Cleavage Flashcards

1
Q

early stages in human development

A
fertilized egg = zygote
2 cell stage
4 cell stage
11 cell stage morula
blastocyst
late blastocyst
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2
Q

post-fertilization events of the zygote

A
  1. becomes metabolically active
  2. cleavage = mitosis
  3. travels down oviduct – takes days
  4. loses zona pellucida before implantation
  5. implantation
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3
Q

zygote does mitosis to become 8 cell embryo, ______ continues and ______ occurs

A

cell division
compaction

note zona pellucida is still intact here

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4
Q

4 days post fertilization, _____ is transported into ? and results in the formation of a ?

A

water
ball of cells = morula 16 cells

blastocoel - the result of cavitation

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5
Q

blastocoel formation requires?

A

Na/K ATPase transporters

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6
Q

when is the embryo referred to as a blastocyst?

A

58 cell stage

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7
Q

features of the blastocyst

A
  1. zona pellucida
  2. large central blastocoel
  3. consists of 2 cell types
  4. polarized
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8
Q

what are the cell types in the blastocyst?

A

outer cells = trophoblasts

inner cells = inner cell mass

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9
Q

trophoblasts

A

form extraembryonic structures such as the placenta

outer cell layer of blastocyst

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10
Q

ICM

A

forms embryo proper plus some extraembryonic structures

inner cell mass of blastocyst

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11
Q

what causes polarity of the blastocyst?

A

because of the eccentric placement of blastocoel and inner cell mass

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12
Q

embryonic pole vs. abembryonic pole

A

pole of the blastocyst where ICM is located

pole marks opposite pole

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13
Q

control of cleavage

A

maternal genes til 2 cell stage

embryonic genome control by 4 cell stage

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14
Q

what is methylation?

A

addition of methyl groups to specific DNA regions

inactivates genes
including some enhancers/promoters

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15
Q

methylation cycle

A
  1. mature eggs/sperm highly methylated
  2. demethylation of ma/pa genomes shortly after fertilization
  3. remethylation of ICM
  4. levels fall after primordial germ cells enter genital ridges
  5. remethylation late in gemetogenesis
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16
Q

remethylation occurs later is gametogenesis and may lead to ?

A

maternal/paternal imprinting

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17
Q

what does polarization of blastomeres cause?

A

at 8-16 cell stages creates recognizable apical and basal surfaces

determines whether cells are destined for ICM or outer layer

18
Q

what are the 2 theories of polarization?

A

inside-out hypothesis

cell polarity model

19
Q

inside-out hypothesis

A

fate of blastomere is determined by its position w/in the embryo

not from intrinsic properties

20
Q

cell polarity model

A

–depends on plane of cell division during cleavage

–cleavage plane parallel to outer surface of embryo = can become either

–cleavage plane perpendicular to outer surface of embryo = only trophoblast destiny

21
Q

developmental potential =

A

potency

potency is greater than fate

22
Q

genes involved in differentiation?

A

cdx-2
oct-4
nanog
sox2

23
Q

Cdx-2

A

essential for trophoblast cell differentiation

antagonistic to oct-4

24
Q

Oct-4

A
  1. expressed by oocytes and zygotes
  2. required for cleavage
  3. expressed in all morula cells
  4. role in maintenance of undifferentiated cells

w/o this inner cells become trophoblasts

25
Q

Nanog

A
  1. produced by ICM
  2. maintain integrity of ICM
  3. w/o this inner cells become endoderm
26
Q

Sox2

A

first expressed in 8 cell stage

along w/ oct4, helps control regulation of genes involved in differentiation

27
Q

define genomic imprinting

A

is differential gene expression depending on whether a chromosome is inherited from ma or pa

certain genes derived from egg differs from expression of same genes derived from sperm

28
Q

what causes genomic imprinting ? examples

A

due to DNA methylation differences in sperm and eggs

ex. prader-willi and angelman syndromes

29
Q

parental imprinting

A
  1. occurs during gametogenesis
  2. involves methylation
  3. imprinted genes can be maintained for life
30
Q

relate imprinting and rounds of gametogenesis

A

imprinting is erased and reestablished w/ each round of gametogenesis

31
Q

Prader-Willi Syndrome

A
small hands and feet
short
poor sexual development
retardation
usually obese

mutation always inherited from father – deletion long arm chr15

32
Q

Angelman Syndrome

A

exhibit frequent laughter
uncontrolled muscle mvt
large mouth
unusual seizures

mutation always from mom
deletion long arm chr15

33
Q

X inactivation

A

occurs in humans in first few weeks of development

once inactivated it remains that way in all daughter cells then on

brought about by xist gene

34
Q

XIST gene

A

X inactivation specific gene

located on x chr

produces RNA molecule that coats X chr and induces inactivation

35
Q

RNA coat X chr

A

causes:

  1. removal of acetyl groups from histones
  2. methylation of histones
  3. alteration of histone composition
36
Q

_____ region escapes X inactivation

A

pseudoautosomal

37
Q

Barr body

A
  • -found by murray barr

- -mary lyon proposed barr body = inactive x chromosome

38
Q

define regulation

A

refers to ability of embryo to compensate for removal of structures or for addition of structures

39
Q

list experimental methods

A
  1. chimeras or mosaics
  2. fate mapping
  3. totipotency
  4. production of tetra - hexparental embryos
  5. production of interspecies chimeras
  6. deletion/ablation exp.
  7. addition exp.
  8. transgenic embryos
  9. knock-out experiments
40
Q

need book for further definition reviews

A

clinical correlation 3.2