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Basic Developmental Biology > Basic Developmental Biology Deck 3 > Flashcards

Basic Developmental Biology Deck 3 Flashcards

1
Q

What is forward genetics?

A

Isolation of mutants followed by gene ID: phenotype precedes genotype.

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2
Q

What is reverse genetics?

A

exploring gene function through targeted manipulation of the genome.

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3
Q

In the hedgehog pathway:

1) what is ligand?
2) what is receptor?
3) what is inducer?
4) what is effector?

A

1) one of three hedgehog molecules (ex. Shh, Ihh)
2) ptch1 (ordinarily inhibits smoothin)
3) smoothin, which effects Glis.
4) Gli1/2/3, in absence of signal, Gli 3 is in repressor form, no Gli 1 and 2. With signal, all are activated transcription factors.

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4
Q

In the TGF-beta/BMP pathway:

1) what is ligand?
2) what is receptor?
3) what is inducer?
4) what is effector?

A

1) lots of ligands >20.
2) receptor is S/T receptor, dimerize in presence of signal
3) active Smad / Co-smad factor.
4) transcription factor that binds Smad/cosmad.

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5
Q

In the FGF signaling pathway:

1) what is ligand?
2) what is receptor?
3) what is inducer?
4) what is effector?

A

1) FGF, in cooperation with Hspg
2) tyrosine kinase receptor, dimerizes.
3) cascade -> Ras/Raf/Mek?Erk.
4) Erk
with cascade, you get on/off, no graded (dose dependent) output.

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6
Q

In the Notch/Delta signaling pathway:

1) what is ligand?
2) what is receptor?
3) what is inducer?
4) what is effector?

A

1) Notch / Delta ligands.
2) same
3/4) notch intracelular domain

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7
Q

In the Retinoic Acid signaling pathway:

1) what is ligand?
2) what is receptor?
3) what is inducer?
4) what is effector?

A

1) Vitamin A (retinol)
2) RXR-RAR transcription factors already in the nucleus.
Note: hydrophobic signal, goes to nucleus. In non-target tissue, retinoic acid is degraded.

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8
Q

In Eph/ephrin signaling pathway:

What are key points?

A

Eph/ephrin are membrane proteins, can have effect on either cell or both. Modulate cell shape, axonal cell migration.

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9
Q

What occurs in second week of development?

A

Implantation, yolk sac formation, AP axis patterning, initiation of gastrulation.

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10
Q

What signals get you from totipotent cell to epiblast?

A

Oct4 for ICM, Nanog for epiblast.

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11
Q

What signals get you from totipotent cell to primitive endoderm?

A

Oct4 for ICM, Gata6 for primitive endoderm.

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12
Q

What signals get you from totipotent cell to trophectoderm?

A

Cdx2 for trophectoderm.

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13
Q

In Nodal signaling:

1) what is the signal
2) what is the receptor / co-receptor
3) what is the effector
4) what is the signal outcome, including range and timing.

A

1) Nodal
2) Type 1 / Type 2 activin receptors, with Cripto and Cryptic co-receptors.
3) Smad-co-smad enter nucleus
4) upregulate Nodal, first, Lefty second. Lefty inhibits Nodal, is transcribed second but travels further faster.
Pathway is BMP pathway (S/T kinase pathway).

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14
Q

What causes AP axis differentiation?

A

Nodal / nodal inhibitor signals (Lefty and Cerberus) on opposite ends of embryo. Initially, all cells are producing Nodal.

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15
Q

What is Heterotaxia?

A

discordant and randomized organ position.

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16
Q

What is isomerism?

A

describes phenotype of organ, mirror image duplication, ex. 3 lobes of both lungs.

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17
Q

What are the two mechanisms for somitogenesis?

A

1) segmentation clock (cell autonomous.
2) wavefront (extrinsic signal that says do / don’t respond to signals of the clock.).
As tail bud extends and segmentation clock becomes further from tail, segmentation clock can kick in.

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18
Q

What is the signaling pathway of the segmentation clock?

A

1) Delta-like1,3 binds Notch, causes NICD to be cleaved and enter nucleus.
2) NICD activates Hes1,7 and Lfng.
3) Lfng inhibits NICD cleavage (stops Delta/Notch signaling).
4) Hes1,7 inhibits inself and lfng (allowing Delta/Notch signaling to resume).
Also: Retinoic acid is released from somites, fine-tunes the system.

19
Q

What is wavefront portion of clock?

A

FGF/wnt being released from tail, causes continued growth of tail and sends signal back towards somites to ignore segmentation clock.

20
Q

How do somites progress and differentiate?

A

1) epithelialize.
2) subdivide into compartments, first ventromedial region undergoes EMT to form sclerotome. Overlying tissue is called dermamyotome.
3) dermomyotome separates into dermatome and myotome.

21
Q

What does sclerotome become?

A

highly migratory, becomes vertebral bodies.

22
Q

What does myotome become?

A

delaminates, becomes musculature.

23
Q

What does dermatome become?

A

delaminates, becomes dermis.

24
Q

What is syndetome, where does it form?

A

becomes axial tendons, forms at myotome / sclerotome border. develops last.

25
Q

Where do the following limb elements originate?

1) skeleton
2) tendons
3) muscle
4) motor innervation
5) sensory innervation
6) skin

A

1) lateral plate mesoderm.
2) lateral plate mesoderm.
3) somite (paraxial mesoderm)
4) spinal cord (neural tube, ectoderm)
5) dorsal root ganglia (neural crest, ectoderm)
6) ectoderm.

26
Q

What is the auto activating feedback loop that allows for limb bud formation?

A

lateral plate mesoderm releases FGF10, signal received by ectoderm, which releases Wnt3a, FGF8, signals received by lateral plate mesoderm, loop maintains its own signaling. (Different FGF receptors for FGF8 and FGF10).

27
Q

What is proximal-distal signaling pattern and signals in the limb?

A

RA released at flank, dominant at short distances. FGF/Wnt/shh released at AER, induces distal patterning. As limb grows away from flank, RA signal is smaller. FGF is permissive, doesn’t cause the specific distal fat.

28
Q

How is Anterior-posterior signaling controlled in the limb?

A

Controlled by ZPA at posterior edge, Shh is signal, dose dependent. Knocking out Shh leaves a single digit.

29
Q

How is dorsal ventral signaling controlled in the limb?

A

Instructive Wnt signal from dorsal ectoderm induces Lmx1b, which defines dorsal identity. Ventral BMP signals prevent Wnt expression on ventral surface. Deletion of Lmx1b causes los of dorsal limb pattern.

30
Q

What are dysostoses and what causes them?

A

abnormality in location and shape of skeletal elements. Tend to be due to problems in Hox genes. Patterning problem.

31
Q

What are dysplasias and what causes them?

A

abnormality in skeletogeneis, problems in bone structure, growth and modeling.

32
Q

Why is Sox9 critical?

A

allows for chondrocyte differentiation. No Sox9, no cartilage, not much bone, incompatible with life.

33
Q

Why are Ihh and PTHrP critical in bone growth?

A

Cause maturation and hypertrophy of chondrocytes and bone formation.

34
Q

What causes neural crest to delaminate?

A

Intermediate amounts of BMP and Wnt signals (a lot = ectoderm; little = neural crest)

35
Q

What are the fates of migratory neural crest cells that travel dorsally and ventrally to the somites?

A

dorsal root: melanocytes

ventral root: enteric nervous system, dorsal root ganglia, sensory ganglia, schwann cells.f, adrenal medulla.

36
Q

What is Hirschsprung’s disease?

A

Defects in ability to respond to the GDNF signal or Ret (tyrosine kinase receptor for GDNF) that signals path for neural crest cell migration. Causes aganglionosis of terminal colon, causes megacolon. prominent among Mennonites.

37
Q

What signals cause enteric neural crest cells to migrate to appropriate parts of gut?

A

GDNF = neural crest chemoattractant, gets enteric NC cells to cecum (where GDNF expression is greatest). Endothelia 3 (ligand) gets enteric neural crest cells to terminal colon.

38
Q

What is signaling from ectodermal progenitor to:

1) hairless skin
2) hairy skin

A

1) BMPs / Notch (stratified epidermis, no hair).

2) BMPs / Wnts (hair follicle skin)

39
Q

What is Robin Sequence?

A

Sequence caused by small mandible. Causes tongue to stay elevated, cleft palate, constriction of airway, failure to thrive.

40
Q

What is Treacher Collins Syndrome?

A

TCOF1 mutation, failure of neural crest.

41
Q

What is a stem cell?

A

Cell that can self-replicate and give rise to at least one other cell fate. Must be able to live for a long time, otherwise it’s a progenitor.

42
Q

What are the paracrine signals during migration that cause neural crest cells to adopt the following cell fates?

1) Sensory neurons
2) autonomic neurons
3) adrenal medulla
4) melanocytes
5) Schwann cells

A

1) Wnt
2) Bmp
3) glucocorticoids
4) Endothelin + Wnt
5) GGF

43
Q

What do we get from epidermal progenitor to a hair follicle?

A

1) BMP+Wnt is expressed in epidermal progenitor.
2) Wnt induces Shh, which drives placode formation.
3) DKK is released next to the growing placode, which inhibits Wnt, preventing diffuse follicle growth, so follicle grows only in a local spot.

Basic Developmental Biology (4 decks)

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