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preimplantation Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what are the 6 basic steps of development?

A

fertilisation, cleavage, blastocyst, gastrulation, neuralation, organogenesis

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2
Q

what does the ectoderm form?

A

skin, nervous system

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3
Q

what does the mesoderm form?

A

muscle, blood, organs, bone

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4
Q

what doe the endoderm form?

A

gut lungs pancreas

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5
Q

what does ingression involve?

A

cells migrating through the primitive steak and node to form the mesoderm

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6
Q

what is conditional specification?

A

the fate of a cell being induced via cell to cell signalling

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7
Q

what is autonomous specification?

A

the fate of a cell being determined by molecular components within the cytoplasm

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8
Q

what are 3 signalling mechanisms?

A

diffusion, cell contact, gap junctions

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9
Q

what is a neuroblast?

A

a stem cell in dros. cells from the ectoderm which delaminate to become neural stem cells. there fate is determined by whether the initially produce more achate scute that the surrounding cells, this causing a positive feedback system in which they suppress the others, increasing the superiority in secretion

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10
Q

what are the stages of cell lineage?

A

totipotent, specification, determination, differentiation

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11
Q

what is the simple time line for an oocyte?

A

released from the ovary, travels down oviduct where it is fertilised, release from zone pellucida, implanted

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12
Q

how long does it take for a mouse egg to implant?

A

4.5 days

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13
Q

what is the role of the zone pellucida?

A

prevents the egg from implanting in the oviduct and causing an ectopic pregnancy

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14
Q

how long does it take for the first cell division to occur in the mouse embryo?

A

1.5 days (very slow)

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15
Q

how long does it take to reach the 8 cell stage in a mosque embryo?

A

2 days

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16
Q

how long does it take for a mouse embryo to become a morula?

A

2.5

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17
Q

how long does it take for murine egg to become a blastocyst?

A

3.5

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18
Q

what is the difference between a morula and a blastocyst?

A

morula is solid ball of cells but a blastocyst is hollow and contains a blastocoel

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19
Q

until what stage is the morula loosely organised?

A

8 cell stage

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20
Q

what happens at the 8 cell stage to the morula?

A

compaction

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21
Q

what occurs during compaction

A

cell surface molecules such as cadherins become expressed. which causes cell to cell contact to greatly increase, microvilli also form, holding the cells together so that fluid can’t enter the embryo.

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22
Q

how do cells communicate after compaction?

A

via gap junctions

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23
Q

after compassion how does the blastocoel form?

A

the external layer of cells are polarised along their apical to basolateral axis, this means that they are able to pump sodium into the centre of the embryo, which pulls water with it through water potential (?)

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24
Q

what is the phenotype of the external cells not long after the blastocyst has formed? what about the internal cells?

A

the cells become flatteend and large- they will become the trophectoderm. the internal cells for the inner cell mad which will form the epiblast or the primitive endoderm

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25
Q

what will the trophoblast become?

A

the chorion which is the embryos part of the placenta

26
Q

what genes do the trophoectodrm cells express?

A

cdx2 and eomesodermin

27
Q

what genes do all ICM cells express?

A

Oct4

28
Q

what is the role of Oct4

A

supressed cdx2 and eomesodermin- preventing the development of TE cells inside the cell

29
Q

what is the action of cdx2?

A

it suppressed oct4

30
Q

what are the two subgroups of gene expression within the ICM?

A

the primitive endoderm expresses GATA6 and sox 17

the epiblast expresses Nano and stat3 and sox 2

31
Q

what is the interaction between the genes in the epiblast and those in the primitve endoderm?

A

GATA6 represses Nanog it also induces GCNF which represses OCT4. nano represses GATA6

32
Q

up until what point are all cells in the embryo totipotent ?

A

8 cell stage- can form chimeras

33
Q

what ar the two cell fat decision that the mouse embryo must induce before implantation?

A

segregation of the trophoectoderm and inner cell mass

segregation of the epiblast from the primitive endoderm

34
Q

what does the primitive endoderm form?

A

the amnion- extra embryonic

35
Q

what are the two theories depicting how the trophoectoderm differentiates from the inner cell mass?

A

polarisation model and the inside out model

36
Q

what is the polarisation model?

A

polarisation occurs before compaction, this laters the distribution of cytoplasmic determinants and that this asymmetric distribution determines cell fate

37
Q

what must be proved in order for the polarisation model to be true?

A

the inner cell mass cells must result from an asymmetric division from an external cell.

38
Q

what is the inside out model?

A

that the trophoectoderm is patterned based on the microenvironment that they are exposed to and the cytoplasmic determinants determine the cell fate

39
Q

what is the support for the inside out model?

A

he environemtn that the cell is exposed to determines its fate: if this is true then you should be able to move inside cells to the outside and it will become TE and vice versa- 97% of cells no matter where they were from, when put on the outside because TE. however for the other way round it is only 60%. which isnt as conclusive but the experimenters argue that some may slip bak out to the outside and not remain on the inside
need to know what the signalling molecule is. developmental genetic support for inside out model: TEAD4 mutants lack cdx2 expression from trophoectoderm fails to develop. Tead 4 regulates CDx2 expression. how does it do this? needs a cofactor called yap. TEd4 initially in cytoplasm and if it was able to bind to yap then would go into the nucleus and cause cdx2 expression. (how could this be measured.
yap and lats are part of the hippo signalling pathway
hippo is a transmembrane receptor- when it binds to ligand, lats phosphorylates yap which allows it to be degraded via ubiquitination- so when hippo is activated it yap cant bind to the Tead4 and cause cdx2 expression
why is hippo stimulated in inside cells- hipp is actiavted by cell contact- seen in tumours because cell contact prevents cell division - on the inside of the embro there is a lot of cell contact but on the otuside cells there isnt a lot of cell contact- long and flat

40
Q

what is the hipp pathway and why is it relevant?

A

supports the inside out theory that the trophoblast and inner cell mass are determined by their micoenvironements. hippo is a transmembrane receptor- when it binds to ligand, lats phosphorylates yap which allows it to be degraded via ubiquitination- so when hippo is activated it yap cant bind to the Tead4 and cause cdx2 expression.

41
Q

what is the hipp pathway and why is it relevant?

A

supports the inside out theory that the trophoblast and inner cell mass are determined by their micoenvironements. hippo is a transmembrane receptor- when it binds to ligand, activates lats. lats phosphorylates yap which allows it to be degraded via ubiquitination- so when hippo isnt activated, yap can bind to the Tead4 and cause cdx2 expression.

42
Q

what is the support for the inside out model?

A

he environemtn that the cell is exposed to determines its fate
need to know what the signalling molecule is. developmental genetic support for inside out model: TEAD4 mutants lack cdx2 expression from trophoectoderm fails to develop. Tead 4 regulates CDx2 expression. how does it do this? needs a cofactor called yap. TEd4 initially in cytoplasm and if it was able to bind to yap then would go into the nucleus and cause cdx2 expression. (how could this be measured.
yap and lats are part of the hippo signalling pathway
hippo is a transmembrane receptor- when it binds to ligand, lats phosphorylates yap which allows it to be degraded via ubiquitination- so when hippo is activated it yap cant bind to the Tead4 and cause cdx2 expression
why is hippo stimulated in inside cells- hipp is actiavted by cell contact- seen in tumours because cell contact prevents cell division - on the inside of the embro there is a lot of cell contact but on the otuside cells there isnt a lot of cell contact- long and flat

43
Q

what is the hippo pathway and why is it relevant?

A

supports the inside out theory that the trophoblast and inner cell mass are determined by their micoenvironements. hippo is a transmembrane receptor- when it binds to ligand, activates lats. lats phosphorylates yap which allows it to be degraded via ubiquitination- so when hippo isnt activated, yap can bind to the Tead4 and cause cdx2 expression.

44
Q

what could be done to test the inside out theory?

A

: if this is true then you should be able to move inside cells to the outside and it will become TE and vice versa- 97% of cells no matter where they were from, when put on the outside because TE. however for the other way round it is only 60%. which isnt as conclusive but the experimenters argue that some may slip bak out to the outside and not remain on the inside

45
Q

how is the second cell fate decision made?

A

it was always assumed that the differentiate between the epiblast and the primitive endoderm was the micoenvironemnt- the blastocoel. however, this is not the case- labelling of the respective genes in each cell type found that they were randomly distributed amongst the ICM.

46
Q

what experiment showed how the second cell fat decision was made?

A

when you use gene expression probes- you seen that in early blastocysts all cells are mixed up together this would not happen in microenvironment model was true at around 3.5 they are random and by 4.5 they are organised in a epiblast primitive endoderm way.
stochastic model: proposed that initially you get randomly cells that produce more nanog or gata6. then cells that were in the wrong place would move to the right location or die.
there are variants

47
Q

what is disputed about the inside out theory?

A

how stochastic the cell fate is:
time outside-time inside model: when cells decide to go in was a factor of whether they were more likely to become epiblast or primitve endoderm
the first cells to internalise 8-16 cell stage tend to be epiblasr (nanog) or bipotent (both)
where as cells that internalise later (16-31 cell stage) start to express gata6 and become prE.
however these studies are quite hard to do
they both find different things in their small sample sizes.
whether this is an artefact of the experimental set up

48
Q

what is elf5 implicated in?

A

TE patterning and supports the expression of cdx2 and Eomesodermin

49
Q

make sure read the facts from the essay plan

A

…

50
Q

what theory of how the PE and epiblast are formed in similar to the inside out model?

A

the theory that all the cells within the inner cell membrane are homogenous and then differentiate depending in the microenvironment that they are exposed to- the PR because it is facing the blastocoel

51
Q

what are 4 pieces of evidence that the ICM is not a heterogenous environment?

A
  • a subset of ICM cells express the extra embryonic lineage-specific cytokeratin ENOD-A
  • lineage specific markers for EPI and PE are expressed in non overlapping regions of in the ICM in early blastocysts before segregation
  • individual ICM cells have distinct empi like or Pe link gene expression- salt and pepper
  • labelled ICM cells can contribute to either PE or empi but not both
52
Q

what receptor is associated with gata 6 expression? what is the evidence for this? what does this implicate

A

fibroblast growth factor family of receptor tyrosine kinases. in garb mutant mice PE fails to form: grb2 encodes an sh2/sh3 adaptor protein- implicating Ras, MAP kinase pathway in gata6 expression

53
Q

when are the two different periods of cell production in the ICM?

A

8-16 , 16-32

54
Q

what is the theory about the length of time that a cell spends in the inner cell mass?

A

the less time spent out the outside, and the longer spent on the inside is supportive for pluripotency: cells internalised in the first wave up regulate expression of pluripotency transcription factor Sox2

55
Q

what does the first wave if cells internalised do in terms of gene expression and how doe this implicate the cell fate

A

cells internalised in the first wave up regulate expression of pluripotency transcription factor Sox2- they will become epiblasts

56
Q

what is a piece of evidence that supports the timing-inside, timing outside theory of the second cell fat decision?

A

if a ‘surplus’ of inner cells is generated by the 1st wave, these can differentiate to ultimately form PE. But it is much less typical for inner cells from the 2nd wave, already biased to form PE, to eventually contribute EPI. This suggests that the time a cell spends on the outside of the embryo and therefore its extent of cell polarisation/differentiation is inversely related to the degree of pluripotency and the ability to provide future EPI progenitors

57
Q

what is the apical polarity complex?

A

par3, par 6 and PKC- thought to control microtubule organisation and excludes basolateral portions such as lgl from the apical pole

58
Q

how is is thought that the polarisation complex becomes localised in the apical pole?

A

via cadherins- par6 doesn’t become localised when cultured in a calcium free environment

59
Q

what is thought to happens to cells that don’t inherit the polar complex?

A

become apolar- icm

60
Q

what is the link between the apical complex and polarity thought to be?

A

somehow mediates cdx2 transcription -those that don’t inherit it don’t inherit cdx2 expression- icm

Biology of development (6 decks)

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