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CMMB 403 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

A pro-nuclei is

A

The mothers egg and the father sperm in one egg

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2
Q

Development starts when

A

the egg and sperm fuse

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3
Q

A zygote is a

A

single cell

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4
Q

Developmental bio is not a series of phenotypic event but instead

A

a combo of various processes like using diff cells and tissues to grow

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5
Q

How do you determine the developmental functional of a gene

A
  1. Determine where in the embryo the gene is expressed
  2. Then you can remove the function of the gene (make a knockout)
  3. Phenotypes
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6
Q

Haploinsufficiency is

A

when one functional copy of a gene is not enough to provide enough protein for normal funtion

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7
Q
A
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8
Q

heterozygote loss-oof function mutations cause an

A

abnormal phenotype when a gene is haploinsufficient

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9
Q

The first clue to the functions of a protein is

A

where is this gene expresses during development.

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10
Q

What is WISH

A

A method to tell where in an embryo a given gene is transcribed. (it glows!)

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11
Q

The stages of embryogenesis starts with

A

fertilization which is the fusion of sperm and egg to produce a zygote

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12
Q

it continues with

A

cleavage which si rapid mitotic division

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13
Q

Then is

A

gastrulation which is cell movements that create the three germ layer

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14
Q

followed by

A

organogenesis which is the tissues and organs form the germ layers

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15
Q

in some species this is followed by the larval stage which is

A

only in some stuff and sexually immature form that undergoes metamorphosis to become mature

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16
Q

finally is gametogenesis

A

which is the formation and differentiation of germ cell (starts in the embryo gamtes differentiate in adults)

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17
Q

the front is

A

anterior

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18
Q

back is

A

posterior

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19
Q

butt is

A

dorsal

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20
Q

boobs are

A

ventral

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21
Q

cutting anterior and posterior is

A

cross-sectional (transverse plane)

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22
Q

cutting dorsal and ventral is

A

horizontal (separating boobs and butt)

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23
Q

Embryos are cut through

A

horizontal so dorsal-ventral

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24
Q

cutting both laterally is

A

(right down the middle, symmetric) midsaggital

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25
Q

Early cell division is rapid

A

synchronous cell division during cleavage is followed by asynchronous and relatively slow cell division during gastrulation

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26
Q

Size and volume of the embryo do not significantly increase until

A

organogenesis has started

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27
Q

So yk how like hundreds of cells divide but!

A

the size doesn’t increase!!

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28
Q

How do u know organogenesis

A

as soon as formation of neural tube

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29
Q

A blastomere is any cell

A

of a cleavage stage embryo

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30
Q

Slide 8 (presentation 2)!

A

memorize

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31
Q

The beginning of gastrulation is

A

cells moving inwards

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32
Q

Holoblastic cleavage is

A

complete so isolecithal or mesoleithal

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33
Q

in holoblastic the cytoplasm is

A

equally distributed to cells

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34
Q

meroblastic cleaving is

A

incomplete so telolecithal or centrolecithal

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35
Q

why does the yolk remain separate in meroblastic

A

cuz its thick and doesn’t allow cell division so yolk remains separate and had no cells

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36
Q

Holoblastic - isolecithal has 4 types explain each

A

radial cleavage - evenly distributed yolk and spars radial cleavage
spiral cleavage - like a tent with legs
bilateral cleavage - weird circles
rotational cleavage - around a round

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37
Q

holoblastic - Mesolecithal is

A

displaced radial cleavage so like a globe but slightly off

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38
Q

Meroblastic - telolecithalhas 3 types explain

A

bilateral cleavege - makes cracks?
discoidal cleavage - fish, reptiles, birds buds pop over

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39
Q

Centolecithal has the

A

yolk in the center and cells dividing around it

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40
Q

Gastrulation is when

A

the germ layers are formed and the nervous system is induced

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41
Q

what is the mesodermal structure necessary to induce the nervous system

A

the formation of the notochord

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42
Q

In vertebrates the notochord

A

disappears and its not even present in invertebrates

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43
Q

epithelial cells are

A

attached in a sheet-like form (need to be connected to a neighbour or die)

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44
Q

Mesenchymal cells are

A

individualized cells and can be individual and motile

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45
Q

Invagination is

A

making a hollow

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46
Q

Ingression is

A

the migration of individual cells from the surface to the interior of the embryo (become mesenchymal)

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47
Q

Involution is

A

inward expansion of cells so it end up covering the internal cells

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48
Q

Delamination is

A

splitting of a cellular sheet into 2 or more or less parallel sheets. (resembles regression but is actually forming a new epithelial layer)

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49
Q

Epiboly is

A

several cells layers of cells merging into each other and the entire layers are moving, so it expands and move inwards

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50
Q

Convergent extension

A

It merges vertically and so grows horizontally

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51
Q

Specification -> _____ -> ______

A

Determination –> Differentiation

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52
Q

Specification is

A

when a cell is committed to a certain fate but its still reversible, so it’ll differentiate a certain way unless signal or its environment change

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53
Q

Determination is when

A

the commitment is irreversible and it’ll happen regardless of its environment if it changes

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54
Q

Differentiation is when

A

it develops into a specialized into a certain cell type. its a certain type both functionally and biochemically

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55
Q

How do we know a cell is a specified cell

A

if you put 2 diff cells in the same neutral environment and they both turn into their own diff cell types we know they are specificated

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56
Q

Autonomous specification is when

A

blastomeres acquire determination factors from egg cytoplasm (the mother supplies the determination?)

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57
Q

Conditional specification is when

A

embryonic cells are specified by signal from their neighbouring cells

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58
Q

So only in amphibians does

A

autonomous specification starts from a zygote

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59
Q

Fate maps of vertebrates refer to

A

a cells future path of differentiation like a statistical likelihood

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60
Q

In an autonomous manner at the “8-cell stage”

A

its already determined

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61
Q

Even our first two cells contribute

A

unequally to the human embryo therefore specifies

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62
Q

A syncytium is only present in insects and

A

is a cytoplasm containing many nuclei, the cell membrane haven’t formed between nuclei (double check)

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63
Q

A morphogen is a

A

long-range signalling molecule that forms a concentration gradient in the embryo and so the specification/determinations depends on the concentration of the molecule.

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64
Q

In contrast a determinant influences cell fate

A

in the cell where it is found or produced

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65
Q

Transcription Factors are

A

proteins that regulate gene expression, genes have to be turned on at the right time and place for development

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66
Q

Secreted signaling molecules are involved in

A

cell-to-cell communication by signalling transduction cascades

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67
Q

Cell surface receptor proteins are

A

responsible for receiving signals and propagating them intracellularly.

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68
Q

What is essential for development to proceed?

A

Differential gene expression and cell communication

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69
Q

All animals share what

A

the same classes of transcription factors and signalling molecules.

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70
Q

8 histone proteins and 4 types of histone proteins which are

A

H2B, H3, H4, H2A AND THEY HAVE TAILS!!

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71
Q

Condensed nucleosomes have histone tails that are

A

mostly methylated

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72
Q

Uncondensed nucleosomes have histone tails that are largely

A

unmethylated and acetylated

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73
Q

So how does methylation work?

A

methyls have a lysine which is positive and since the backbone of DNA in negative they get super close!!

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74
Q

What do enhancers and promoters really do?

A

promoted initiate, enhancers regulate speed/rate

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75
Q

Transcription factors, and functions for Hox

A

hoxa1, hoxb2…; Axis formation

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76
Q

POU

A

Pit1, Unc-86, Oct2; Pituitary, neural fate

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77
Q

Lim

A

lim1, forkhead; head development

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78
Q

Pax1

A

Pax1 ect; neural specification, eye + muscle developmetn

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79
Q

Basic helix-loop-helix

A

MyoD, MITF, Daughterless; muscle + nerve specification, pigmentation, sex in drosophila

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80
Q

Basic leucine zipper

A

Cebp, AP1, MITF; liver, fat cells

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81
Q

Standard zinc-finger

A

WT1, KRUPPEL, Engrailed; kidneys, gonad and macrophage development

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82
Q

Nuclear hormone receptors - zinc-finger

A

Glucocorticoid receptor, estrogen, testosterone, retinoice receptors; Secondary sex determ, limbs

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83
Q

Sry-sox

A

Sry, SOxD, Sox2; Bend DNA, mammalian primary sex determ, ectoderm

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84
Q

The three major domains of a transcription factor are

A
  1. DNA Binding domain
  2. trans-activating domain
  3. protein-protein interaction domain
    (watch smth?)
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85
Q

What are the two ways u can modify a nucleosome through methylated DNA?

A
  1. add a methyl group and take away an acetyl therefore compacting DNA (deacetylase comes in)
  2. add more than one methyl
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86
Q

What binding protein is attracted to methylated regions

A

MECP2

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87
Q

The 2 DNA methyltransferases are

A

Dnmt3 (de novo methyltransferase) -recognizes unmethylated cytosines

Dnmt1 (perpetuating methyl transferase)- recognized methylated c’s and methylates the c on the opposing strand

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88
Q

Where does DNA get methylated?

A

on cytosine (CpG islands play a role on this too)

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89
Q

cassest exon

A

cutting out the middle keeping the ends

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90
Q

Mutually exclusive exons

A

1 gene cut two ways will give 2 products?

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91
Q

Alt 5’ splice site exons

A

retains the 5’ region

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92
Q

Alt 3’ splice site exons

A

retains the 3’ region

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93
Q

Homotypic exclusion/self-avoidance is when

A

a neuron avoids making a protein or smth that the same as other ones cuz it can sense its neighbour?

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94
Q

What are cadherins?

A

transmembrane proteins that are critical for the segregation of cell types in embryo (cadherin are the molecule in morphogenesis)

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95
Q

How do epithelial cells sort?

A

by the type of cadherin proteins present in their cell membranes

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96
Q

for example, epithelial cells transition to mesenchymal cells when

A

e-cadeherin expression is repressed (cuz e-cadherin is needed for cells to stick)

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97
Q

What is a primitive streak

A

it allows cells to move inwards and form the ecto, endo and mesoderm

98
Q

Juxtacrine signalling is when

A

two cells exchange signals through contact

99
Q

Paracrine signalling is when

A

two cells close to each other or neighbouring cells exchange signals

100
Q

Endocrine signalling is when

A

secreted signalling proteins like hormones enter the blood and find their target cell / tissues

101
Q

They did a reaggregation experiment, what did they find

A

when they took cells from diff parts (neural tube and ectoderm epidermis) they stuck em together yet they moved and clumped with their own cell types, this means that they are already expressing their kind of cadherin so they stick together

102
Q

What are cadherins dependant on?

A

calcium

103
Q

so when theirs calcium arounf they

A

stick to other cells and form dimer - dimer bonds

104
Q

EC1 AND EC2-5 Respectively are…

A

ec1 is a adhesive recognition site, ec2-5 are calcium binding sites

105
Q

slide 4 on 5 , 6- spet 16

A

pleasies

106
Q

what if there is no calcium availble

A

then they let go

107
Q

catamines bind to

A

the cytoskeleton

108
Q

What is induction?

A

The process by which a cell population influences the development of a neighbouring cell by close-range interactions

109
Q

What is competence?

A

The ability of the signal-receiving cell to respond to the cells sending the signalling through induction

110
Q

slide 8 -0 sept 16

A
111
Q

Pax 6 is needed or smth im very confused

A
112
Q

Morphogen gradients can be created through

A

diffusion (continuous gradient)

113
Q

Inducer molecules are often paracrine factors only some being morphogens what does this mean?

A

It’s determined by a threshold, morphogens are usually proteins.

114
Q

Think about a graph of distance from source to amount of morphogen what does it look like and how do thresholds tie in?

A

So obvi the closer you are the higher the amount of morphogen but also there are thresholds to get something going so if a cell is too far its not gonna have a response.

115
Q

Explain the typical pathway for signaling for example a simplifies RTK

A

Upon ligand binding the receptor will dimerize and undergo self-phosphorylation so that it can function as a kinase (basically turning it on)
so basically a ligand which is a paracrine factor will attach to the ligand binding domain and inside will be phosphorylated then that was done using ATP, the protein then gets phosphorylated and activated.

116
Q

How many fibroblast growth factors (FGF) ligands?

A

over 20 diff ones

117
Q

What is RAF, MEK and ERK, gef

A

Raf - Map kinase kinase kinase
Mek - Map kinase kinase
ERK - Map kinase
GEF - guanine nucleotide releasing factor or exchange factor - gap-GTPase activating factor.

118
Q

Okay now describe the RTk pathway for FGFs (fibroblast growth factors)

A

Ligand (FGF) attatches to ligand domain (RTK) which phosphorylates the RTK (RTK is a transmembrane protein) and then turns on an adaptor protein named GEF, which turns on RAS which makes GDP TO GTP (lower energy ton more energy), so RAS turns into RAF (now has energy), turn on MEK which turns on ERK which goes into the nucleus and activated transcription factor and then transcription occurs.

119
Q

What about the JAK- stat pathway which is casein gene activation (FGFs an also activate this pathway)

A

Prolactine the ligand attaches to its receptor, whichphosphorylats to turn on jak2, which turns on stat5, which dimerizes to another stat5 and starts transcription so its a transcription factor.

120
Q

Achondroplasia is the heterozygous

A

gain-of-function of FGFR3, causing dwarfism, (glycine goes to arginine)

121
Q

Now description the sonic-hedgehog signal transduction pathway for when its not present

A

Hedgehog (the ligand) is not present so the pathced protein inhibits the smoothed protein and so PKA and Slimb are on and they promote the phosphorylation of Ci and that’s 2 pieces so one of those pieces will act a a repressor for hedgehog responsive genes.

122
Q

Now sonic hedgehog for when hedgehog is present

A

Hedgehog the ligand will bind to the patched proteins and therefore turn on the smoothened protein which can then inhibit PKA and Slimb which makes a full 2-piece Ci and this full ci will activate transcription.

123
Q

Ci stand for

A

cibitus interruptus

124
Q

So the Sonic hedgehog pathway is kinda like

A

a on/off switch

125
Q

knOW SLIDE 11?

A
126
Q

One of the phenotypes for when sonic hedgehog signaling is inhibited is

A

cyclopia so one eye

127
Q

Also without SHH (sonic hedgehog) what happens

A

they embryo will develop wihtout a vertibular column cuz shh from the notochord its needed for induction of vertebrae development

128
Q

What is Wnt4 necessary for?

A

For kindey formation and female sex determination.

129
Q

Hoe many types of Wnt in humans?

A

19

130
Q

In contrast hoe many beta-catenins?

A

only 1 type, so onyl 1 gene codes for it

131
Q

Describe the cellular process when wnt canonical is not present

A

Obvi no wnt ligand on the proteins receptors so beta-catenin stays ubiquitinated and phosphorylated by GSK3? and then gets destroyed by the beta-catenin destruction complex. as such transcription remains off.

132
Q

Okay so what if WNT canoncial pathway is present?

A

WNT binds to r-spondin, LRP5, and frizzled proteins or ligand receptors and this turns on dishevelled which then turns off GSK3, which then turns off the beta-catenin destruction complex which leaves beta-catenin in the cytoplasm. Beta-catenin still living goes the TCF and binds which is on the gene and this turns on transcription.

133
Q

Where is beta catenin present?

A

nucleus, cytoplasm and intracellular cadherin

134
Q

Describe the wnt planar cell polarity pathway (does not involve b-catenin)

A

Wnt attatches to frizled and frizled and lrp. this makes dishevelled and ryk and ror go to Rho gtpase which turns on JNK and cytoskeleton reorganization and this turns on genes and changes cell shape and behaviour respectively.

135
Q

What is required for planar cell polarity (PCP)?

A

wt signalling so the hair cells in the ear which we need to hear are ordered a certain direction cuz of wnt, so not dishevelled and drosophila have this too on their wings

136
Q

Two major domains of the TGF-BETA superfamily

A

1) BMPs
2) all other members

The difference is what kind of smad they turn on

137
Q

okay first lets describe the pathways for activin, nodal or TGF-beta ligan

A

so these two things receptors ser/ thr kinase domain and receptor type 1 will like to bind when tgf-beta-like ligands bind to them and stick together. The sticking together makes the intracellular part like phosphorylate and this in turn phosphorylate smad 2 or 3 and dimerizes to smad 4 (co-smad) and turns transcription on

138
Q

Okay now describe thr pathway for BMP ligands

A

so these two things receptors ser/ thr kinase domain and receptor type 1 will like to bind when BMP ligands bind to them and stick together. The sticking together makes the intracellular part like phosphorylate and this in turn phosphorylate smad 1 or 5 and dimerizes to smad 4 (co-smad) and turns transcription on

139
Q

What does smad pathways activated by tgf-beta superfamily require?

A

it needs a surface molecule receptor, type 1 or type 2

140
Q

Now the hippo pathway also called the yap + taz pathway

A

When hippo is active yap/taz is inhibited, and so theres no tracription cuz it basically turns on a transcription factor, howverr when hippo isnt present itll just not turn on lat1/2 obvi and then yap/taz will just keep going and and transcire stuff.

141
Q

What kind of signaling is notch

A

juxtacrine - so directly connects cell to cell

142
Q

What is the point of notch

A

it forms the vestibular column

143
Q

Describe notch pathway

A

delta ligand-receptor from a neighbouring cell will attach to both ligand receptors which makes it attach to protease. protease makes it release from the intracellular membrane, it gets into the nucleus and allows transcription

144
Q

3 concept of stem cells and exompain what they mean

A
  1. single-cell asymmetry - so a stem cell can make a differentiated cell or make another stem cell
  2. Population asymmetry - thye do th ame things with cell pops depending on what u need so if u need more of a cell itll focus on that if not make more stem cells?
  3. the 4 types of stem cells go from multipotent to committed to progenitor (short lived replicates a bunch before to make its destine cell) and then differentiated.
145
Q

Is a zygote a stem cell?

A

yes cuz its able to divide and differentiate

146
Q

totipotent stem celsl mean

A

these can generate all the cell types in the embreyo and the extra-embreyonic tissue (part of the placenta, or choroin, the amnion and the yolk sac) - important for regeneration

147
Q

pluripotent stem cells can

A

can generate all the cell types of the embreyo but no Extra - embryonic tissue like placenta (cant put these cells in mother and expect smth to come to of it when pregnant)

148
Q

Multipotent stem cells means that

A

it can generate many cell types or a signal cell type in a tissue - specific manner.

149
Q

unipotent is when

A

only produce 1 type of cell

150
Q

slide 5

A
151
Q

Howd these two canadian figure out stem cells

A

They gave mouse lethal radiation and it died, then did the same but injected with bone marrow of healthy mouse and it lived

152
Q

So stem cells can maintian their own

A

pops but also differentiate

153
Q

Where are enterocytes found and what happens to them?

A

They are in the intstine and we lose about 10^11 of them every single day

154
Q

Name the 5 small intestine cells in the epithelium and what they do

A
  1. Enterocytes :absorpative cells that uptake flid and nutrients
  2. Enteroendecrine cells: produce hormones necessary for intestinal function
  3. Goblet cells: secrete mucus

4.Tuft cells: chemosensors/ T cells activators

  1. Paneth cells: produce antimicrobial molecules.
155
Q

Generally how does this system work? (intestines)

A

so its arranged like stem cell - paneth - stem cell - paneth and lower theres a long of wnt2b and as u go higher it more bmp4 so their like opposite gradients. this is cuz stem cells need more wnt and less bmp

156
Q

What are some examples of adult mammalian tissues and organs that have adult somatic stem cells

A

Blood
Intestine
Lungs
Brain
Skin
Muscle
Mesenchymal stem cells (reside in bone marrow)
Adipose tissues
Heart

157
Q

Why are planarian adults cool

A

cuz not matter where you cut it from itll regenerate its entire self. so each piece becomes its on organism

158
Q

What 3 things define a cell types

A
  1. shape
  2. function
  3. gene function and the amount expressed
159
Q

So what are pluripotent cells like in humans

A

we only have them for a very short time and in only 1 stage of development

160
Q

Where do u get pluripotent embryonic stem cells from?

A

from blastomeres of the inner cell mass.

161
Q

The pluripotent cells from embryos can be

A

incorporates into all three germ layers of other embryos to form chimeras

162
Q

Where can you get pluripotent embryonic germ cells from?

A

the fetuses primordial germ cells.

163
Q

Stem cells are so important cuz of self renewal so they have to be

A

be maintained forever

164
Q

What 3 aspects if each stem cell pool are finely regulated`

A

Maintenance
Rate of proliferation and self-renewal
Differentiation of stem cell progeny

165
Q

Name 2 extra-cellular mechanisms and explain them

A
  1. Physical - like hippo pathway is a mechanoreceptor
  2. Chemical - endocrine - insulin, paracrine - wnt ligands
    juxtacrine - notch ligand
166
Q

Name the 3 intra-cellular mechanisms

A
  1. cytoplasmic - notch> NICD, asymmetric (hippo), symmetric (Beta-catenin, destruction complex)
  2. Transcriptional (Smads, B-catenin, Yap/taz)
  3. Epigenetic (dna accessibility varies between stem cells and their differentiating progeny)
167
Q

(inner cell mass) ICM formation involves what 3 things

A

Apical basal polarity,
asymmetrical hippo signalling activation, asymmetrical cell division

168
Q

Learn hippo

A
169
Q

The first differentiation event is

A

the formation of the icm

170
Q

So basically there are to ways the cells can divide between the apicalsurface and basal surface, describe both

A

symmetrical (apical) where it divides like horizontal
Asymmetrical (basal) where it divides vertically

171
Q

When it divides symmetrically the

A

trophectoderm expands(this is the like outside cell ayer)

172
Q

When is divides assymetrically a

A

an icm cell is created (daughter cell looses exposure to outside)

173
Q

Two apical proteins are

A

Par: partitioning defective
aPKC: atypical protein kinase C

174
Q

What does notch differentiation drive?

A

It drives differentiation

175
Q

Notch inhibits what and causes what

A

inhibits secretory cells (EE cells) and causes absorptive cells enterocyte (EC)

176
Q

Stem cell niche refers to the

A

microenvironemt that houses stem cells and protects their pool and control self-renewal

177
Q

Can we control stem cell function?

A

yes by controlling their niche

178
Q

What does reprogramming refer to?

A

process of converting differentiated adult cells toa more primitive or immature form or a stem cell! so that means erasing its memory 9gene expression profiles)

179
Q

Howd they make dolly?!?

A

A blackface sheep gave the egg like capsule and the nucleuswas given from an udder cell. and so an exact clone dolly was made so the mom is black the kid is white (clones to the nucleus not birther)

180
Q

But thats wasnt the first time the process was used, explain the first use in frogs

A

Took unfertilized frog egg and a nucleus and out in in differential cells of a tadpole ?

181
Q

And this other guys showed that u can reverse

A

reverse a differntiated cell into a pulripotent cell using mice

182
Q

How does directed differentiation work?

A

Oct3/4, c0Myc, sox2 and Klf4 are always active and so now u have induced pluripotent cells and can turn them into basically anything except placental obvi

183
Q

Whys iPSC (induced pluripotent stem cells) good?

A

Because if you introduce it to humans its their own cells and so it wont be rejected

184
Q

Primitive gonads can become

A

either male or female

185
Q

Soamtic cells determine if the

A

gonad will become testies or ovaries

186
Q

so its the developments of testies/ovaries that will

A

that will make the actual germ cells

187
Q

XY sex-reversed females would have either

A

deletion/mutation of SRY or haploinsufficiency of SOX9

(these are males that develop to females)

188
Q

XX Sex reverses males would have either

A

translocation of SRY to another gene
a mutation of Rspo1

(these are females that develop as males)

189
Q

Whats the procces of becoming female somatic cell wise

A

precurse cell of gonads -(gets Rspo1 and wnt4)-> granulosa cells -> ovaries and organogenesis

190
Q

What is the procces of becoming male somatic cell-wise

A

precurse cell of gonads -(gets Sry which becomes sox9)-> sertoli cells - (gets anti-mullerian factors ad hormones) -> testies and organogenesis

191
Q

What are the 4 categories of mesoderm?

A

Intermediate: Kidney, gonads
Chorda: Notochord
Paraxial: Head, somite
Lateral plate: Somatic. extra-embryonic, splanchnic

192
Q

The mesonephros is the intermediate..

A

kidney which si then replaced by the metanephros which are the permanent kidney

193
Q

so what do the mesonephros become?

A

in men they become part of their wollfian in women become mullerian

194
Q

What funtions as the mesonephral duct in early embryo?

A

Wolffian duct

195
Q

What are these ducts

A

Wolffiand and Mallerian ducts are produced by all fetus but males will keep Wolffian and females mullerian, the other will dissapear

196
Q

What hormones help men keep the wolffian duct

A

Testosterone (maintains wolffian dict) plus anti-mullerian factor/hormone (degenerates mallerian )

197
Q

What hormones help woman keep the mallerian duct

A

No test or anti-mullerian factos, since no testoterone the wolfian duct degenerates

198
Q

Where is SRY locate?

A

On the smaller arm of the y chromosome

199
Q

What IS THE hmg-BOX od SRY?

A

A dna binding domain

199
Q

SRY is a HMG-somain containing

A

transcription factors and is related to SOX-9

200
Q

Why are xy females common in humans but not mice

A

cuz the sry is on the same side whereas in mice it’s on the opp side so its easy to translocate

201
Q

SRY was found by analyzing

A

sex-reverses individuals and seeing what was mutated

202
Q

What does SRY do to tunr a gonad into testies?

A

Chronological sequence of SRY and SOX9 expression during sex determ and early testis development

203
Q

so in mice the timeline is like

A

SRy super high at 11.5 dpf, and then sox9 get on as sry drops and just stays stable after that

204
Q

Id you put sox 9 in a female

A

theyll become male

205
Q

Primary sex determ is a funtion of

A

the somatic cells of gonad not germ cells

206
Q

Define primary sex determ

A

Specificationand differentiation of the gonads as either ovaries or testies

207
Q

Secondary sex determ is

A

the sex-specific phenotype outside gonads, from external genitalia and ducts to sex-specific

208
Q

Lec 09 oct 7h - slide 16

A
209
Q

Theca cells produces what and leydig cells

A

theca produce estorgena nd leydig produce testosterone

210
Q

Pathway for sex determ in men mice

A

Genital ridge -> Sry _> sox9 (block b-catenin) -> fgf9 forward feedback loop - >testies

211
Q

Pathway for sex determ in girly mice

A

(rspo1) Wnt4 -> beta-catenin (block sox9) -> ovaries

212
Q

If rspo1 isnt present in females what happens

A

itll become testies

213
Q

What is rspo1 and where was it discovered

A

its a ligand the amplifies WNT signaling and stabilized b-catenin
discovered in a consanguineous family.

214
Q

Primordial Germ Cells (PGCs) form where?

A

At the posterior portion of the epiblast

215
Q

Primordial Germ Cells (PGCs) the gastrulate where?

A

through the primitive streak where they associate with the endoderm that will form the gut.

216
Q

Intially how many primoridal germ cells are present?

A

50

217
Q

What is required in PGCs?

A

Oct-4

218
Q

So basically some cells don’t lose oct-4 (the 50) but all others do and so those 50 that keep it will

A

those 50 will be deposited to posterior portion, become active again once genital ridges appear and start moving through there

219
Q

In mice this happes at – , and for humans at –

A

e11, humans at 6weeks

220
Q

What contians the genital ridges?

A

Mesonephros

221
Q

What 3 things happen after the germ cells migrate to the gonads?

A
  1. They divide mitotically to produce millions of germ cells
  2. They undergo meisosi ( diff for sperm vs eggs obvi) - Jomolohous ch synapse and recombine, - they reduce in ch. number so diploid to haploid
  3. The gametes differentiate into sperm or mature oocytes
222
Q

Okay so timing is obvi diff for males vs femalse, lets start with male

A

Before birth: Mitotic prolif -> mitotic arrest
Before puberty: Mitotic prolif
Puberty: meiotic entry (germ cell divides to 4 sperms)

223
Q

Okay so timing is obvi diff for males vs females, now females

A

Before birth: Mitotic prolif -> meiotic -> meiotic arrest (some die here)
Before puberty: Follical formation
Puberty: Ovulation so the gg is being made or they start dying again

224
Q

What is a precursor to sperm called?

A

Spermatogonium

225
Q

What is the acrosome made up of?

A

Made of golgi apperatus and lots of digestion enzymes so when the acrosome fuse itll burst and help the sperm in through the eggs extracellular matrix

226
Q

How does the amount of eggs change through a woman life?

A

Before bith theres this giant shoot up and then a bunch die, then again they continue to dies after birth a but then stabilize, then at puberty a couple die again

227
Q

Nutritice proteins are for

A

energy and amino acids to supply early embryo vis yolk proteins accumulated in the egg

228
Q

Ribosomes and tRNA is to

A

to meed the needs of structural protein and enzymes, the mebryo uses pre-exsisting trnas in oocytes (has a way to synthesize ribosomes too)

229
Q

Messenger RNA

A

the oocyte accumulates mRNA essntial for early embryonic development whichch remain inactive until after fertilization

230
Q

Morphogenetic factors

A

Asymmetrical distribution of transcription and paracrine factors in the egg and guides embryonic cell differentiation during early development

231
Q

Protective chemicals

A

the egg have like ultraviolet filter, dna repair enzymes, and antibodies to safeguard the embryo form enviro or micorbes

232
Q

5 steps of gene transfer (sperm and egg)

A
  1. Sperm contacts the jelly layer
  2. Acrosome reaction
  3. Digestion of jelly layer (proteolytic enzyme)
  4. Binding to vitelline envelope
  5. Fusion of acrosomal membrane and egg membrane - now the haploid nucleus and centriole will enter the egg
233
Q

Whats specific about repli in early development

A

unlike normal repli where there ar four phases G1, S, G and mitosis, in early development there’s only 2 phases s and m no gap phases

234
Q

What helps the cell enter mitosis?

A

Cyclin B and cdc2 breaks the cell to move into the S phase

235
Q

What is the mid-blastula transition (MBT)

A

Trancription of the zygotic genes begin also called maternal zygotic transition or MZT

236
Q

What 3 things happen maternal to zygotic transition or MZT

A

Maternal mRNAs are degraded
The cell cycle lengthens and gap stages are added
The synchronicity of cell division is lost.

237
Q

Until the MZT what is the embryo running on?

A

It runs on maternal resources, (the mrnas and protein in the egg at the time of fertilization)

238
Q

WHat is the timing of MBT/MZT critical for?

A

To understand the fucntions of maternal effect genes in diff species.

239
Q

So three stages zygote, minor wave, major wave

A

zygote - maternal transcripts
Minor wave (4 cells - 48) maternal being used up - things become totipotent
major wave(8 cells -72 hrs) - zygotic transcripts, any remaining maternal rna is degraded

240
Q
A

CMMB 403 (2 decks)

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