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Human Embryology > Common Signalling Pathways > Flashcards

Common Signalling Pathways Flashcards

1
Q

What is cell signalling?

A

Communication between cells to govern basic cell activities and actions

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2
Q

What happens in signal transduction?

A

cells convert one kind of signal or stimuli into another

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3
Q

What are the 3 types of INTERCELLULAR SIGNALLING

A
  • Autocrine signalling
  • Paracrine signalling
  • Endocrine signalling
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4
Q

List the different molecular signalling pathways

A
  • morphogens
  • notch/delta
  • transcription factors
  • receptor tyrosine kinases (RTKs)
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5
Q

What are the two proteins needed for intercellular communication?

A
  • gap junctions (connexon)
  • cell adhesion molecules (cadherin, immunoglobin super family)
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6
Q

The anterior, posterior and anteroposterior axes of the embryo does what?

A

They determine the correct locations for things like the limbs and nervous system patterning

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7
Q

What does excessive retinoic acid lead to

A

Because retinoic acid posteriorizes the body, when there’s excess, structures have a more posterior nature

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8
Q

A more anteriorized body structure is caused by what?

A
  • insufficient retinoic acid
  • Defects in retinal aldehyde dehydrogenase (produces retinoic acid)
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9
Q

Retinoic acid receptors are _________ and they __________ when activated. Their main targets are ______

A
  • Transcription factors
  • Regulate downstream gene expression
  • Hox genes
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10
Q

Explain the metabolic production of Retionic acid

A

Dietary vitamin A (retinol) is oxidized by retinol dehydrogenase which creates retinal. Retinal is oxidized by retinal aldehyde dehydrogenase creating the bio active form of ATRA (All Trans Retinoic Acid) all which cellular binding proteins are controlling their concentration.
Retinoic acid can be actively degraded into inactive metabolites by an enzyme (CYP26)

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11
Q

What are the members of the TGF-ß superfamily and their function

A
  • TGF-ß, BMPs, activin and nodal.
  • Contribute to dorsoventral patterning, cell fate decisions and formation of specific organs
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12
Q

What are morphogens?

A
  • diffusible molecules that say where a cell is generated in the body and where they go till they get to their destination
  • they can be expressed in opposing gradients (dorsal ventral etc)
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13
Q

Name examples of morphogens

A
  • Retinoic acid
  • Transforming Growth Factor ß(TGF-ß)
  • Sonic Hedgehog (patterns the ventral neural tube)
  • Wnt proteins
  • Bone Morphogenic Proteins (BMPs)
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14
Q

The Wnt-secreted glycoproteins are vertebrate orthologs of _______

A
  • The Drosophila gene Wingless
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15
Q

What do Wnt proteins do?

A
  • The control apoptosis, cell migration & cell fate specification
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16
Q

Explain the Wnt/ß-catenin pathway when Wnt is present

A
  • Wnt binds to Fzd (its receptor) with coreceptor LRP5/6
  • Active Fzd phosphonylates DVL which is activated
  • Active DVL binds to a complex to phosphorylate GSK3
  • GSK3 with phosphor is inactive and cannot phosphorylate ß-catenin
  • ß-catenin goes to nucleus and activates target genes with TCF (transcription factor)
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17
Q

Explain the Wnt/ß-catenin pathway when Wnt is absent

A
  • No Wnt to activate Fzd (cell surface receptor)
  • No Fzd to phosphorylate DVL
  • Inactive DVL cannot bind to protein complex
  • GSK3 (a kinase) is active, (not phosphorylated) and it phosphorylates ß-catenin marking it for degradation
  • No ß-catenin available to activate target genes
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18
Q

What is different when Wnt is present versus absent

A
  • When Wnt is present target genes in the nucleus are activated
  • When Wnt is absent target genes in the nucleus are inactivated
19
Q

Sonic Hedgehog was the first mammalian ortholog of _______ to be identified

A
  • The drosophila gene hedgehog
20
Q

What is different when Sonic Hedgehog is present versus absent

A
  • In the presence of Shh, Gli becomes an activator (Gli-A) for target genes
  • In the absence of Shh, Gli becomes a repressor (Gli-R) for target genes
21
Q

Explain the pathway of an absence Shh

A
  • PTCH (shh receptor) inhibits smoothened (Smo) both transmembrane receptors
  • Inactive Smo cannot act on Cos2 in a complex (Cos2, Fu, Gli)
  • Another complex with activated GSK3 (kinase) phosphorylates Gli
  • Phosphorylated Gli (Gli-R) is cleaved and goes into nucleus
  • Gli-R represses target genes
22
Q

Explain the pathway of a present Shh

A
  • Modified Shh ( post transcriptional addition of cholesterol to n-terminal) inhibits PTCH
  • Smo is activated and acts on complex
  • Complex conformation changes and Fu binds to SuFu (its suppressor)
  • Gli is not phosphorylated and cleaved so it goes into nucleus as an activator
  • Gli-A binds to CBP (transcription complex) which activates target genes
23
Q

How can an enzyme be switched ‘On’ or ‘off’

A
  • By phosphorylation (kinases)
  • by de-phosphorylation (phosphates)
24
Q

What is autocrine signalling?

A
  • This is when the same cell that produces the ligand (signalling molecule) also produces the receptor
  • This allows a cell to produce a signal for itself
25
Q

What is paracrine signalling?

A
  • This is local signalling between cells
  • a cell produces the signalling molecules to bind & activate surrounding cells
  • enabled by diffusion
26
Q

What is endocrine signalling?

A
  • This is the signal transfer in distant body sites
  • a signal is produced by a cell and transferred to a distal portion of the body through the bloodstream
27
Q

Explain the active TGF-ß/SMAD signalling pathway

A
  • This pathway is active when TGF-ß binds to its type II receptor which an inactive kinase domain. The type II receptor transphosphorylates its type I receptor, activating the kinase domain
  • Then the type I receptor phosphorylates the receptor-associated SMAD protein (R-SMAD)
  • The R-SMAD protein binds to its common-partner (SMAD4) creating a complex that translocates to the nucleus
  • This complex then function as a transcription factor by directly binding to DNA which will up-regulate target genes
28
Q

Explain the gradient between Shh and BMP on the dorsoventral place of the neural tube

A
  • The notochord and the floor plate of the neural tube secretes high levels of shh
  • The dorsoventral concentration of Shh is higher on the floor plate and lower on the roof plate (ventral-to-dorsal)
  • a member of the TGF-ß family (BMPs) is highly secreted on the roof plate in the opposing gradient of Shh (dorsal-to-ventral)
  • Together, they determine dorsoventral cell fates
29
Q

How many families of Wnt and Fzd are there?

A
  • Wnt: 19 families
  • Fzd: 10 families
30
Q

What is the purpose of the notch/delta pathway

A
  • To specify the fate of precursor cells
  • to maintain stem-cell niches
  • proliferation, apoptosis & differentiation
31
Q

Explain the notch/delta pathway

A
  • This is a intercellular interaction
  • The delta/jagged ligand from one differentiating cell binds to the notch protein (receptor that’s attached to NICD) on another progenitor cell
  • this binding event causes the cleavage of NICD from notch then it goes to the nucleus & binds to a TS complex, activating target genes (HES) which inhibits differentiation in progenitor cells
32
Q

Explain the role and function of transcription factors

A
  • They are proteins that regulate gene expression by activation/repression
  • The bind to the promoter region sequences to regulate the rate of target gene transcription by interacting with accessory proteins
33
Q

What is the difference between a transcriptionally active and inactive chromatin

A

ACTIVE
- transcription factors are able to bind
- histone acetylases and kinases are activated to modify chromatin (histone activated)
- histone deacetylases are inhibited
INACTIVE
- TFs can’t bind
- acetylases and kinases are inhibited
- deacetylases are activated

34
Q

Examples of transcription factors

A
  • HOX proteins (heart)
  • PAX genes (eyes)
  • basic helix-loop-helix TF (muscle)
35
Q

What is the purpose of receptor tyrosine kinases (RTKs)

A

They are essential for:
- cell proliferation
- apoptosis
- migration
- The growth of new blood vessels

36
Q

Name 5 abnormalities for Vitamin a (retinol)

A
  • Spina Bifida
  • otosclerosis (the hardening of the ear)
  • Anophthalmia ( AACI the eyes)
  • Hypoplasia (insufficient formation or the lungs)
  • Spongy myocardium
37
Q

Name 3 abnormalities for Shh

A
  • Holoproencephaly
  • Grig’s and Pallister Syndrome
  • Gorlin’s Syndrome
38
Q

Name 2 abnormalities for the Wnt/ß-Catenin pathway

A
  • Williams-Beuren Syndrome
  • Osteoporosis-Pseudoglioma Syndrome
39
Q

Name 2 abnormalities for the Notch/Delta Pathway

A
  • Alagile Syndrome
  • CADASIL
40
Q

Name 2 abnormalities for transcription factors

A
  • Rubinstein-tayabi
  • Alpha-thalassemia/X-linked mental retardation
41
Q

Name 2 abnormalities for HOX proteins

A
  • Cardiac atrial-septal defects
  • Lissencephaly Syndrome
42
Q

Name 3 abnormalities for PAX genes

A
  • Occular defects
  • Alveolar rhabdomyosarcoma
  • Waardenburg’s Syndrome
43
Q

Name 2 abnormalities for RTKs

A
  • Milroy disease
  • cancer
44
Q

what is the difference between a differentiating and a progenitor cell?

A
  • in a differentiating cell, notch signalling is inactive
  • in a progenitor cell, the regulation of target genes, inhibits differentiation

Human Embryology (14 decks)

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