BIO 310 > Lec. 8 (Development) > Flashcards

Lec. 8 (Development) Flashcards

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1
Q

What are the 3 main features of developmental processes?

A

1) Growth (proliferation) –> Need to make more cells to create a complex organism out of the single-cell zygote

2) Shaping –> The overall shape of an organism + its structures must be determined by cells organizing themselves

3) Patterning –> Cells need to organize what the orientation of the organism will be (pattern of cells from head to toe needs to be established)

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2
Q

List the steps of development in order:

A

1) Rapid Proliferation

2) Patterning

3) Shaping + Growth

4) Organization + Specification of local structures

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3
Q

What is the first step in development?

Explain what occurs in this step

A

RAPID PROLIFERATION

== The single cell zygote must undergo rapid division to generate a lot of cells quickly SO a period of rapid proliferation characterized by cell division WITHOUT GROWTH occurs

Results in a lot of cells that take up the same space as the original zygote

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4
Q

What does the cell cycle consist of during rapid proliferation?

A

Solely repeating cycles of S and M phases == rapid replication of DNA followed directly by division

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5
Q

List 3 key regulators of cell cycle

A

1) M-Cyclin
2) Cdc-20
3) Cdh1

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6
Q

What happens when M-cyclin is in HIGH concentration?

A

High conc. of M-Cyclin promotes M-Phase

AND

promotes accumulation of Cdc-20

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7
Q

What causes Cdc-20 to accumulate? What is a consequence of this?

A

High conc. of M-cyclin causes Cdc-20 to accumulate leading to high conc. of Cdc-20

== As Cdc-20 is an inhibitor of M-cyclin, this increase in Cdc-20 results in inhibition of M-cyclin which terminates M-phase

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8
Q

What occurs to Cdc-20 upon its inhibition of M-cyclin?

A

As M-cyclin drops, Cdc-20 conc. will also drop!

== M-cyclin levels will then either begin to rise again (==another M phase) OR another M-cyclin inhibitor will take over (== G phase)

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9
Q

What occurs in normal cells as M-cyclin + Cdc-20 levels drop?

A

Cdh1 is activated! == Inhibits M-cyclin, thus preventing M-phase and allowing for a G-phase to occur!

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10
Q

Cdh1 is a _________ of the _________ phase

A

Cdh1 is a key initiator of the growth phase

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11
Q

How come early embyonic cell division lack G-phase?

A

Due to a lack of Cdh1 presence!

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12
Q

Why is Cdh1 NOT present in early embryonic cells?

A

Because early embryonic cells are not expressing any of their own genes yet! == all RNAs + proteins in the zygote came from the MOTHER!

–> No maternal Cdh1 encoding RNAs or proteins are loaded into the early zygote from the mother BUT M-cyclin + Cdc-20 ARE! == No G-phase promoter, so when Cdc-20 levels drop, another M-phase initiates!

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13
Q

What process is correlated to the transition of lack of G phase to presence of G-phase in embryonic cell cycle?

A

Maternal to Zygote Expression Transition

(RNAs and proteins loaded from mother are depleted and the zygote begins to express its own genes to accommodate) == Cdh1 begins to be produced which initiates G-phase in the cell cycle!

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14
Q

What are morphogens?

A

Signaling molecules expressed at one place that are then dispersed across a distance with a gradient of concentration

–> cells respond to the LEVEL/AMOUNT of morphogen they receive! (specifically via activation of certain Hox genes!)

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15
Q

What type of signaling contributes to patterning?

A

Gradient Signaling!

== Morphogens present in a gradient control which genes get expressed in cells depending on how close the cells are to the source of the signals + therefore the amount of morphogen they are receiving (genes have threshold levels needed for activation!)

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16
Q

What is the “french flag model”?

A

Cells possess threshold-sensing mechanisms; they activate different genes depending on whether they detect high, medium, or low concentrations of morphogens

== Similar to a French flag’s stripes, high concentration areas activate a “blue” fate, lower concentrations activate “white,” and low/no concentration results in “red,” providing a system for patterning.

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17
Q

How is the morphogen gradient established in embryos?

A

The gradient is predetermined by loading mRNA encoding for morphogens into the embryo at ONE END!

== by localizing RNA to one end, a gradient of protein concentration can be generated!

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18
Q

When is mRNA encoding for morphogens loaded into an embryo? How does this loading occur?

A

mRNA encoding morphogens is loaded in during oogenesis by NURSE CELLS

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19
Q

What are nurse cells?

A

Cells localized next to developing eggs whose sole job is to make a bunch of stuff + put it into the developing egg

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20
Q

Other than establishing early patterning in an embryo, what else is morphogen gradient signaling used for?

Provide an example

A

Used later in development to establish patterns!

Ex: Limb development in mammals!

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21
Q

What morphogens contribute to mammalian limb development? How are these morphogens paired and what do they direct?

A

(1) Opposing gradients of retinoic acid and FGF
== Determines the pattern of a limb (what cells will be the forearm vs. the hand)

(2) Opposing gradients of Shh + Gli3R
== determines the orientation of a limb (which side is the thumb vs. pinky side)

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22
Q

In terms of determination of limb orientation by pinky vs. thumb side, what morphogens are involved?

A

Shh (sonic hedgehog) == high conc. is side of pinky

Gli3R == high conc. is side of thumb

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23
Q

Do morphogens function in isolation or combination? Explain

A

Morphogens act in COMBINATION to produce distinct body segments

–> Each body segment will contain a group of cells exposed to unique combinations of morphogen levels + therefore have unique gene expression patterns

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24
Q

After morphogen-gradient signaling determines body segments, what determines what each segment will become?

A

The Hox genes!!

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25
Unique combos of morphogen concentrations activates a specific body plan by controlling ______________
Unique combos of morphogen concentrations activates a specific body plan by controlling **HOX GENE EXPRESSION**
26
Why are hox genes considered "master regulators"?
Because activation of a hox gene turns on the entire program needed to make whatever structure a given hox gene encodes
27
Explain the organization of hox genes within the genome:
Hox genes are ALL located in ONE region of the genome called the **Hox locus** == in this locus, hox genes are arranged in ORDER of the location of the body structure they encode (i.e. the hox gene encoding for the most anterior body part will be at one end of the locus and the hox gene encoding for the most posterior body part will be at the opposite end of the locus)
28
What is the **principle of posterior prevalence**?
The principle that the MOST POSTERIOR HOX GENE expressed in the locus is the one that has an effect + determines what structure forms!
29
What happens when there is a LOF mutation in a hox gene?
The anterior pattern encoded for by the hox gene anterior to the hox gene that has lost function will expand to "fill the space" of the other! (causes an extended body section due to loss of another one)
30
What happens when there is a GOF mutation in a hox gene?
Can cause a Hox gene to be expressed in a region it should not be, therefore resulting in an extension of POSTERIOR body segments == a posterior body segment may develop where it should not
31
What step of development determines the body plan of an organism?
The second step == PATTERNING (morphogen signaling + control of Hox genes)
32
What is the third step of development?
Tissue growth and shaping
33
How is tissue growth connected to tissue shaping?
Depending on WHERE, in what direction, and how much cells grow can determine the shape of a tissue
34
List the 4 determinants of tissue size (and therefore shape) Explain how each contributes an effect on tissue size
**1) Cell growth** == cells get bigger, tissue gets bigger **2) Cell divisions (with growth phase)** == more cells that grow between divisions, tissue gets bigger **3) Cell death** == directs the shape of a tissue by having specific cells die (Ex: Webbing between fingers) **4) Matrix deposition** == increased matrix deposition between cells increases the space between the cells which overall increases SA of tissue
35
What is a major challenge of tissue growth?
As a tissue grows, its center becomes very dense while its periphery becomes very sparse
36
Do tissues grow uniformly? Why or why not? How does growth occur INSTEAD then?
NO: Tissues cannot grow uniformly due to the problem that arises with the center of a tissue becoming more dense than the periphery INSTEAD: growth must vary depending on the cell density of a given region of a tissue == **cells in the periphery of a tissue must grow more and cells in the middle of a tissue must grow less**
37
What pathway regulates growth of cells in a tissue based on cell denisty?
The Hippo pathway
38
What are the main components of the Hippo pathway? Explain the components
**1) Hippo** == A factor activated by cell-cell contacts (denoting high density) that in turn activates the inhibitor Warts **2) Warts** == An inhibitor of Yorkie/Yap and thus an inhibitor of cell growth **3) Yorkie/Yap** == A TF that activates cell growth related genes
39
What condition activates Hippo? What is the result of this in the pathway?
**Cell-cell contacts indicating high cell density activates Hippo!** Resultingly, Warts is activated which then functions to inhibit yorkie which inhibits cell growth! == prevents growth of cells that are already dense
40
What condition inhibits Warts? What occurs as a result?
Signals demonstrating low cell density such as: 1) Loss of cell junctions 2) Cytoskeletal tension == Inhibits Warts which results in activation of Yorkie/Yap, leading to increased cell growth
41
When Hippo is ACTIVE, _________ is NOT, causing ____________. When Hippo is INACTIVE, __________ IS ACTIVE, causing ___________
When Hippo is ACTIVE, **Yorkie** is NOT, causing **inhibition of cell growth in areas of high cell density**. When Hippo is INACTIVE, **Yorkie** IS ACTIVE, causing **increased cell growth in areas of low cell density**
42
What occurs when Yorkie is overexpressed?
Tissues become overgrown which alters structural shape + therefore impacts function
43
While growth can be a determinant of tissue shape, what other 2 factors can impact tissue shape?
1) Cell movement 2) Intercalation
44
What is **gastrulation**?
A process in which one part of the blastula (ball of cells) invaginates, generating 3 layers of cells in the embryo which determine the inside vs outside of an organism
45
What are the 3 layers of cells generated by gastrulation?
1) Ectoderm (outer layer) 2) Mesoderm (middle layer) 3) Endoderm (inner layer)
46
Gastrulation is carried out by...
Large coordinated cellular movement! (AKA. Collective Cell Migration)
47
What is Collective Cell Migration?
Large coordinated movement of a group of cells
48
What are the main methods of collective cell migration?
Two main methods 1) Epithelial Migration 2) Mesenchymal Migration
49
What is epithelial migration?
The movement of a group of cells that is directed by a few leading cells that actively move + respond to signals to direct the movement --> The remaining cells in the group do not actively move but instead are moved due to adherence to the moving cells (cells get dragged along)
50
What is mesenchymal migration?
The movement of a group of cells in which each cell responds independently to a signal and moves accordingly (all cells in the group respond independently to the same signal)
51
In what scenarios are epidermal vs mesenchymal migration more beneficial?
**Epidermal Migration ==** Better for large-scale tissue movements **Mesenchymal Migration ==** Better for direction cells to a general area in which each cell will have a different end point
52
What form of collective cell migration is inappropriately activated in Cancer? What does this lead to
In Cancer, mesenchymal migration is often inappropriately activated resulting in metastasis
53
What is Intercalation?
A cell rearrangement process in which a group of cells is "squished", causing reorganization of the cells such that the tissue becomes elongated
54
How does intercalation occur?
Via rearrangement of which cells are contacting each other
55
What is the final step of development?
Organization and specification of local structures
56
What type of signaling directions local structure specification?
**INDUCTIVE SIGNALING** == Certain cells within an "organizer" complex release inductive signals which get received by neighboring cells = "tells them" what type of cell they should be!
57
How is inductive signaling different from morphogen-directed signaling?
Inductive signaling does not involve a gradient of response (as in morphogen signaling), all cells that receive an inductive signal respond in the same way!
58
What is one of the most prevalent inductive signaling systems?
TGF-β signaling pathway
59
Explain the general TGF-β pathway
1) Organizer cells release TGF-β 2) TGF-β binds to the R(S)TKs on nearby cells 3) TGF-β binding causes the R(S)TKs to autophosphorylate AND transphosphorylate Smad proteins 4) 2 phosphorylated smads and 1 unphosphorylated smad form a trimeric complex that then can act as a transcription regulator that can impact gene expression
60
How are local cell patterns in a tissue formed?
Lateral inhibition via the NOTCH pathway!
61
Explain the notch pathway
1) All cells initially express the notch receptor and release the delta ligand 2) Two cells send delta to each other and receive delta from each other BUT one will eventually reveive more delta than the other cell 3) The cell receiving more delta gets its own delta production shut down 4) == two populations of cells are generated: receivers and senders --> These populations take on a specific pattern within a tissue
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