which are expressed in cells that are on their way to adopt a neural fate

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11
Q

Where are sox2s expressed and when?

A
  • In the neural plate
  • Later confined to the forebrain (telencephalon, diencephalon)
  • Just after the anterior endoderm/ prechordal mesoderm has involuted
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12
Q

What do TFs, such as sox2, determine?

A

Anterior fate of the neural plate

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13
Q

How does the neural plate get longer?

A

ACTIVATION-TRANSFORMATION MODEL:

  • Signals from the notochord (underneath the neural plate) cause the back end of the neural plate to proliferate - BMPS?
  • At the same time, DIFFERENT signals from the notochord transform these cells from an anterior to a posterior identity (represses Ant TFs) - Wnt, FGFs, RA etc
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14
Q

What is the ‘anterior CNS’?

A

Forebrain (telencephalon, diencephalon) and brain derivatives (eg. optic nerve)

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15
Q

What is the ‘posterior CNS’?

A

Hindbrain and spinal cord

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16
Q

How are BMP antagonists maintained in the prechordal mesoderm?

A
  • By transcription factors siamois and goosegoid
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17
Q

In the anterior endoderm, what is induced by siamois and goosegoid and what do these molecules do?

A

Secreted molecules cerberus, frzb, dickkopf

Which inhibit the Wnt signalling pathway

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18
Q

What is needed in order to get anterior neural plate cells?

A

Inhibition of BMP AND Wnt signalling, by BMP and Wnt antagonists from the axial mesoderm

19
Q

Where is Wnt signalling repressed?

A

In the neural plate, directly above the anterior endoderm

20
Q

What do FGFs do and where are they high/low?

A

Maintain the proliferation of cells

Highest at the posterior end of the neural plate, low at the anterior - forms a gradient

21
Q

What happens to Wnts at the notochord extends?

What does this form?

A

Wnts are upregulated

Forms a gradient, where Wnts are low anteriorly and high posteriorly

22
Q

What causes the neural plate to posteriorise?

A

Upregulation of FGFs, Wnts and RA in a gradient manner as the notochord extends

23
Q

Where does the extreme anterior fate arise? (forebrain)

What signal allows this?

A

Where there is NO Wnt signalling AT ALL

  • Signals from the anterior endoderm (cerberus)
  • Inhibits BMPs, Wnts and Nodal
24
Q

What does retanoic acid do?

A
  • Diffuse through the membrane and becomes bound by a cytoplasmic receptor
  • When bound, goes through the pores in the nucleus adn binds to the promoters of genes
  • Regulates gene transcription of HOX genes
25
Q

What happens when RA is expressed in high concentrations compared to if low concentrations?

A
  • Different subset of TFs turned on, dependant on the concentration of RA that the cells see
26
Q

How is a gradient in the nervous system turned into step-like units (segmented)?

What model is this?

A
  • Lewis Wolpert model
  • X axis is distance from the source
  • Y axis is concentration of the molecule
  • Different cells respond differently to different threshold concentrations of the molecule by adopting different fates in a stepwise identity

(in relation to low, medium and high concentration)

27
Q

What organisms is segmentation first seen in?

A

Segmented worms and drosophila larvae

28
Q

What is segmentation controlled by in drosophila larvae and how?

A

Hox genes - expressed in different segmentation patterns in the forming embryo, control the segment identity of each domain

29
Q

How do we know that hox genes specify AP segment identity in drosophila and provide positional information?

A
  • Many different Hox genes
  • Hox genes are evolutionarily conserved across species (with each hox gene having a homologue)
  • Each hox gene is expressed in a specific region along the AP axis (from early stages of development through to adulthood)
  • Up-regulated in response to RA
30
Q

What are Hox gene up-regulated in response to?

A

Retanoic acid

31
Q

Which Hox gene is turned on in responce to very high RA levels?

A

Hox 11

32
Q

Which Hox gene is turned on in responce to very low RA levels?

A

Hox 5

33
Q

What do Hox genes do?

A

Set the identity of the segment - tell which nerves to form (thoratic, lumbar, sacral,caudal etc)

34
Q

What causes segmentation of the drosophila nerual axis?

A
  • Retanoic Acid concentration gradient from low at the anterior end, to high at the posterior end
  • Different levels of RA determines which Hox genes are upregulated (expressed)
  • Changes the transcriptome, fate and function of that cell
  • Different Hox genes confer different identities to the segment, in regards to neurons etc
35
Q

What happens if knock out the genes which code for Hoxa1 and Hoxb1?

What does this show?

A
  • Fail to get rhombomere 4
  • Fail to get facial neurons
  • Shows that Hoxa1 and Hoxb1 are required to specify rhombomere 4
36
Q

What are rhombomeres?

A

‘Bulges’ of the developing brain

37
Q

What induces midbrain cells?

A

An interaction at the boundary between the forebrain and hindbrain cells

38
Q

Why are there multiple Hox genes which all code for the same protein in humans?

A

As a ‘back up’ incase one Hox gene fails

39
Q

In the embryo, where does Sox2 eventually become confined to?

A

The forebrain - diencephalon, telencephalon

40
Q

What does cerberus do?

A

Inhibits Wnt, BMP and nodal

Induces extreme anterior fate - forebrain

41
Q

What does the procencephalon become?

A
  • Dienchephalon

- Telenchephalon

42
Q

What is the procencephalon?

A

Developing forebrain

43
Q

What does the rhombencephalon become?

A

Metencephalon

Myelencephalon

44
Q

What is the rhombencephalon

A

Developing hindbrain

BMS 249 - Developmental Neurobiology (16 decks)

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