Concepts And Terminology Flashcards

1
Q

Remind yourself of the basic points

A
  • Embryo implants at blastocyst stage (between 32 and 64 cells)
  • Blastocyst has 2 layers = trophoectoderm and embryoblasts
  • Trophoblasts consist of cytotrophoblasts which form syncytiotrophoblasts which invades the decidua to form placenta
  • Embryoblast forms epiblast and hypoblast
  • Epiblast becomes embryonic epiblast which gives rise to embryonic ectoderm and primitive streak (which involutes to form embryonic endoderm and embryonic mesoderm)
  • Hypoblast becomes extraembryonic ectoderm then yolk sac
  • Development is determined by restriction of cell fate.
  • Once the blastocyst differentiates into trophoblasts and embryoblasts, the cells are committed. They cannot switch (this is a general rule but there are some exceptions)
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2
Q

How is cell fate controlled? What are the 2 possibilities?

A
  • Controlled by molecular changes
  • There are 2 possibilities
  1. Mosaic development (cell autonomous specification):
    - instructions/information are inherited from parent cell hence cell’s fate is pre-determined
  2. Regulative development (conditional specification):
    - cell isn’t committed to a particulate fate, instead it is influenced by its surrounding/positions within embryo.
    - the cell initially has the potential to become any type of cell
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3
Q

What did Weismann’s nuclear development?

A
  • Proposed that nuclear determinants are unevenly segregated during cleavage
  • E.g in the diagram, you can see the determinants go into different cells so each daughter cell has different nuclear determinants hence their cell fate will be different
  • Represents mosaic development

(The one about nuclear/maternal determinants)

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4
Q

What did Roux’s experiment on determination state?

A

-He tested Weismann’s theory and mosaic development using frogs

  • He ablated one cell (but not remove) of a 2 cell embryo - this resulted in half an embryo which supports the mosaic development
  • However, this was not the correct interpretation of the results
  • When the experiment was repeated, but the 2 cells of the embryo were separated than being ablated, you get 2 perfect tadpole embryos
  • This supports regulative development
  • It was able to regulate and develop without any missing parts
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5
Q

What is invariant cell fate in C.elegans?

A
  • C.elegans = nematodes
  • They are used to study embryonic development
  • They are completely transparent so we can see every single cell within embryo
  • Everytime you observe a C.elegans embryo, they follow the same developmental pattern
  • We start off with one cell which divides into 2 which have known cell fates
  • The cells divide into other cells with different cell fates but these cell types are always the same
  • By the time the embryo is fully developed, there are 558 cells; each can be traced back to a specific origin, it never varies —> suggests mosaic development
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6
Q

How did Driesch demonstrate regulative development?

A
  • An intact 4-cell sea urchin embryo generates normal pluteus larva
  • When the 4-cell embryo is removed and each cell is isolated, each cell can form a smaller but normal pluteus larva

-The 4 larvae derived this way were not identical despite their ability to generate all the necessary cell types

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7
Q

What are development and decisions based on?

A
  • Both mosaic model and regulative development
  • Also more complex interactions exist and provide combinations of these 2 —> these allow robustness in embryonic development

A theoretical example:

  • normally, the initial cell gives rise to 2 cells - one which forms skin and head tissue; the other would give rise to trunk and tail
  • if we ablated a cell at 2-cell stage and mosaic development was the sole method of controlling cell fate, the embryo would develop either skin+head tissue or trunk+tail - not both
  • if we ablated a cell at 2-cell stage and regulative development was in charge of controlling cell fate, the embryo would overcome the issues and all tissues would be present (as cells don’t have a predetermined fate)

An experiment in C.elegans:

  • in the embryo, the pharyngeal tissue usually develops from the Aba cell, with its sister cell Abp giving rise to trunk and tail
  • When the position of Aba and Abp are exchanged, the tissues they give rise to swap as well - Aba give rise to trunk and tail; Abp give rise to pharyngeal tissue
  • This implies that the position of a cell within the embryo determines its fate - this is regulative development as the cells do not have a predetermined fate

(In the diagram, Aba and Abp are connected to a P cell in a different way, so it’s the interaction with the P cell which is responsible for regulation of development)

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8
Q

What are the decisions of fate and commitment?

A
  • Fate = what will normally happen to a cell during development
  • Committment = specification (what tissues will develop in an autonomous environment). Determination (irreversible change in potential). When a cell is determined, it’s committed to a certain fate
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9
Q

What are the definitions of potential/potency and differentiation?

A
  • Potential/potency = range of tissue which a cell can give rise to
  • Differentiation = restriction of potential with molecular and biochemical changes (describes the transition to a mature cell type)
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10
Q

How do you test fate and committment?

A
  • If you take a piece of tissue from an early embryo labelled with a dye, and then you graft it into an unlabelled host embryo at different times and locations, we see different effects
  • If we graft it into the same place at the same time or to a different location, the embryo will develop as normal and the cell will have normal fate
  • If we take a graft from a later embryo, normal development will not occur because determination would have already occurred
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11
Q

What is induction?

A
  • Restriction in potential depends on inductive interactions from neighbouring cells
  • Competence = ability to respond to inductive signal
  • Spermann and Mangold did an experiment that demonstrated cell-cell communication is important for regulating cell fate; one group of cells can act as an ‘organiser’ of embryonic pattern formation
  • Hensen’s node plays this role in the primitive streak
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12
Q

What are the 2 types of inductive interactions?

A
  • Permissive induction
  • Instrcutive induction
  1. Permissive induction
    - where tissues create an environment where other factors can then act to induce changes
  2. Instructive induction
    - oppositional and morphogen gradient
    - Appositional induction = instruction is passed by coming together of 2 tissue types
    - Morphogen gradient = a localised signal is crested and diffuses outward. Different concentration along the morphogen gradient induce different responses
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13
Q

What is a morphogen?

A
  • Diffusible molecule that triggers different cell fates at different concentrations e.g transcription factors
  • Different concentrations induce different cells
  • Can provide positional information within embryo
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14
Q

What are HOX genes?

A
  • They confer positional identity
  • Mutation of the annapedia gene (member of HOX family) causes Drosophila antennapedia mutants to have legs instead of antennae on their heads
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15
Q

What are homeotic genes?

A

-Regulate development of anatomical structures

  • In a theoretical animal, a morphogen gradient specifies 4 distinct segments
  • Morphogen concentration is highest at caudal end compared to cranial end
  • The morphogen induces the expression of all 3 genes
  • At the highest levels (tail/caudal end), all 3 genes are expressed
  • At lower concentrations of morphogen, genes 1 and 2 are expression
  • At even lower concentrations, just gene 1 or no genes are expressed

-If we alter the morphogen gradient, we alter gene expression in different regions and alter the phenotypic identity of the segment

  • Without knowing the identity of certain genes, we can begin to deduce their functions and how they interact
  • E.g we can determine which gene is important for which segment
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16
Q

What are complex patterns from simple rules?

A
  • Turing proposed that there is a diffusible activator that activates a diffusible inhibitor of itself
  • So as the activator concentration reaches a certain amount, the inhibitor is produced, preventing more activator production
  • This then inhibits the inhibitor production
  • Now the activator can return

-Turing also suggested that changing concentrations of activator/inhibitor and surface area leads to production of different patterns

17
Q

What happens in gene organisation?

A
  • Morphogens regulate genes
  • Upstream of genomic DNA, there is regulatory region (containing introns and exons)
  • At the start of genomic DNA, there’s the transcriptional start site
  • Regulatory region recruits RNA poly II to start transcribing
  • Primary transcript is formed which contains introns and exons
  • Secreted factors and other signals allow cells to communicate
  • Individual transcription factors don’t act alone so their effects can vary in different cell types
  • There are also additional control at the level of translation, post-translation and epigenetic changes
  • Primary transcript is spliced, called and polyadenylated to create mRNA
  • This is translated to protein except 5’ and 3’ UTRs
18
Q

What are gene regulatory networks?

A
  • Transcription factors don’t work alone, they interact with each other in large gene regulatory networks
  • E.g if we have 3 genes (A, B and C) and we inactivate A, we can compare the expression pattern to that when all 3 genes are active
  • Normally genes A and C are expressed and gene B is not
  • However, when we inactivate gene A, we find that gene B is expressed and C is no longer expressed
  • We can use that to workout the regulatory network:
  • Gene A is constitutively expressed
  • Gene A activates gene C expression
  • Gene A represses gene B expression