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Developmental Biology > Chp 1&2: Development > Flashcards

Chp 1&2: Development Flashcards

0
Q

Cleavage

A
  • process of creating blastomere (smaller and smaller cells due to division) ->blastula
  • leads to a cavity in all organisms called the blastocoel/blastopore
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1
Q

Fertilization

A

Brings together 2 genomes
Ex: frogs have chemical signal that tells them to produce gametes
Females->produce yolk->zygote

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2
Q

Gastrulation

A

-gastrula
-germ layer formation (3 layers):
Endoderm: lining of intestines/lungs
Ectoderm: skin, nervous system
Mesoderm: skeletal, muscles, parts of organs, blood, becomes gametes
-moving of the blastomeres resulting in the germ layers

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3
Q

Organogenesis

A

-interactions, rearrangements, migrations

Ex: notochord= works as a signal for different tissues -> nervula

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4
Q

Metamorphosis

A
  • larval stage (non sexual) to sexually competent adult

- different depending on group of organism

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5
Q

Germ cell - Gametogenesis

A

-tends to be isolated during development due to the different signals

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6
Q

Development

A

Aristotle 350 BC- used chickens
Limited to multicellular except in yeast cells
Embryology= old name
Continues past gestation (humans late 20s)

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7
Q

3 approaches to dev bio

A

Anatomical
Experimental
Genetic

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8
Q

Anatomical

A

Blastomeres-cells & fate
Comparative embryology - dev diff
Evolution
Teratology- teratogens: result in birth defects
-observe deformities to inform what went wrong
Mathematical- pos. & neg. feedback
-chemical

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9
Q

Ovoviviparity

A

Eggs w/ yolk

Hatch internally

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10
Q

Oviparity

A

Egg layers: birds, frogs, insects, monotremes

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11
Q

Viviparity

A

Placental mammals

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12
Q

After Aristotle …

A

Nothing happens bc of religion

  • William Harvey (1651)
  • late 1600s: Enlightenment->science kicks in
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13
Q

William Harvey

A

“All animals are from eggs”
NO spontaneous generation
Tried to find the mammalian egg
-used deer

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14
Q

1672: Marcello Malpighi

A

Microscopes
-microscopic accounts of chick
How dev. occurs?
-epigenesis -> organs from scratch vs. preformation -> everything is already there, it’s just miniature
-no cell theory, so no limits on how small something was

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15
Q

Kasper Wolff

A

Supports epigenesis

Watches late tissue formation

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16
Q

1820s: several German scientists

A

Germ layers
Microscopes get perfected
-new staining techniques that allowed them to see small structures
*ectoderm, endoderm, mesoderm
-interaction was critical
~of the layers: to know what they’re purpose is
-relationship among early embryos and their structures across species
-the closer related… The longer it takes to distinguish embryos (humans + chimps)
-as dev progresses, characters go from generic -> specific

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17
Q

2 kinds of cells

A

Epithelial - sheets

Mesenchymal - wanderers

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18
Q

Morphogenesis

A

Due to a limited amount of cell activities of cell activities
*where they go + how much they divide can have cell shape change
Mesenchymal-> epithelial-> tube-> sheet

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19
Q

Fate mapping

A

-almost the point where medicine comes in
-end up with cell lineages
Each cell is a daughter
-tunicates
Look like tadpoles as larvae -> bag of goo
Cytoplasm had diff colors BC of germ layers
Test fates by removal of mesodermal cells

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20
Q

Genetic Labeling

A

1920: Hilde Mangold + Hans

Chimeras

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21
Q

Chimeras

A 
2 genetically diff species mixed 
-1st ones done on newts
-chick + quail: easily identified cells 
      >Condensed dna 
      >have specific antigens
      >neural crest cells
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22
Q

Transgenic chimera

A

Today: put in green fluorescent + protein (GFP)

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23
Q

Life Cycles (review)

A 
-Fertilization>hatching=embryogenesis
1 cleavage
2 gastrulation
3 organogenesis 
4 gametogenesis
5 metamorphosis
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24
Q

Cleavage

A

Rapid mitoic division
Zygote> blastula
*volume stays the same

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25
Q

Gastrulation

A

Cell movement resulting in germ layers

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26
Q

Organogenesis

A
  • formation of organs
  • a lot of cell communication
  • some organs = multiple germ layers
  • cells migrate
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27
Q

Metamorphosis

A

-maturity> related to gametogenesis (“not ready”) where germ cells are set aside for reproduction + protected
*fated of cells depends on what they’re next to
>all other cells are somatic (46 chromosomes, go towards creating the body)

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28
Q

Frog Life Cycle

A

-when conditions are good (enough sun, good temps) females will make yolk in the liver which is packed into the eggs
-Fertilization
>germ cells move into the gonads from a hiding spot in the endoderm
-eggs come from oognia
-sperm comes from spermatogonia

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29
Q

Mitosis (in frog)

A

Germ cells from oognia or spermatogonia

Primary oocyte spermatocyte> meiosis(2n->1n) > homologous chromosome pairing shuffling daughters = haploid> 1n - secondary oocytes

-in the egg meiosis stops early + sits in stage of haploid
Until it reaches sperm…egg complete
-nucleus in the egg = “pronucleus”
-nucleus + pronucleus combine to form zygote (2n)
-as sperm hits egg> cytoplasmic rearrangement (change of color, movement)

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30
Q

Cleavage (in frog)

A
  • volume remains the same
  • blastula= 10s of thousands of cells
  • animal pole divides quickly (sm. cells)
  • vegetal pole is slow (large cells)
  • blastocoele forms (fluid cavity)> animal pole
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31
Q

Gastrulation (in frogs)

A
  • sperm entry defines dorsal surface of organism
  • as cells migrate in through blastopore (lip, gray crescent) they become mesoderm
  • the cells outside > ectoderm
  • blastopore becomes neural groove eventually
  • the large yolk-filled cells in the vegetal pole> become endoderm
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32
Q

Organogenesis (in frogs)

A

Mesoderm in the most dorsal
-neural groove
-neural tube> nervous system
Ectoderm above notochord becomes tissue in your spine
Embryo> neurula
Ectoderm grows over the neural tube (birth defect if doesn’t grow)
Mouth & anus form
Muscles form (dev point when start moving, where it hatches)

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33
Q

Cell specification

A

“Presumptive tissue”
1) specification: if put in a neural environment, no signals> follows fate
2) determination: follow fate regardless of environment, irreversible
Ex: tunicate- in the cleavage stage, the 1st blastomeres determine fate

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34
Q

Types of specification

A

1) autonomous >specific blastomeres translates to specific tissues/parts determined by cytoplasmic constituent
*proteins- transcription factors
*mRNA
>fates are invariant
>most invertebrates
2) conditional specificity
-all vertebrates a few invertebrates
-fate is determined by your “friends”(environment)> happens a little later
-little invariant fate assignment
-can frequently switch fates (good thing)
-cell rearrangement> migrations> specificity: *development gets regulated which allows cells to acquire a variety of characters
3) syncytial specificity
-mostly insects (all insects do this)
-localization of cytoplasmic constituants

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35
Q

Genetics

A

-visible mutations on the chromosome lead to the nucleus being determined as holding the info/DNA (variable)

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36
Q

Cell Fates & Cloning

A

-do cells become differentiated?
-easy in the 1950s (thought of in 1890s)
>remove nucleus from oocyte, remove the donor nucleus from cell, transplant donor into oocyte

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37
Q

Somatic nuclear transfer (cloning)

A

1956: King + Briggs
-used tail bud nuclei for a SNT
>result: nothing
-used germ cells nuclei
>result: frog
*establishes that the DNA is being modified/responsible

DNAs fate= determined
Clones= twins

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38
Q

1975: serial Transplantation

A

Took adult frog foot web cells
>ectoderm (skin, nervous tissue)
>very specialized
-do the SNT>embryos>gastrulation
-go into blastula (pregastrulation)>take nucleus + transplant into another oocyte which survives up until tadpole stage then dies
*proved reversible differentiation is potential in all cells

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39
Q

1997: Dolly (sheep)

A

-G1 stage: mammary cells (diff breed) from one sheep
-enucleated an oocyte (in 2nd meiotic phase)
-fused the cells w/ electroshock (used to get the egg cell to believe it was fertilized) in this case>membrane fusion
-did process with 343 cells
>result: 1 Dolly

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40
Q

Totipotent

A

Creat every cell possible

  • no genes have been lost/mutated during differentiation
  • phenotype is not identical
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41
Q

How do you turn on/off genes?

A

1) every cell w/ a nucleus (RBC don’t have nucleus) is the same DNA
2) unused genes are not destroyed so potential for expression exists even if everything’s shut off
3) only a small % of the genome is expressed in a cell
>RNA should be specific

42
Q

Fruit fly gene expression

A

-used polytome chromosomes
-DNA replication but no mitosis 2^9 vs. 512
-150 times the normal amount
-found that regions of the chromosome
>”puff out” when transcribed
-DNA rep. found in salivary glands

43
Q

Other gene expression studies

A
  • confirmed point 3> DNA RNA hybrids

- label DNA or RNA seq of interest and put them in w/ RNA isolated from cell

44
Q

Diff. Gene Expression Techniques

RT PCR

A 
RT= reverse transcriptase (virus)
PCR= polymerase chain rxn
  • take RNA + turn that into DNA using RNA virus (RT)
  • in the PCR, polymerase is used
45
Q

Diff gene expression technique

cDNA

A

Complementary DNA sequence bound to a plate

46
Q

Insitu hybridization

A
  • labeled anti sense RNA (radioactive or dyed)
  • look for areas of expression
  • can look at quantity of expression
47
Q

Transgenics

A

-allows you to look at gene function during normal dev
-doesn’t damage dev of organisms
-can inset cloned DNA into cells
>microinjection
>transfection -low intake
>electroporation -speed intake by shocking EX: sodium shock

48
Q

Transposable Elements

A 
"I am legend" movie
-retroviral vectors (Gene therapy) 
  >near 100% insertion (you'll get results)
  >replace viral proteins w/ phyload
    -marker product (GFP)
49
Q

Chimeras (mice)

A
  • take a blastomere from mouse A + put it in mouse B early, it contributes to all tissues
  • took from inner cell mass then they were totpotent
50
Q

Gene Targeting

A
  • from knockouts
  • if they have 1 good copy then the organism will develop
  • if knockouts are crossed then you’ll get heterozygotes
  • break gene l, microinject, then cells swap out bad gene for good gene
  • Bone morpho protein/BMP 7 Knockout: the heterozygote develops normally + the knockout has no eyes or kidneys
51
Q

Newer: Antisense RNA

A

-inject a large amount of it into cell which makes the cell destroy both sense and antisense forms of RNA
>cell does all the work
-Morpholino Antisense (permanent poison)
>hard for the cell to destroy RNAs
>double stranded RNA triggers an antiviral response

52
Q

Differential Gene Expression

A

~25,000 protein encoding genes
-dev genetics
>how do you take same genes + create diff cells/tissues
>how do you go from genotype -> phenotype
*diff from cell or molecular bio is the level of interest
>want to find out how the cellular processes function on a tissue/cell level

53
Q

Gene Expression

A

-proteins lead to everything else except ribosomes
-occurs at multiple levels:
1) Diff Expression -> RNA
2) Selective nRNA processing
-which nRNA->mRNA goes to cytoplasm
-intron + exon splicing (antibodies)
3) Selective Translation
>RNA to protein
4) Differential Protein Modification
>degradation
diff signals to express here AND for how long
>activation

54
Q

Chromatin (active or repressed)

A

> complex of DNA + proteins (histones)
-nucleosome= basic unit of chromatin-> DNA (2loops) wrapped in 8 histones
~140 base pairs

55
Q

Chromatin

A

String of nucleosomes which are connected by H1 linker proteins (histones)

56
Q

Histone

A

Cause nucleosomes to get wound tight

-organize DNA strands into nucleosomes by forming molecular complexes around which the DNA winds.

57
Q

H1 confirmation represses transcription

A

(take yarn off ball when knitting)

-when H1 linkers are removed, it allows transcription factors to get in there

58
Q

Nucleosomes and H1

A

Limit access to DNA
-default condition = repressed
-specification/diff. -> cell/tissue specific change to the repressed state
> use histone acetyltransferase(can add acetyl groups)

59
Q

Methyl + acetyl groups

A

Location: on tails

  • tighten or loosen nucleosome
  • remove methyl= loosen
  • remove acetyl= tighten
  • histone methyltransferase adds methyl groups (tightens)
60
Q

Introns + Exons

A 
Introns= loose
Exons= exits nucleus/keep
61
Q

What is “the gene”?

A

*promoter: polymerase binding/initiation
>upstream (5’)
*transcription + translation termination helps form poly-A tail
-before leaving nucleus:
>nRNA will get a 5’ cap of methylated guanine
>reverse polarity so there’s no 5’ end
*poly-A tail
>needed to bond to ribosome
*3’ poly-A tail
>protects from exonucleus

62
Q

Promoters & Enhancers

A

-determine when + where genes are expressed

63
Q

Promoter

A

Upstream- bind polymerases and also transcription factors

64
Q

Basal transcription factors (TFs)

A

Necessary for polymerase binding

Ex TATA binding protein (TBP)

65
Q

TFIID

A

Fraction of a cellulose extraction

  • foundation of the complex of proteins needed for initiation
  • stops nucleosome formation
66
Q

TFIIA

A

(Larger protein)

  • binds w/ TFIIB so that RNA polymerase can bind
  • factors E, F, H release RNA polymerase + unwind helix (like helicase)
  • regulated by TBP Associated factors
67
Q

TBP Associated Factors (TAF)

A

Can help modulate activity of the RNA polymerase activity-bound upstream of promoter + is tissue specific

68
Q

Enhancer

A

Control efficiency and rate for a specific promoter
*importnat in tissue specific exp.
-can be 1000s of base pairs away but on the same chromosome (limit)
-5’ (upstream) or 3’ (downstream)
-function= combine w/ transcription factors
-nothing can bind to it
-removing methyl groups
-most genes require enhancer activity
-multiple enhancers + multiple TF can all work on 1 gene
>want to have enhancer to work the right way + same place
-enhancers can also inhibit
-mixed activity

69
Q

Transcription Factors (TF)

A

-proteins that bind to enhancers (DNA seq) and promoters
-activate or repress (variably) a lot or little
-grouped into families
>small amino acid changes, change binding

70
Q

Hox Genes

A

-codes for TF
-axis formation
Pou= pituitary and neural fates
Lim= head
Pax= neural and eye dev
-basic structure= combination of Leucine zippers, Helia loophelia, zinc finger

71
Q

3 TF domains

A

1) DNA binding domain
2) Transactivating domain
>important in activating/suppressing transcription
>binds to proteins (TFIIS modifying histones)
3) protein-protein interaction domain
>other TFs or TAFs(transcription associated proteins) can come in and modify activity

72
Q

Ex 1 of TF domains

MITF

A

-TF that’s active in ears and pigment cells
-heterozygote (1 functioning form of MITF)
>deaf, multi colored eyes, white forelock
>helix loop helix structure
*protein-protein domain allows it to dimerize w/ MITF
*can then bind to DNA
*transactivating domain binds w/ a TAF (acetyl transferase)

73
Q

Ex 2 of TF domains

Pax 6

A
  • active in mammalian eye, nervous system + pancreas
  • contains 2 DNA binding domains
  • pax 6 binding seq. found in lens gene enhancers and endocrine cells in pancreas that are important in insulin/glucagon (Diabetes)
  • can activate or suppress
  • pax 6 + sox 2 have to be present together for lens dev (eyes won’t form)
  • sox 2 is only present in ectoderm that’s been exposed to optic vesicle
74
Q

3rd Binding site of Pax 6 TF domain

A
  • repression or activator
  • critical in stopping lens formation outside eye
  • when expressed it does a positive feedback (becomes permanent enhancer)
75
Q

Transcription Factor Cascades

A

-TFs are activated by TFs
>Pax 6 is turned on by TF: MBX which is expressed in late gastrulation
-Activation of TFs
>may need a signal to be competent

76
Q

Silencers

A

Repressed that repress transcription
Ex: neural restrictive silencer enhancer (NRSE)
>causes promoter only to be active in neurons
-expressed in all other cells
-works as deacetylase

77
Q

Methylation

A

-DNA methylation
>how expression becomes stable -> adulthood
-promoters can become methylated
CpG seq because cytosine gets methylated but only if followed by guanine
-methylated cytosines stabilizes nucleosomes
>results in TF not binding

78
Q

Genes during development

A

-genes only active in sorry or some active in egg
-methylation of CpG
-imprinting
>disadvantage: lethal alleles exposed

79
Q

How does methylation stop transcription?

A

-interaction w/ histones
-methylated DNA attracts enzymes that further methylated DNA
-methylated DNA stabilizes nucleosomes beyond stabilized methylation of histones
*Mecp2 (protein)> selectively binds methylated DNA and also binds deacytelases
(H1 linker histone) ->attracted to methyl DNA

80
Q

Clones

A

Compare to normal formation -> methylation is messed up

81
Q

Normal DNA methylation

A

maintained during mitosis by DNA methyl transferase (1 strand methylated + the copied strand will be methylated)

82
Q

Loss of methylated transferase (mice)

A

Small shortly after birth, die because of multiple malignant tumors

83
Q

Insulators

A

Seq that binds proteins “insulators” stops activation of adjacent promoters often located between enhancers and promoters

84
Q

Dosage compensation

A 
Inactivation 
   Ex: X chromosome 
      X converted to heterochromatin
      Heterochromatin remains condensed 
      Replicates later than the other chromosome
      Forms Barr body
    *if not shut down; death because only want same X chromosome shut down in every cell
    *early inactivation critic
Shut down isn't always 100% 
   -15% could still be active (alleles)
   -germ s will cause reactivation
85
Q

Inactivation

A

= a chain reaction:
MeCP2 > methylated DNA
Stabilized nucleosomes > deacytelases

EZH2 > methylates DNA & histones
H1 highorder folding (nucleosome)
*all of this initiated by RNA seq that never leaves nucleus
-methylated promoters

86
Q

Differential RNA processing

A 
(DNA>nRNA>mRNA>proteins)
After transcription> translation
1) mRNA (introns, cap, tail) 
2) move from nucleus> cytoplasm
3) translation> post-translation changes
-diff in cells=diff in proteins
-same pool of RNAs but diff sets make it to the ribosomes (called censorship) 
-splicing: exons + introns
   *combine multiple exons differently 
   *nRNA contains introns
       >pre mRNA 
   *by processing diff subsets
87
Q

Example of differential RNA processing

A

Sea urchin blastula vs gastrula

  • more genes are transcribed than expressed
  • the stuff not sent out = degraded within nucleus
88
Q

Alternate RNA splicing

A

-normal vertebrate RNA has many introns + exons that get spliced together> shorter seq
-splice sites (introns) decide if it’s cut out or left
-spliceosomes= bind to splice sites
>made of combination of RNA + protein (splicing factors)
-diff spliceosomes = diff results
-splice site recognition is 5’

89
Q

Alt. RNA splicing example

Tropomyasin

A

-1 gene for Tropomyasin
BUT diff kind (slight modifications) of Tropomyasin in brain, liver, skeletal muscle, etc.
Multiple protein forms
*called: splicing isoforms

90
Q

Alt. RNA splicing example

BC1-X

A

1 form inhibits apoptosis

Other fork induces apoptosis

91
Q

Alt. RNA splicing example

Fruit flies

A

1 gene in drosophila has 38,016 potential isoforms

*genome and protenome are not equal

92
Q

Differential Splicing

A

Enhancers etc.->DNA->RNA
-diff proteins recruiting to splice sites
>changing splice activity

93
Q

Translation

A

Controlling protein creation

  • mRNA longevity> stabilized RNA leads to more protein
  • stability is a function of poly A’ tail
94
Q

Untranslated region

A

UTR
(Not turned into proteins)
-determines length
-when experiment alters UTR it increases or decreases the half life of mRNA
-caesin mRNA: half life= 1.1 hours (during lactation= 28 hours)
>protein found in milk

95
Q

Oocyte translation

A

Make and store mRNA that is used much later after fertilization

  • necessary for chromatin, membranes, cytoskeleton components
  • early cell divisions rely on this
96
Q

Bicoid & nano translation

A

(Insects)

Localize (mRNA) to specific parts of cell

97
Q

Translation regulation

A

-tends to be negative
-default state= on
-5’ cap 3’ tail is where this occurs
>important in ribosome binding
*no cap/tail = no translation

98
Q

mRNA

A

Circular
5’ held to 3’ by proteins *important in unwinding double stranded RNA
3D structure

99
Q

Ex of mRNA

EIF4G

A

Binds 3’
Binds ribosome
Ribosome binds 5’ initiation factor

100
Q

Ex of mRNA

EIF4G

A

Binds 5’ cap
Interacts with G
So oocytes produce RNAs without cap
-fertilization >capping

101
Q

Cytoplasmic localization

A

3’ UTRs
-vegetal localization (yolk rich)
-bicoid (anterior) nanos (posterior)
>if 3’ UTR from bicoid and add to RNA it knows where to go

102
Q

Post translational

A

Structural
Enzymes
Phosphokinase
TF

103
Q

For many proteins to become active…

A 
Need something else:
-dimer
   >MITF - hemoglobin
-cleaved - insulin
-ribosomes - tubules
-ion binding

Developmental Biology (1 decks)

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