Concepts and Language of Development Flashcards

(53 cards)

1
Q

How is polyspermy prevented after the sperm penetrates the zona pellucida?

A

sperm enters oocyte - biochemical changes are triggered in the zona pellucida’s coat proteins
- alters structure = prevents additional sperm from penetration

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2
Q

what features define the one-cell zygote stage post-fertilisation?

A
  • two unfused pronuclei (one from sperm, one from oocyte)
  • surrounded by zona pellucida
  • fluid-filled perivitelline space with one/two polar bodies
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3
Q

What are polar bodies and when are they produced?

A

polar bodies = small, non-functional cells formed during asymmetric divisions in oogenesis
- first polar body forms after meiosis I
- second polar body forms only if fertilisation occurs and meiosis II is completed

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4
Q

Why do polar bodies contain little cytoplasm?

A

asymmetric meiosis division - most of the cytoplasm is retained in the oocyte to support early embryo development

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5
Q

What happens to the size of cells during early cleavage?

A

total size of the embryo stays the same due to the rigid zona pellucida, so each mitotic division results in smaller cells

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6
Q

what is compaction? when does it occur?

A

around 12-16 cell stage (morula)
- outer cells flatten and tightly adhere to form an epithelial barrier, setting up for blastocoel cavity formation

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7
Q

what characterises the blastocyst stage?

A

(day 4/5) - fluid-filled cavity (blastocoele) forms
- outer epithelial layer of trophoblast cells
- inner cell mass that will form the embryo

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8
Q

What must occur for implantation to take place?

A

zona pellucida must be enzymatically shed (hatching) - allows the blastocyst to interact with and embed into the uterine wall

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9
Q

What do trophoblast cells contribute to after implantation?

A

begin differentiating into structures that will form the placenta (extra-embryonic structures)

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10
Q

What is formed from the inner cell mass after implantation?

A

bilaminar embryonic disc (epiblast & hypoblast)

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11
Q

What is the primitive streak and why is it important?

A

midline structure that forms from the caudal end, where epiblast cells migrate and differentiate—this initiates gastrulation and germ layer formation

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12
Q

what role does Henson’s node play?

A

signalling centre - secretes growth factors to r regulate behaviour of migrating cells during gastrulation

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13
Q

How are the three germ layers formed during gastrulation?

A

gastrulation = bilaminar embryonic disc (epiblast and hypoblast) transforms into a trilaminar disc with three distinct germ layers (ectoderm, mesoderm, and endoderm)

  1. primitive streak forms from caudal/posterior end
    - extends anteriorly along embryo midline (establishes body axes & site for cell migration)
  2. Henson’s node as signalling centre (anterior end of PS)
    - secretes growth factors (Wnt, Nodal, BMP antagonists)
    - Wnt & Nodal promote primitive streak formation, cell migration, mesoderm specification
    - BMP antagonists inhibit BMP = promote neural and mesodermal fates.
    - directs differentiation and movement of epiblast cells during gastrulation
  3. epiblast cells move laterally, converge towards PS & undergo EMT - break cell-cell junctions and transforming into mesenchymal, migratory cells
  4. ingression and formation of the germ layers:
    - first wave of epiblast cells moves through the streak, displaces the hypoblast, and forms the definitive endoderm
    - second wave migrates between the epiblast and the newly formed endoderm, forming the intraembryonic mesoderm
    - remaining epiblast cells that do not ingress become the ectoderm, forming the embryo’s outermost layer
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14
Q

(!!) signals from Henson’s node that influence gastrulation?

A

Wnt, FGFs & Nodal signalling - promote EMT (loss of E-cadherins/cell-cell junctions) & mesodermal specification

BMP antagonists - inhibit BMP; promote neural and mesoderm specification

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15
Q

what is neurulation? what structure does it form?

A

process that forms the neural tube from the neural plate - later develops into the brain and spinal cord

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16
Q

How does the neural tube close?

A

through a zipping mechanism from the middle outward, with cranial and caudal neuropores being the last to close

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17
Q

what condition arises due to failure of the NT to close anteriorly?

A

anencephaly

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18
Q

what condition arises due to failure of the NT to close posteriorly?

A

spina bifida

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19
Q

What does the ‘cloth purse’ model describe in embryology?

A

escribes the folding of the flat embryonic disc into a 3D cylindrical body—like tightening a drawstring purse

forms a closed gut tube, connected to the yolk sac via the vitelline duct and to the developing bladder via the allantois

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20
Q

What is mosaic development? What experiment supports mosaic development?

A

form of development where a cell’s fate is autonomously determined — encoded within the cell itself; unaffected by its environment

Roux (1888): destroyed one cell of a 2-cell frog embryo → surviving cell only formed half an embryo → suggested pre-programmed fate.
- BUT flawed = the dead cell remained in place, possibly interfering with development
- repeated with separation instead - each frog blastomere developed into a full embryo = regulative development confirmed.

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21
Q

What is regulative development? What experiment supports regulative development?

A

cell’s fate & development is influenced by its position, environment, and interactions with neighbouring cells — not predetermined

Driesch: separated sea urchin blastomeres with a hair - each developed into a complete embryo, showing plasticity and environmental influence

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22
Q

is development purely mosaic or regulative?

A

no - most embryos use a combination of both; allows for:
- compensation if something goes wrong
- developmental flexibility
- stronger outcomes

23
Q

what is a fate map? how is it made?

A

labelling a region of tissue and grafting it into the same position in a host embryo - tissue follows its normal developmental path & structure it forms

24
Q

What happens when tissue from later-stage embryos is grafted heterotopically (into a different location)?

A

doesn’t change fate - tissue fate is determined and has an irreversible commitment to a specific developmental path

25
difference between specification and determination?
specification = reversible - fate can change in new environments - earlier cells are specified, not determined determination = irreversible - fate locked in (even with diff signals) - later cells become determined & progressively more restricted
26
What is induction in embryonic development?
process where certain cells/tissues send signals that influence the fate of neighbouring cells seen in organiser activity - send inductive signals to nearby competent cells, induces host tissue to change fate
27
What is an organiser in developmental biology?
region of the embryo that can induce major changes in the fate of surrounding cells — directs axis formation and patterning
28
What is competence in the context of induction?
ability of cells to respond to inductive signals
29
what is permissive & instructive induction - as two major types of inductive interactions?
permissive = inducing tissue provides a supporting environment - doesn't directly instruct cell fate but allows other factors to act instructive = inducing tissue gives specific signals to guide cell fate (more directive)
30
two types of instructive induction - appositional induction & induction via morphogen gradients - what are they?
appositional induction - two tissues in direct contact; one sends signals to other to change fate induction via morphogen gradients - morphogens secreted from a localised source diffuse, form a conc. grad across tissue - different concs = different cell fates (spatial patterning)
31
How does competence change over developmental time?
early cells: highly competent, flexible, responsive to signals later cells: more determined, less responsive - reduced developmental plasticity
32
How are induction, organiser activity, and competence interlinked?
- induction relies on signals from organiser regions - success of induction depends on whether nearby cells are competent - together, they coordinate tissue patterning and fate decisions
33
What is a morphogen? How do morphogens influence positional identity?
**diffusible molecule** secreted from a localized source that **forms a concentration gradient** and induces different cell fates at different concentrations - cells “read” the local morphogen concentration - express different genes depending on the concentration = distinct cell type differentiation
34
What are Hox genes? How do Hox genes contribute to body patterning?
Hox genes = group of homeotic genes, arranged in clusters (Hox A-D); control segmental identity along AP axis activated by morphogen gradients regulate development in specific body regions - mutations can transform one body part into another (homeotic transformations)
35
What happens when a Hox gene is knocked out?
segment it controls may take on the identity of a neighbouring segment - **mispatterning**
36
What happens with constitutive activation of a Hox gene?
all segments may adopt the fate conferred by that gene - **loss of segmental diversity**
37
How are morphogens and Hox genes linked?
morphogens act as upstream signals that establish broad positional identity Hox genes then refine this into specific anatomical structures
38
What is Turing’s reaction-diffusion model?
theory explaining self-organising spatial patterns via: - activator that stimulates its own production and an inhibitor - inhibitor spreads faster and suppresses activator nearby = periodic patterns creates stripes, spots and labyrinth/interlocking patterns
39
What determines the type of pattern formed in reaction-diffusion?
diffusion rates - slow activator, fast inhibitor = stripes - similar diffusion = spots, intricate patterns
40
How do morphogen gradients and reaction-diffusion systems work together?
morphogen gradients provide positional info reaction-diffusion sharpens and refines this into precise spatial patterns - ensures complex 3D organisation of the embryo
41
list 6 factors that affect the first cell fate decision
1. presence of localised maternal determinants + early polarisation 2. Cdx2 mRNA localisation 3. Tead4 and Hippo signalling 4. Oct4 kinetics between fated TE vs ICM cells 5. epigenetic regulation of cell fate 6. expression of fate-specific TFs
42
what TFs are specific to trophectoderm cells?
Tead4 CDX2 Gata4
43
what TFs are specific to ICM cells?
Nanog Oct4 Sox2 Sall4
44
what role does the presence/absence of localised maternal determinants play in early cell fate decisions?
presence of localised maternal determinants = when they're unequally distributed in the oocyte, it leads to asymmetrical inheritance during division - directly specifies different cell fates early on no localised maternal determinants = external influences like sperm entry establish polarity, and cell fate decisions are influenced later by position, signalling, and environment
45
how does cell division at the 8-16 cell stage contribute to cell fate?
outer cells are more likely to undergo symmetrical division = become trophectoderm (TE) cells inner cells often undergo asymmetrical division = form the inner cell mass (ICM)
46
how does Cdx2 mRNA localization affect cell fate?
Cdx2 mRNA is more localized in outer cells = leads to the inheritance of TE characteristics Inner cells receive less Cdx2 due to asymmetric division (one daughter cell inherits more) = inner cells with less Cdx2 tend to develop into ICM cells Cdx2 represses ICM pluripotency TFs (Nanog, Oct4) via mutual inhibition and promotes TE cell fate
47
what is the role of Tead4 and Hippo signalling in trophectoderm (TE) regulation?
polarised outer cells - Hippo signalling pathway suppressed & inactivates kinase complexes upstream - no Yap protein phosphorylation - Yap protein translocates from cytoplasm to nucleus and partners with Tead4 - Tead4 induces expression of TE-specific TFs (Gata4, Cdx2) = mutual inhibition of ICM-specific genes to reinforce TE fate
48
how does cell polarity influence Yap localization in the early embryo?
in polar cells - Yap protein moves from cytoplasm to nucleus to interact with Tead4 and promote expression of TE-specific genes for TE fate in non-polar cells - Yap remains in the cytoplasm, prevents TE-specific gene expression and favouring ICM differentiation
49
how do Oct4 kinetics influence cell fate?
slower Oct4 binding kinetics due to a more open chromatin structure & more accessible Oct4 binding sites = cells favour asymmetrical division & ICM differentiation faster Oct4 kinetics due to less accessible binding sites & chromatin structure = cells favour symmetrical division & TE differentiation
50
what is the impact of histone modification on Oct4 kinetics and cell fate?
higher levels of H3R26me (histone 3 arginine 26 methylation) increase accessibility to Oct4 binding sites = slow Oct4 kinetics = favour ICM differentiation
51
how does DNA methylation regulate TE and ICM fate during the morula to blastocyst transition?
DNA methylation silences TE-specific genes in ICM cells TE cells maintain the expression of TE-specific genes like Cdx2, through mechanisms like the positive feedback loop with Elf5 when Elf5 is unmethylated
52
what effect does Elf5 methylation have on TE cell fate?
Elf5 methylated = Elf5 expression is repressed = prevents activation of TE-specific genes (Cdx2) this stops the positive feedback loop between Elf5 and Cdx2, leading to ICM fate instead of TE fate
53
how do histone modifications differ between TE and ICM cells?
TE cells have histone modifications (e.g. H3K9me2) = promote TE-specific gene expression and repress ICM genes ICM cells have histone modifications (e.g. H3K9me3) = promote pluripotency and repress TE-specific genes