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BMS2021 > TOPIC E: DEVELOPMENT > Flashcards

TOPIC E: DEVELOPMENT Flashcards

1
Q

what are descriptive studies based on?

A
  • Expression profiles of mRNA
  • Non coding RNAs and proteins
  • Temporal (when) and spatial (where)
  • fate mapping of cells (lineage tracing)
  • comparative studies of organisms
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2
Q

What are manipulative studies and 3 examples?

A

ALTERING SYSTEM AND OBSERVING EFFECTS

  1. Gene knockout or transgenic overexpression
  2. Adding drug or tetragon and observing effects
  3. Translating cells from ONE area to ANOTHER (cell commitment and specification)
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3
Q

What kind of microscopy is a light microscoope used for?

A
  • Brightfiled microscopy
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4
Q

What kind of microscopy is a confocal microscope used for?

A
  • Fluorescence microscopy
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5
Q

What kind of microscopy is an electron microscope used for?

A
  • TEM (Transmission electron microscopy–> can “see” inside cell)
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6
Q

Does temporal gene expression analysis in tissue examine WHEN a gene is expressed?

A
  • YES “when”= time
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7
Q

What does DNA analyis include?

A
  • PCR (promoter and enhancer studies–> plasmids)
  • gene cloning (epigenetics–> methylation of DNA, histone modification)
  • Southern blotting– >gene knockout or overexpression
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8
Q

What does RNA analysis include?

A
  • gene expression analysis
  • RT-PCR
  • RNA -seq
  • Knockdown of mRNAs using RNA intereference (RNAi)
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9
Q

What does protein analysis include?

A
  • Western blotting and immunostaining of tissues
  • Protein structure –> function, phosphorlyation, sumoylation (to do with ubiquitin) , acetylation, glyocsylation
  • Protein-protein interactions by co-immunoprecipiation
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10
Q

WHat does bioinformatics include?

A
  • using computer software to understand biologcial data

e. g. constructing whole genomes, comparing data genes or sets

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11
Q

What is real time PCR?

A
  • Quanititative Reverse Transcription -PCR (q RT-PCR)
  • converts RNA—> cDNA (via reverse trancription)
  • Fluorescent ATCG labells added to mix
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12
Q

What do a lower number of PCR cycling to reach detection indicate?

A
  • More starting RNA
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13
Q

What do a higher number of cycles of PCR cycling to reach detection indciate?

A
  • Less cDNA present therefore less RNA
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14
Q

What does in situ hybridisation look at and what colour stain?

A
  • Study of prenatal development
  • temporal and spatial expression of mRNAs in MODEL embryos (fly, fish, chicken, mouse)
  • Purple stain for cells with the RNA of interest
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15
Q

What is imunofluorescence to do with?

A

WHEN and WHERE a protein is epxressed in a tissue (antibodies against protein of interest)

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16
Q

What does Western Blotting show in terms of the proteins?

A
  • The SIZE of the protein and the relative amount present in a tissue
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17
Q

Does the primary antibody for Western blotting or Immunofluorescne have to be made in the same animal or separate animals?

A
  • Separate animals for different cell strucutres
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18
Q

Does a second degree antibody have to be made in separate animals to target different primary antibodies?

A
  • NO

- Can be made in SAME animal

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19
Q

What does a transgenic mice model involve?

A
  • Carrying foreign gene and we observe the phenotype
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20
Q

What are the 2 methods for creating trasngenic mice?

A
  1. Pronuclear injection

2. Transforming ES cells (embryonic stem cells)

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21
Q

What does modern developmental bio involve?

A
  • Embryology
  • Cytology (cells ) + Histology (tissues)
  • genetics
  • understands the genetic and cell mechanisms that allow 1 cell–> multicomplex cell
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22
Q

What issues does Dev bio help with?

A
  • Cancers, cell therapy for human disease (stem cells) , developmental disorders `
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23
Q

What is pattern formation?

A
  • Once cell–> many cells–> organised cells–> tissues–> organs
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24
Q

Which two processes does pattern formation require?

A
  1. Differential gene expression

2. Signalling between cells

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25
Q

Which 5 things does pattern formation arise from?

A
  1. Cell proliferation
  2. Cell migration
  3. Changes in cell shape and SIZE
  4. Cell differentiation
  5. Cell interaction
  6. Apoptosis (cell death–> not shown on diagram)
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26
Q

What are epithelial cells characterised by?

A
  • TIGHTLY connected to each other
  • don’t move alone (move as a sheet–> mass movement)
  • Polarised, cell-cell junctions, cilia,
  • Sits on basement membrane
  • (Cytokeratin marker gene)
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27
Q

What is the marker gene for epithelial cells?

A
  • Cytokeratin
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28
Q

What are mesenchmyal cells characrterised by?

A
  • Not connected to other cells
  • More in ECM
  • Not polarised
  • No cilia
  • (Vimetin marker gene)
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29
Q

What is the marker gene for mesenchymal cells?

A
  • Vimetin
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30
Q

What plays a major role in cancer matastasis and development?

A
  • EMT–> epithelial to mesenchymal transition
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31
Q

What does polarised mean in terms of epithelial and mesenchymal?

A
  • Strucutres (e.g. nucleus) are on one side of cel and not other
  • (nucleus on basement membrane side)
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32
Q

What is cell fate defined as?

A
  • Given destination of cell if left undisturbed in embryo
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33
Q

What are two types of cell COMMITMENT?

A
  1. Speciifcation

2. Determination `

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34
Q

What occurs in the cell COMMITMENT of specification?

A
  • Cell can autonomously differentiate BUT it can still be REVERSED
    e. g. IF forming neuron but then put in different place, can change into different cell type
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35
Q

What occurs in the cell COMMITMENT process of determination?

A
  • Cell differentiates autonomoously if placed in a dish BUT when placed into another tissue CANNOT BE REVERSED
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36
Q

What does cell FATE compose of?

A
  • CELL COMMITMENT (Specification and determination )

- DIFFERENTIATION (Developmental fate –> final phenotypes e.g. neuron developing dendritic processes)

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37
Q

What is an examples of formation of beta islet cells?

A
  • blastomere–> endoderm cell (SPECIFIED)–> pancreatic bud cell –> endocrine pacnreas cell (DETERMINED) –> Beta islet cell
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38
Q

What is cell fate restriction governed by? (3 things)

A
  1. Cells genome (gene expression )
  2. Cells history (factors it has been exposed to–> where it has been moved from)
  3. Interaction with neighbours
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39
Q

What is an example of a specified cell ?

A
  • Haemotopoetic stem cell
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40
Q

What is an example of a determined cell? (bloodline)

A
  • Common myeloid progenitor
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41
Q

What is an example of a differentiated cell type?

A
  • Myeboblasts (baso neutro eoso)
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42
Q

What is a fate map?

A
  • Diagram that maps adult tissues or structures to regions of embryo that give rise to structure
    e. .g lineage tracing (label group of cells and see where they go)
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43
Q

Is embryonic development conserved in animals and if so, what makes it good for?

A
  • YES! Which makes them good model organisms to study development (model human development)
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44
Q

What are advantages of flies and c.elegan worms for model organisms?

A

Rapid life cycle

  • Key genes are known
  • fate of cells known
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45
Q

What are disadvantages of using flies and c.elegan worms for model organisms?

A
  • Aspects of anatomy and development NOT conserved in humans
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46
Q

What are the advantages of using zebra fish and the clawed frog (lower vertebrates) as model organisms?

A
  • Vertebrates develop OUTSIDE the maternal body
  • Can perform fate mapping in them
  • Easy to keep clean and manipulate
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47
Q

What are the diasvantatges of using lower vertebrates (zebra fish and clawed frog) ?

A
  • Don’t share some features of humans such as mammary glands (so can’t use for breast cancer)
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48
Q

What are avain embryos used to study?

A
  • Embryogenesis–> gastrulation, neural crest cells –> GFP positive labelled neural tube put into quail embryo –> cell fate then follwed
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49
Q

What are the advantages of using avian embryos?

A
  • Easy to obtain (from egg) and manipulate
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50
Q

What are the diadvantages of using avian embryos?

A
  • Longer life cycle (4 months)

- Transgenic strategies worse than mouse (over/under expression)

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51
Q

What are the advantages of the mouse (mammalian model)?

A
  • Same organs as humans and also diseases like obesity
  • Easy to maintain colonies (good transgenics)
  • Transgenic and knockout mice for human disease
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52
Q

What are the disasdvantages of using mammalian model organisms?

A
  • Embryos develop in utero (so harder to access)
  • Expensive –> null mutant generation
  • Models can show DIFFERENT PHENOTYPES to human disease
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53
Q

Which two factors is development driven by?

A
  1. Differential gene expression

2. Interaction b/w TFs and signalling molecules b/w cells

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54
Q

Does each embryo cell retain its own ‘history memory’?

A
  • YES!
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55
Q

What is each gene controlled by?

A
  • Promoters (initate gene expression)
  • enhancers (bind activating factors)
  • inhibitory (bind inhibitory factors)
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56
Q

What are TFs?

A
  • DNA binding proteins –> regulate a array of target genes

- direct development ‘tell’ other genes what to do

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57
Q

What do transactivation domains on Transcription factors do?

A
  • Activate or repress genes

e. g. homeobox genes

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58
Q

What do homeobox genes encode and what does this form?

A
  • Homeobox proteins

- to form homeodomain

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59
Q

Are genes expressed FIRST in drosophilla more posterior or anterior?

A
  • More anterior
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60
Q

What do mutations in Hox genes cause?

A
  • Homeotic transformations–> one body part develops as a different body part (wrong location) e.g. legs where antenae used to be (antennapedia mutation)
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61
Q

What transformation is where one body part develops as different body part?

A
  • Homeotic trasnsformation
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62
Q

Where are the Hox genes expressed in mice and humans?

A
  • Series along the length of the embryo

- genes determine the vertebrae type

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63
Q

What is induction defined as?

A
  • Change in the cell fate due to signals sent from other cells –> signals LIMITED in space and time (can be turned off) e.g. Glycoproteins
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64
Q

What does signalling equal?

A
  • Things that are secreted from cell
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65
Q

Do all organisms use a limited repertoire of inductive signals?

A
  • Yes!
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66
Q

What is embryonic induction?

A
  • One tissue sends signals to direct the development of ANOTHER tissue
    e. g. Newt (ball of cells) –> dorsal blastophere
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67
Q

What does the dorsal blastophere do?

A
  • Acts as the organiser by releasing signals to neighboring tissues
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68
Q

What does the spemann organiser do?

A
  • Can induce a SECOND BODY AXIS through INDUCTION (duplicated neural tube)
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69
Q

What occurs in sequential induction?

A
  • One type of cells (B lets say) can release inductive signals (e.g. glycoproteins) to another type of cells (lets say A) to allow certain cells in A to produce a NEW type of cells (type C) etc until many different cell types form
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70
Q

What determines how cells respond differently to signals? (i.e. what is it based on?) (2 things)

A
  1. Other signals that it is receiving (combinatorial combined effects)
  2. Cell memory (what other signals it has had in the past–> chromatin marks)
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71
Q

Will a cell with a different signalling history respond in the same way to a cell?

A
  • NO!
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72
Q

What is lateral inhibition?

A
  • When cells send inhibitory signals to neighboring cells –> alters behavior of receptive cells
    e. g. neuronal differentiation (one cell forms a neuron and other cells don’t)
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73
Q

What is the notch signalling pathway for lateral inhibition?

A
  • DIRECT INTERACTION b/w cell surface receptor (Notch) and ligands (delta or Jagged or Serate)
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74
Q

In the Notch signalling pathway of lateral inhibition, what is the cell surface receptor and what are the most common ligands?

A
  • Cell surface receptor= Notch

- Ligands= delta, Jagged , Serate

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75
Q

A part from the nervous system development, where is the delta notch pathway of lateral inhibition important?

A
  • Heart, kidney and pancreas development
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76
Q

What is an example of autocrine signalling?

A
  • IL-2 in T cell proliferation or IL-1 in monocytes
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77
Q

What are examples of paracrine signalling?

A
  • Diffusable factors, neighboring cells (adjaent cells)

e. g. Fibroblast growth factor (FgF)

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78
Q

What is the morphogen gradient?

A
  • type of inductive signal
79
Q

What is a morphogen?

A
  • “Secreted, diffusable molecule that can influence the fate of a field of neighboring cells via concentration gradient”
80
Q

With morphogens do cells respond differently based on the concentration of a molecule?

A
  • YES!

e. g. Sonic hedgehog for digit formation

81
Q

What can the distance of the morphogen from the source indicate?

A
  • Which set of genes is activated
82
Q

What are the 4 different paracrine signalling factors?

A
  1. FgF (fibroblast growth factor)
  2. Hedgehog signalling protein
  3. Wnt
  4. TGF-beta (Transforming Growth Factor Beta)
83
Q

Which two cell surface receptor types/pathways do the 4 families use?

A
  1. Protein kinases (FgF, and TGF-beta)

2. Second messenger system–> kinase activation

84
Q

What do FgFs promote?

A
  • Involved in cell proliferation

- - Promote angiogenesis

85
Q

Which paracrine signalling pathway can FgFs activate or repress?

A
  • The Wnt pathway
86
Q

What is FgF8 sufficient to form?

A
  • Sufficient to form another limb
87
Q

What is the role of TGF-beta?

A
  • Cell specification
  • ECM formation
  • Cell division and death
88
Q

What do the phosphorylated serine/ threonine residues activate in the TGF-beta family pathway?

A
  • Activates the Phosphorylation of smads (proteins) which enter the nucleus and activate target genes
89
Q

What are examples of some classes of TGF-beta family?

A
  • Nodal
  • TGF-beta
  • Bone Morphogenic Proteins (BMPs)
90
Q

What can BMPs regulate?

A
  • Chondrogenesis–> cartilage formation

- Deleted BMP receptors –> skeletal defect in mice

91
Q

What is the Wnt signalling pathway important for?

A
  • Needed for gastrulation (3 layers)

- (dorsal side of embryo, neural tube formation, cell proliferation and differentiation)

92
Q

Which membrane receptor does Wnt bind to?

A
  • Frizzled
93
Q

Which important factors are associated with Wnt signalling pathway?

A
  • Frizzled (Wnt binds to it )
  • Dsh (Dishriveled) attaches and beta-catenin no longer degraded and thus stabilised –> enters the nucleus to activate target genes
94
Q

What is Wnt4 required for?

A
  • Kidney formation (knockout of gene–> no kidneys develop)
95
Q

What are the three types of Hedgehog genes in mammals?

A
    1. Sonic
      1. Indian
      2. Desert
96
Q

What does the hedgehog signalling pathway play a role in?

A
  • major role in development (mutated in skin cancer)
97
Q

what do most cells have in terms of the context of the Hedgehog signalling pathway?

A
  • A primary cilium
98
Q

What happens when there is NO hedgehog acting on a cell?

A
  • Gli usually gets phosphorylated into fragments –> represses target genes
99
Q

What happens when Hedge hog comes along and binds to PTC on cell surface ?

A
  • SMO (smoothened) is no logner inhibited –> SMO goes up primary cilium –> stops Gli from being broken down
  • Gli travels down from cilium –> activates target genes in the nucleus –> induces EFFECTS
100
Q

In the hedgehog pathway, what does PTC (patch) usually CONSTANTLY inihbit?

A
  • PTC usually conatantly inhibits SMO (smoothened) -without hedgehog binding
101
Q

What does sonic hedgehog pattern and what is an example of when this signalling is inihibted ?

A
  • Tissues such as limb, neural tissue
  • Cyclopedia–> one eye
  • this occurred from weed killer eaten by mother sheep –> weed eaten inhibits cholesterol synthesis which is required for Hedgehog production thus NO HEDGEHOG and only one eye :(
102
Q

What is morphogenesis?

A

“Organisation of form–> groups of SIMILAR cells that have formed tissues ORGANISE with other tissues into SPECIFIC shapes and sizes”

  • Cells–> groups–> tissues–> organs
103
Q

What are the two drivers of morphogenesis?

A
  1. DIRECT cell-cell adhesion

2. Cell migration

104
Q

How can boundaries between cells be made?

A
  • By cells having different types and amounts of cell surface molecules (cell adhesion molecules–> Cadherins)
105
Q

What are Cadherins and what do they do?

A
  • Calcium dependent ADHEsion Molecules
  • They ESTABLISH and MAINTAIN intracellular connections
  • Spatial segragation of cell types and morphogenesis
106
Q

What are E-cadherins?

A
  • Early embryonic cells –> thin epithelial tissue
107
Q

What are N-cadherins?

A
  • Neural Cells (deletion –> no grouping to form neural tube)
108
Q

What are P-cadherins?

A
  • Placental cells
109
Q

Which two signals is cell migration a combination of?

A
  • Motility and glucan* signals
110
Q

Can BOTH eputhelial and mesenchymal cells migrate?

A
  • YES!

- But epithelial cells can ONLY migrate as a sheet/tubes

111
Q

What is the pathway for cell migration from change in polarity (signal like 4 families bind) ?

A
  • Polarity changes
  • Actin filaments at leading edge (mechanical force) –> align with myosin aswell for motility
  • Integrins interact and grip cell with ECM –> myosin provides the motile force
112
Q

What provides the motile force for polarity changes in epithelial to mesenchymal transition?

A
  • Myosin
113
Q

Which experiment do you do to show something (gene) is NECESSARY?

A
  • Knock it out to see if necessary (like the kidney example)
114
Q

Which experiment do you do to show if something is SUFFICIENT? -

A
  • Put it in structure and see if it induces it
115
Q

What are the major phases of embryo development?

A
  • Fertilisation (sperm + egg–> zygote)
  • Cleavage (Rapid cell division without any growth-same size)
  • Blastocyst formation (hollow ball of cells)
  • Implantation in uterus (formation of bilaminar disc)
  • Gastrulation (3 germ layers form)
  • Neurilation (neural tube forms)
  • Growth and organogenesis
116
Q

What are the major phases of HUMAN EMBRYONIC DEVELOPMENT?

A
  1. Ovulation
  2. Fertilisation
  3. Cleavage (1 cell–>2–> 4–> 8)
  4. Morula forms
  5. Early blastocyst forms and travels through fallopian tube
  6. Late blastocyst (day 6) –> actually implants in uterus
  7. gastrulation
  8. Organogenesis
117
Q

What do cells show in the major phases of emryonic development?

A
  • Progressive fate restriction (cells–> tissues–> organs)
118
Q

On day 6, where does the embryo ‘hatch’ from and were does it go?

A
  • ‘hatcher’ is from zona pellucida and implants in wall of uterus
119
Q

What does the inner cell mass (ICM) form?

A
  • Embryo (also the site of stem cells)
120
Q

What does the outer layer of the trophoblast form?

A
  • Forms placenta and outer membrane
121
Q

What are the two layers of the bilaminar disc?

A
  • Epiblast (‘upon’-top)

- Hypoblast (‘under’-bottom)

122
Q

By which week/day has the bilaminar embryonic disk formed?

A
  • By the second week (day 14)

- consists of epiblast and hypoblast

123
Q

What is gastrulation?

A

Where the bilaminar disk differentiates into 3 germ layers

124
Q

What happens after approx. day 15 after fertilisation?

A
  • Primitive streak forms (caudal end of epiblast)
125
Q

What does the primitive streak form?

A
  • Caudal end of epiblast

- Defines the major axes of embryo (cranial and caudal end + left and right sides of embryo)

126
Q

What does the primitive streak expand to form?

A
  • Primitive NODE (has primitive PIT- depression) –> continues towards caudal end of streak forming a GROVE
127
Q

What happens after the primitive GROVE is formed?

A
  • Cells migrate towards streak–> detatch from epiblast and go beneath to the INTERIOR of embryo (invagination)
  • The first cells displace the hypoblast cells and are replaced –> definitive endoderm (new cell layer) thus forms
128
Q

By day 16, what are the remaining cells from the epiblast known as (After the hypoblast cells have been replaced) ?

A
  • Ectoderm
129
Q

What do the cells that have resided in the spece b/w the epiblast and new definitive endoderm form?

A
  • Germ layer –> mesoderm
130
Q

When cleavage occurs (cell division) does the embryo increase in size?

A
  • NO! The cells divide with NO size increase
131
Q

What is cell potency?

A
  • The ability to differentiate into different cell types

- increased potency can mean that cells differentiate into more cell types

132
Q

What can totipotent cells become and what is an example of a totipotent cell?

A
  • Can become ANY cell type (zygote)
133
Q

What can pluripotent cells become and example of one?

A
  • MOST cell types e..g inner cell mass of blastocyst
134
Q

What can multipotent cell types become and what is an example of one?

A
  • Lineage restricted

e. g. Embryonic germ layers

135
Q

What can unipotent cells become and what is an example?

A
  • One cell type

e. g. RBC, neuron

136
Q

Which stage of lineage specific gene expression is gene expression the highest in?

A
  • Highest in the unipotent stage
137
Q

What is cleavage defined as?

A

“period of RAPID cell DIVISION (without growth) after fertilisation”

138
Q

What are individual cells called after fertilisation and in development?

A
  • Blastomeres
139
Q

What happens when the blastomeres reach the 8 cell stage (what process do they undergo)?

A
  • they undergo COMPACTION
  • tightly joined via E-cadherin then divide to form MORULA
  • Inner cells move to one side then cavity forms (blastocyst –> inner cell mass + trophoblast)
140
Q

What is the inner mass a source of?

A
  • ES cells
141
Q

What is an example of cell lineage specification?

A
  • When cells of the embryo make decision to form inner cell mass or trophoblast
142
Q

What are the two hypotheses that give idea of how cells decide whether to form a trophoblast or inner cell mass?

A
  1. Inside out hypothesis

2. Cell polarity model

143
Q

What occurs in the ‘inside out hypothesis’?

A
  • Those cells that are on outside when dividing (physical forces) become trophoblast and cells on inside become inner cell mass
144
Q

What occurs in the ‘cell polarity model’?

A
  • If cells are parallel to the zona pellucida (protective layer around the blastoderm) surface, they become TROPHOBLAST and if the cell division is perpendicular to the zona pellucida, they become inner cell mass
145
Q

What are pluripotent factors that make the inner cell mass pluripotent?

A
  • OCt4, NANOG, and SOX2! (trancription proteins)
  • these stop the cells from dividing
  • When the genes are expressed, they form proteins Oct4, Nanog and Sox2
146
Q

What form of strucutres does immunostaining detect?

A

Proteins

147
Q

What does lineage specification in the early blastocyst depend on?

A
  • LOCAL microenvironment of cells that are influencing the expression of TFs (Oct4, Cdx2, Nanog, Gata6)
148
Q

For Oct4, where is the transcription factor expressed in the blastocyst and what is the pattern of expression?

A
  • In the INNER CELL MASS (Cdx2 downregulated)

- Expression pattern is uniformly spread

149
Q

What is Oct4 repressed by in the outer cells of the blastocyst?

A
  • Repressed by Cdx2
150
Q

What does Oct4 inhibit expression of in the inner cell mass?

A

Inhibits expression of Cdx2 in the inner cell mass

151
Q

What is Cdx2 expression like in the 8 cell stage?

A
  • Stochastic (unpredictable)
152
Q

Where is the Cdx2 expression limited to in the morula stage?

A

– Outer cells

153
Q

Where is the Cdx2 expression limited to in the blastocyst stage?

A
  • Cdx2 expression in trophoblast specifically
154
Q

What is Nanog expression like in the 8 cell stage?

A
  • Stochastic
155
Q

What is Nanog expression like in the blastocyst stage?

A
  • Nanog has a ‘peppered’ expression in the inner cell mass –> epiblast -becomes embryo proper
156
Q

What is Gata6 expression like in the 8 cell stage?

A
  • Stochastic
157
Q

Where is Gata6 epxression limited to in the morula stage?

A

-the inner and outer layers

158
Q

What causes the repression of Nanog cells to not be expressed where Gata6 is?

A
  • Grb2
159
Q

Where is Gata6 expression limited to in the Balstocyst stage?

A
  • Gata6 “peppered” expression in the INNER CELL MASS –> hypoblast becomes the yolk sac (taken over by placenta in humans)
160
Q

What can the hypoblast be called?

A
  • Visceral/ primitive endoderm –> it is displaced by the first cells migrating from the proper endoderm
161
Q

What shape is the mouse embryo compared to the human embryo?

A
  • Mouse embryo is cup shape whereas human embryo is flat disk shape
162
Q

What are the two signalling centres that are in the early mammalian blastocyst?

A
  1. Specialised group of cells in hypoblast (AVE–> Anterior Visceral Endoderm in mouse)
  2. PRIMITIVE streak
163
Q

What is a signalliong centre?

A
  • Groups of cells releasing growth factors that influence the behavior of other cells
164
Q

Where does the primitive streak form opposite?

A
  • Forms opposite side to the AVE

- AVE sends signals to allow the Primitive streak to form opposite it

165
Q

What does BMP4 (bone morphogenic protein) do?

A
  • Instructs the EPIBLAST cells to make Wnt and Nodal signalling moleucles
166
Q

where does BMP4 come from?

A
  • Somewhere other than the embryo
167
Q

How does the primitive streak form? (inductive signals)

A
  • BMP4 acts on epiblast cells to make Wnt + Nodal (signalling molecules)
  • AVE (from hypoblast) causes production of Lefty1 + cerebrus in EPIBLAST
  • they RESTRICT Wnt and Nodal to other end (posterior-right pole)
168
Q

which two signalling molecules are secreted at the anterior end of the epiblast?

A
  • Noogin and Chordin
169
Q

What is the TF that is expressed at the anterior end of epiblast?

A
  • Goosecoid
170
Q

What are the signalling molecules that are expressed at the posterior end of the epiblast?

A
  • Nodal, Wnt, FgFs
171
Q

What is the TF that is expressed at the posterior end of epiblast?

A
  • Brachyury
172
Q

What are 3 things that the Anterior Visceral Endodoerm does (AVE)?

A
  1. Key signalling centre in the late blastocyst
  2. Establishes anterior-posterior axis
  3. Dictates where the primitive streak will form
173
Q

What are 3 things that the primitive streak of the epiblast does?

A
  1. Initiates gastrulation and embryonic germ layer formation
  2. HELPS establish anterior-posterior axis
  3. regulates L-R assymetry
174
Q

What does the anterior-posterior axis during gastrulation involve?

A
  • Concentration gradients of signalling molecules
175
Q

What is the primitive node?

A
  • DYNAMIC mass of cells at ANTERIOR tip of streak
176
Q

What do cells that migrate through the primitive node form?

A
  • ANTERIOR part of notocord
  • Parts of the neural tube
  • Head structures
177
Q

What is the FgF gradient due to?

A
  • mRNA decay as cells divide from tip
178
Q

From which structure does the embryo develop?

A
  • Epiblast
179
Q

What does the trophoblast form? (two parts)

A
  • Cytotrophoblast
  • syncytiotrophoblast
  • Makes the fetal part of the placenta
180
Q

What does the inner cell mass form?

A
  • Embryonic disk (epiblast–> embryo + amnion and hypoblast–> yolk sac)
181
Q

What is regulative ability?

A
  • Produce normal structures of tissues even if some cells are removed e.g. identical twins
182
Q

Which cells can show regulative ability?

A
  • Cells of the early embryo
183
Q

What does the ectoderm give rise to?

A
  • Epidermis of skin and sweat glands and their hair follicles
  • Nerves (brain and CNS) + eyes
  • Pituitary gland and adrenal medulla
  • jaws and teeth
  • Neural crest cells (craniofacial bones and cartilage peripheral nerves )
184
Q

What does the mesoderm give rise to?

A
  • Skeleton and muscle
  • Circulatory and lymphatic systems
  • Excretory and repro systems (except germ cells)
  • Dermis of skin
  • Adrenal cortex
185
Q

What does the endoderm give rise to?

A
  • Epithelial lining of digestive tract and organs (liver, pancreas)
  • Epithelial lining of respiratory, excretroy and resproductive tracts
  • thymus, thyroid and parathyroid glands `
186
Q

What is organogenesis?

A
  • Differentiation of tissues from the 3 germ layers and arrangements into organs
187
Q

Which 4 tissue types do the 3 germ layers give rise to?

A
  1. EPITHELIUM (endo (gut lining) meso (kidney cortex), extoderm (skin) )
  2. CONECTIVE TISSUE (mesoderm–> collagen, bones)
  3. MUSCLE (mesoderm)
  4. NERVES (ectoderm)
188
Q

What is neurilation?

A
  • The formation of the neural tube
189
Q

What is the notocord?

A
  • Forms towards the end of gastrulation (solid rod of msoderm)
  • Sends inductive signals to neighboring ectoderm to form the NEURAL TUBE
190
Q

What does the notocord send inductive signals to form the neural tube via?

A
  • SONIC HEDGEHOG
191
Q

What does the sonic hedgehog signalling from the notocord cause the ectoderm to form?

A
  • Causes the ectoderm to fold up and form the NEURAL GROOVE –> then folds over to form the NEURAL TUBE
192
Q

What is the neural tube?

A
  • FUTURE BRAIN
  • forms the neural plate via neurilation
  • grows in a cranial to caudal direction
193
Q

Which type of signalling occurs in the induction from the notocord to form the neural tube (neurilation)?

A
  • Sonic hedgehog signalling

BMS2021 (7 decks)

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