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lecture 15 Flashcards

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1
Q

is there a central controller for development

A

no; everything happens in individual cells

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2
Q

what is a domino

A

a signaling/developmental process in a specific tissue

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3
Q

what is the first domino to fall

A

fertilization of the egg

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4
Q

what is inevitable after first domino (fertilization of egg)

A

proliferation, differentiation thru expression of unique transcriptional regulators, all the way till adult organism

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5
Q

what happens as you transition from one stage of development to another

A

expression of specific transcriptional regulators

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6
Q

what happens when a transcriptional regulator is experssed

A

not just one protein that gets expressed, but ALL the genes that are controlled by that transcriptional regulator can be turned on/off leading to cell specialization

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7
Q

what are those transcriptional regulators controlling (what are some dominos)

A

promote/inhibit cell-cell interactions, promote/inhibit cell movement, proliferation thru pathways, up/downregulating actomyosin contractility to help w tissue morphogenesis

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8
Q

is there a master organizer of development

A

no. no CNS dictating what happens when, no master cell or central microchip

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9
Q

what’s controlling all these things in individual cells

A

every cell acts on its own in response to changes in transcriptional regulators expressed

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10
Q

give an example of every cell acting on its own rather than a central controller

A

steps leading to formation of an eye, instructions are contained in the cells that express first step of differentiation

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11
Q

what happens if u take cells that express initial precursor transcriptional regulator (that is gonna put cell and its progeny into developmental path to become an eye) and put it anywhere else on the embryo

A

its gonna become an eye (maybe not functional, but will still form)

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12
Q

why would it become an eye if we put precursor cell at a different location

A

b/c all the info you need (cascade of dominos gonna fall) for embryonic cells to become an eye are all in the cells itself

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13
Q

describe image B (eye like structure forming on diff parts where they shouldn’t be

A

dissected out embryonic eye cells and transplanted them to diff parts of cell –> they became eyes even at the wrong location cuz its just a series of dominoes that fall (same events are gonna happen in that new location, now you’re going to get an eye like structure there)

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14
Q

describe the system that controls development

A

highly conserved –> same processes in mice, humans, flies, equid, etc.

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15
Q

what is Pax6

A

transcriptional regulator, when expressed initiates a series of dominoes that have to fall over to convert pax6 expressing cell into a fully differentiated eye cell

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16
Q

what happens when they expressed pax6 from a squid in flies (where its not supposed to be expressed)

A

still does the same thing –> makes an insect eye (even tho its squid Pax6)

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17
Q

what does this show

A

common origins of multicellular life

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18
Q

what is initial fertilization event

A

single cell undergoes cleavage (goes from one cell to many cells) and forms blastula

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19
Q

what is blastula

A

hollow sphere surrounded by cells or blastomeres

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20
Q

what is initial stage where you get series of cleavage events

A

fertilized egg to blastula

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21
Q

what happens as u go from a single cell to bastula

A

proliferation but not growth; size does NOT change

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22
Q

what happens in gastrulation

A

blastula is turned inside out to form primordial gut (blastula to gastrula)

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23
Q

what can you notice in gastrulation

A

it is noticeably getting bigger, growth is happening, cell movement is happening

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24
Q

how do we know cell movement is happening

A

it has turned inside out

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25
Q

what else kicks into play as you go from blastula to gastrula

A

initial differentiation (you get 3 early cell fates, mesoderm, endoderm, ectoderm) AND morphogenesis (tube is formed)

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26
Q

what are 3 fates of cells that go to form many differentiated cell tyeps

A

ectoderm, endoderm, mesoderm

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27
Q

what is ectoderm

A

remains on outside of gastrulation embryo

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28
Q

what does ectoderm give rise to

A

skin and nervous system

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29
Q

what is endoderm

A

cells on inside of gastrulated embryo

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30
Q

what does endoderm give rise to

A

primitive gut & associated organs –> digestive system, esophagus, stomach, lungs, pancreas, liver, etc.

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31
Q

what are endoderm and ectoderm

A

looking to form epithelial like tissue where cells are forming cell-cell junctions and love being in contact w/ each other

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32
Q

what kinda tissue are endoderm and ectoderm similar to

A

epithelial tissue

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33
Q

what else is happening in ectoderm and endoderm

A

cadherins holding them together, belt of actomyosin contractility near apical surface

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34
Q

what is mesoderm give rise to

A

everything else: muscles, heart, blood, connective tissues (extracellular matrix rich tissues), kidneys

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35
Q

describe mesoderm; what is it similar to

A

more mesenchymal; like fibroblasts

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36
Q

how is mesoderm like fibroblast

A

forms single cells, doesn’t like forming cell-cell contacts w/ each other

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37
Q

can you tell sides apart in blastula

A

no; looks same, top, bottom, left, right

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38
Q

can you tell sides apart in gastrula

A

yeah; can tell top from bottom

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39
Q

how can you tell top from bottom in gastrula

A

opening to embryonic/primordial gut (at bottom)

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40
Q

can u tell left from right in gastrula

A

no; its symmetrical

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41
Q

what happens a few hours after gastrulation

A

profound asymmetry

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42
Q

what is symmetry breaking or axis specification

A

step going from symmetrical to us being to morphologically tell front from back, head from tail, left from right

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43
Q

when does symmetry breaking/axis specification occur

A

early development

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44
Q

why is axis specification a critical step

A

allows subsequent steps of development to follow more of a pattern, to reinforce & expand on this body plan specification that happens early

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45
Q

what is front

A

anteriorw

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46
Q

what is back

A

posterior

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47
Q

what is top

A

dorsal

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48
Q

what is bottom

A

ventral

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49
Q

when is basic body plan established

A

early in development

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50
Q

does basic body plan persist or go away

A

persists for lifetime of organism

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51
Q

what happens to ectoderm

A

ectoderm is still in outer portion of embryo which is where skin is going to form

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52
Q

what else do we now see in ectoderm

A

neural tube; going to become spinal cord and CNS

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53
Q

what is neural tube gonna become

A

spinal cord and central nervous system

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54
Q

what is mesoderm now

A

layer below ectoderm

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55
Q

what is mesoderm gonna become

A

connective tissue, musclesw

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56
Q

where is endoderm

A

in the middle

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57
Q

what is endoderm forming

A

gut cavity lined by endoderm

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58
Q

are these different cell types segregated? and when

A

segregated at early stage

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59
Q

what gives rise to tissue patterning

A

controlled differentiation in space and time (like EVE protein)

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60
Q

what is proper tissue patterning responsible

A

shape and function of adult organism

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61
Q

what happens once you specify body plan

A

can tell it left from right, front from back –> further steps of differentiation and morphogenesis

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62
Q

in early embryo are all cells are same or are they expressing diff things

A

look same but expressing different transcriptional regulators, going to have different face

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63
Q

what is blue part going to form

A

head

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64
Q

what is red (middle part) going to form

A

thorax

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65
Q

what is green (end) part gonna form

A

abdomen

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66
Q

are these relative positions at early stage maintained or not

A

maintained through adult stagew

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67
Q

why does body plan specification happen so early

A

b/c you need a framework to begin to place these different embryonic cells in correct locations, so adult tissues will form in the correct locations

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68
Q

what is tissue patterning

A

above process; body plan specification happening so early (, spatially regulated phenotypic trajectories are imposed on identical cells to generate distinct phenotypic cell domains.)

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69
Q

what does tissue patterning represeng

A

one of the dominoes that can fall during development

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70
Q

what can tissue patterning be a result of

A

several diff upstream cell signaling processes

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71
Q

what is largely responsible for differences between cell types

A

regulatory DNA

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72
Q

in tissue patterning, why do diff cells differentiate into diff fates

A

b/c they express diff transcriptional regulators

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73
Q

describe DNA as it goes from precursor cell/embryo to ultimate fate (muscle cell)

A

DNA isn’t changed

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74
Q

so how is there diff cell types

A

differentiated cells have different transcriptional regulators resulting in unique subset of proteins expressed in each cell types

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75
Q

so basically why are there different cell types

A

different proteins being expressed

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76
Q

why are there different proteins expressed

A

activation/repression of different transcriptional regulators

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77
Q

what does early embryo maintain into adulthood

A

body plan

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78
Q

what is changing in the different examples of tissue patterning we’re going through

A

changing which transcriptional regulators are expressed in different cells

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79
Q

what happens to the developmental potential of cells

A

becomes progressively restricted

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80
Q

what is general principle of development

A

as u go from early embryo/embryonic cell, at the early stage cell has many diff possibilities it can become

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81
Q

what can fertilized egg cell become

A

any cell type in the body

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82
Q

what is this fertilized egg cell fate called

A

totipotent

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83
Q

what happens as these dominoes fall

A

cell divides, generates diff cell fates; basically each step farther down the dev. path where u go from totipotent fertilized egg, to mesoderm endoderm ectoderm, to skin, heart, etc.

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84
Q

can you go backwards in developmental path

A

no; one way trip in terms of developmental fate

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85
Q

progressive restriction meaning

A

as cells differentiate to become more specialized, each step of differentiation there’s less and less things it can be

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86
Q

what do cells undergo

A

one way process of development from pluripotency to terminal differentiation

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87
Q

blastomere

A

hollow blastula stage of development where all the cells are the same cell type

88
Q

what options does blastomere have

A

endoderm, ectoderm, mesoderm [covers all the cell types in adult organisms]

89
Q

what happens once it decides on endoderm

A

ectoderm and mesoderm are no longer an option

90
Q

what happens after endoderm

A

becomes liver, lung, pancreas, all the way down to its final fate

91
Q

why is each step of this pathway happening

A

b/c a different set of transcriptional regulators is being turned on or off to trigger differentiation

92
Q

trigger differentiation of what to what

A

differentiation of cell from its earlier designation (like blastomere) to a more later (developmentally speaking) designation (like endoderm)

93
Q

what is one of the reasons why it’s a one way trip

A

though cells dont have a brain, they have cell memory (can remember what they used to be)

94
Q

what can happen thru cell memory

A

simple signals can generate complex patterns

95
Q

what is cell memory

A

can be epigenetic DNA changes (histone acetylation)

96
Q

what else can cell memory be

A

persistence of macromolecules like regulatory RNAs or transcriptional regulators

97
Q

describe cell memory being an epigenetic change to DNA

A

at earlier step of development, cell had post-translational modifications made to histones associated w/ DNA

98
Q

what is result of cell having post-translational histone modification

A

changes how the transcriptional regulators interact w/ that DNA

99
Q

what is histone acetylation a way of

A

way for cell to remember what has happened

100
Q

what does cell on the left receive

A

signal X, changes some transcriptional regulators and triggers acetylation of histones in nucleus (nucleus turns black)

101
Q

what dos cell on right receive

A

signal Y (nucleus is white, changes trans. regulators, triggers histone acetylation in nucleus)

102
Q

what happens when signal X is removed

A

no longer active in the tissues BUT the cell remembers signal that was there in the past

103
Q

how does the cell remember

A

b/c it carries on histones (specific acetylation that was caused by presence of that signal)

104
Q

what happens when signal C comes in

A

it’s going to have a very specific outcome because of histone acetylation

105
Q

what happens if signal X never came in but signal C came in

A

no DNA modification and no memory, so it would trigger a different outcome in those cells

106
Q

basically describe left vs. right in what signal C triggers

A

triggers different outcome in left vs right

107
Q

what happens in signal Y and Y

A

both had some DNA modification; cell remembers b/c of acetylation changes to DNA; signal C thus triggers 2 diff outcomes

108
Q

what is this [cell memory] an example of

A

one of the dominoes

109
Q

why does this show how development can be complicated

A

way for signals to act on cells to get not just one option but many

110
Q

what is another way for simple signals to generate complex patterns

A

combinatorial control (and cell memory)

111
Q

what is combinatorial signal

A

allows you to get a specific differential outcome by combining signals so they’re there at the same time

112
Q

what are signal A and B

A

paracrine signaling; growth factors expressed by neighboring tissues, acting on cells to trigger differentiation

113
Q

what happens when signal A acts with B

A

you get a green cell; pancreatic duct cell (triggers specific susbet of transcriptional regulators activated that will make this a pancreatic duct cell)

114
Q

what happens when signal A acts w/ signal C

A

triggers diff set of transcriptional regulators that give beta islet cell in pancreas

115
Q

basically what is combinatorial signaling

A

way to get as many cell types from a limited subset of signals

116
Q

what happens in an actual organism (w/r to combinatorial signaling)

A

cell doesn’t just have 3 but hundreds of thousands, putting them together in combos gives you millions of diff cell types

117
Q

what does asymmetric cell division lead to

A

diversity

118
Q

what are 2 ways to dictate how a common precursor can become two different cell types

A

molecular memory of previous signals, combinatorial signals actin on the same cell

119
Q

what is another way to control cell differentiation

A

cell division

120
Q

what does cell division lead to

A

cell can initiate a molecular program which can cause daughter cell to be 2 diff cell types

121
Q

what does 2 diff cell types mean

A

diff set of transcriptional regulators that are activated

122
Q

what is symmetric cell division

A

daughter cells are identical

123
Q

what is asymmetric division

A

generates diversity;

124
Q

describe how asymmetric division generates diversity

A

not everything is uniformly distributed in cytoplasm prior to anaphase and cytokinesis (red dots [ ] on one side of cell)

125
Q

what are red dots

A

vesicles that contain a transcriptional regulator

126
Q

what happens to red dots

A

kinesins w/ microtubules grab those vehicles and move them all to one side of cell b/c that’s where MTs are arranged

127
Q

what happens to red dots after cytokinesis

A

red dots are found in daughter cells

128
Q

describe result of asymmetric division

A

daughter cells are essentially born different

129
Q

why are they considered 2 diff cell types

A

b/c they contain transcriptional regulators

130
Q

what is symmetric cell division

A

cytoplasmic contents of the cell on the left are evenly mixed; when it divides –> 2 identical daughter cells

131
Q

what has to happen in symmetric cell division to trigger differentiation

A

something to enable one cell to differentiate while the other one maintains its initial fate

132
Q

how does this happen

A

even tho cells are the same they are in diff position within embryo; they aren’t on top of each other, diff location (like one closer to endoderm while other is not)

133
Q

what does this different location lead to

A

opportunity for chem environment to be different (albeit small scale) –> triggers differentiation event

134
Q

how can a cell undergoing symmetric division undergo 2 different chemical environments

A

inductive signal

135
Q

what is process of induction

A

after cell division, it needs to differentiate. involves an inductive signal

136
Q

what is inductive signal

A

growth factor expressed (by dark grey) & secreted into extracellular environment

137
Q

how does inductive signal diffuse

A

short distance, binds onto receptors of light gray cells

138
Q

what happens when inductive signal binds

A

triggers signaling pathway that changes which transcriptional regulators are expressed in those cells, thus triggering a SECOND differentiation of light gray into blue

139
Q

basically describe induction

A

dark gray secretes GF short distance, binds onto light gray, triggers light gray’s differentiation into blue

140
Q

simplified definition of inductive signaling

A

two cell types where one in the middle secretes a signal, acts on cells close by to trigger their differentiation to blue

141
Q

why do only the close cells turn blue and not all of them

A

because [ ] of signal was highest there; signal decreases the further down you go

142
Q

what are morphogens

A

long-range inductive signals that exert graded effects

143
Q

describe gradient of signals

A

asymmetric [ ] over a distance; decreases the further you go

144
Q

what can a magnitude of a signal induce

A

different transcriptional regulators and lead to diff cell types and patterning

145
Q

where is the greatest [ ]

A

where it’s being produced; just diffuses thru tissues of developing embryo until it reaches 0

146
Q

what does [ ] correlate with besides triggering differentiation like yes or no

A

instead [ ] correlates with the cell fate that is triggered

147
Q

how can an embryo control where diff cell types are gonna form in space and time

A

tissue can be induced to divide into diff cell types based on [ ]

148
Q

what does the concentration trigger

A

differentiation of diff cell types depending on how they respond to [ ] of morphogen

149
Q

how can cells control shape of gradient

A

can make gradient sharper, make signal transient or stable

150
Q

what is increased signal diffusion

A

can manipulate diffusion by controlling how much it interacts w/ matrix that’s surrounding these cells

151
Q

what happens in increased signal diffusion

A

if it can’t bind to matrix well, it will float on by, increased signal diffusion

152
Q

describe increased signal diffusion

A

lower [ ] at the source, extends farther out into the tissue

153
Q

if we want increased diffusion do we make it bind to the matrix well or poorly

A

poorly; if it was bound 100% it could not leave matrix and diffuse

154
Q

what’s another way to manipulate signal

A

increased signal stability

155
Q

one way cells get rid of a morphogen in environment

A

endocytosis, and degrade it in lysosomes

156
Q

what happens if you decrease endocytosis

A

increased signal stability

157
Q

what happens if you increase endocytosis

A

lowers signal, and thus decreases signal stability

158
Q

what does lateral inhibition do

A

generates pattern of diff cell types

159
Q

what is lateral inhibition

A

stronger a signal a cell receives, weaker a signal it generates

160
Q

what is transient bias

A

signal, force, ‘noisy’ signal

161
Q

what’s another way for cells to control fates to go from one cell type to 2 cell types

A

lateral inhibitiion

162
Q

describe lateral inhibitiion

A

negative feedback loop

163
Q

describe lateral inhibition

A

protein X in cell 1 is trying to turn off protein X in cell 2, protein X in cell 2 is trying to turn off protein X in cell 1

164
Q

what happens if both cells have exact # copies of X

A

nothing will change, both are equally inhibited, stable system

165
Q

what happens if cell 1 has one more copy of X than cell 2

A

cell 1 wins the battle, turns off protein X in cell 2; means that cell 2 can’t turn it off in cell 1

166
Q

what does this lead to

A

self-amplifying asymmetry in protein X; transient asymmetry where one cell is gonna win and thus 2 diff cell types

167
Q

what actually ends up happening

A

bound to get this asymmetry just through random noise; almost guaranteed at one point to trigger self-amplifying symmetry

168
Q

what possibilities are with lateral inhibition

A

can have noise or a very purposeful signal

169
Q

either way what does lateral inhibition result in

A

stable differentiation event where red cell type is present on one side, yellow cell type on other side

170
Q

what is short-range activation and long-range activation

A

combining short acting signal with a longer range signal to get complex cellular patterns

171
Q

first step

A

short range signal (self-amplifying signal) [either thru lateral inhibition or random noise]

172
Q

what happens with just short range signal

A

inevitably go from field of gray cells to field of yellow, because of doominos

173
Q

what can you do to stop this (AKA second step)

A

longer range inhibitor of differentiation that keeps the cluster of differentiated cells limited in scope

174
Q

what happens when you combine them

A

clusters of differentiated/specialized cells in an otherwise uniform field of same cell type

175
Q

what is sequential induction

A

example of combinatorial signaling where depending on what’s present in the cell receiving the signal as well as what cell types produced in/producing the signal, can get rapid increase in complexity of cells within a tissue

176
Q

sequential induction gives rise

A

from 2 cell types to 5 cell types (for example)

177
Q

describe sequential induction steps

A

cell B secretes a signal that acts (short distance) cell A, triggers some of them to become cell C (so we go from A and B to A, B, C)

178
Q

what happens next in sequential induction

A

cell B’s signal turns off, cell C secretes a signal; if cell A receives it turns into cell type D; if cell B receives it turns into cell E (basically whether the signal is received from cell A or B, will give rise to 2 diff cell types)

179
Q

how do animals specify body plan / primary axes of polarization

A

diff mechanism; key first step is movement of transcriptional regulators thru cytoplasm

180
Q

how does it work overall

A

initial dominoes that fall are gonna lead to all other asymmetric changes in developing embryo needed for successful developmental programming

181
Q

what specifies front in back in xenopus development

A

where sperm fertilizes egg

182
Q

what is the first domino that falls that reorients some components of cell (for xenopus)

A

sperm fertilizing egg

183
Q

what happens when xenopus cell divides (after first domino falls)

A

asymmetric cell division, leads to more dominos falling, eventually adult organism

184
Q

what is key first step / domino for drosophila

A

movement of transcriptional regulators is key in establishing the body plan

185
Q

describe this process in drosophila

A

transcriptional regulators are already present in cytoplasm after fertilization, but the key thing is that they are concentrated on one side of embryo or the other

186
Q

what do these processes in xenopus and drosophila have in common

A

diff processes, but the origins of the asymmetry which drive subsequent formation of embryonic body plan and establishment of primary axes of polarization are same

187
Q

what are egg polarity genes

A

created from mothers genetic material, responsible for patterning drosophila embryo

188
Q

what does bicoid create

A

anterior-posterior axis

189
Q

what does toll create

A

dorsal-ventral axis

190
Q

what does bicoid help do

A

helps control expression of Eve

191
Q

what happens before bicoid controls expression of Eve

A

mRNA that expresses bicoid is concentrated on the side of the embryo fated to be the anterior/front

192
Q

what & where is Nanos

A

Nanos is its partner transcriptional regulator, [ ] at posterior

193
Q

what do bicoid and nanos do together

A

where they are [ ] specifies where the front and back are gonna be

194
Q

what does Toll do

A

protein that controls formation of top-bottom axis

195
Q

where is bicoid concentrated

A

anterior

196
Q

once you form these differentiated tissues, how do you maintain an even boundary b/w diff segments of developing embryos?

A

positive feedback loop

197
Q

what does positive feedback triggered by engrailed do

A

helps maintain the segmented pattern

198
Q

is the positive feedback loop always active or only sometimes

A

always; that’s why there’s such sharp boundary between cells

199
Q

what is one cell expressing

A

protein called wingless

200
Q

what does cell w/ wingless do

A

acts on its neighbor to activate the engrailed protein

201
Q

what is the engrailed protein

A

transcriptional regulator that enters nucleus, produces hedgehog protein

202
Q

what does hedgehog protein do

A

acts on first cell to produce more wingless protein –> positive feedback loop

203
Q

what does the positive feedback loop do

A

maintains sharp boundary, keeps them stable in their two different fates

204
Q

what would happen w/o positive feedback loop

A

even lines (in EVE protein in drosophila) would not be as sharp or stable throughout development

205
Q

what does Toll pathway control

A

controls asymmetric activity of Dorsal protein

206
Q

what does D-V signaling genes do

A

creates a gradient of transcription regulator Dorsal

207
Q

what does toll receptor activation in ventral cells trigger

A

translocation of Dorsal protein into nuclei on the same side of embryo, leading to asymmetry in DV axis

208
Q

why is it called dorsal protein

A

b/c its recognized at where the protein is activated (dorsal)

209
Q

what does dorsal protein do and in response to what

A

transcriptional regulator; enters nucleus in response to toll receptor activation

210
Q

what does toll pathway ultimately lead to

A

controls Dorsal protein so it only enters nucleus of cells located on the future ventral side of embryo

211
Q

what happens if you manipulate dorsal protein to be localized in every nucleus of embryo

A

bad things; no dorsal-ventral axis formed; it thinks its all ventral

212
Q

describe the animal body plan

A

ancient & conserved

213
Q

what are cellular memory and inductive signalig

A

important mechanisms of pattern formation

214
Q

what does bicoid form

A

AP axis

215
Q

what does toll form

A

DV axis

bio 211 (18 decks)

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