final Flashcards

1
Q

True or false: plant cells have lots of conserved features when compared to animal/fungal cells

A

True

  • conserved organelles, structures (cytoskeleton), metabolism + processes, genes
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2
Q

How are plant cells glued together? What does this result in?

A

Plant cells are glued together by the cell wall

  • no cell migration because of that (differs from animal cells, think of red blood cells, fertilization, etc)
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3
Q

Are there many types of plant cells?

A

No

~50 types, e.g. mesophyll cells, xylem, phloem.

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4
Q

Describe reprogramming of differentiated plant cells

A

Differentiated specialized cell -> (reprogram/de-differentiation) -> unspecialized undifferentiated cell, e.g. callus cell -> new cell types, e.g. xylem which can form a whole plant as well.

  • can be done in lab or naturally
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5
Q

What is totipotency? Give examples

A

Ability of cell to divide and produce any cell types

e.g. zygote, spore

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6
Q

Give an example of re-programming of plant cells

A

Seedlings -> Digest cell wall using enzymes -> single-cell protoplasts (plant cell with the cell wall removed) -> callus culture, undifferentiated clump that is totipotent -> placed in suspension culture -> proembryonic masses form -> somatic embryo forms -> entire plant forms

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7
Q

What is totipotency important for in biotechnology?

A

Important in the process of making a genetically modified plant

e.g. herbicide resistance.

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8
Q

Describe how transgenic plants used to be made

A

Plant cells bombarded with DNA-coated particles

  • after bombardment, cells that contain the transgene are selected and induced to form complete plants with each of their cells containing the transgene.
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9
Q

What is cytoplasmic streaming? Give an example of where this is seen

A

circular flow of cytoplasm within cells

E.g. seen in root hairs: lots of absorption into the root hair, which is subsequently absorbed into the vascular tissue.

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10
Q

Describe plant root hair growth in general

A

Root grows downward and as it’s growing, many root hairs start to grow out.

  • lots of movement observed at the tip of the root hair
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11
Q

What drives cytoplasmic streaming? Give an example of cytoplasmic streaming (an organelle)

A

Organelle movement

  • driven by myosin, motor on actin filaments

E.g.: Golgi stack movement

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12
Q

What do the plant Golgi stacks move along?

A

Actin filaments that are associated with ER

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13
Q

Describe the model for ER-to-Golgi vesicle transport in plant cells

A

Myosin moves Golgi stack on actin filaments as ER have anterograde movement towards Golgi.

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14
Q

What is the fastest myosin? Describe how it moves

A

Plant myosin XI, movement drives cytoplasmic streaming

  • takes 35 mm steps (1 helical turn in actin per step, if it was > or < 35 mm, actin filament would be rotating)
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15
Q

Describe chloroplast movement in dim light

A

Chloroplasts align perpendicular to the direction of light

  • chloroplasts are trying to maximize the amount of light they absorb
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16
Q

Describe chloroplast movement in bright light

A

Chloroplasts align parallel to the direction of light

  • try to hide a little bit to absorb light but not too much
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17
Q

What allows chloroplasts to detect surrounding light levels? What allows for their movement?

A

Chloroplasts have blue light receptors on their surface.

  • actin filaments pull chloroplasts away from intense blue light.
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18
Q

What cytoskeleton elements do plants have?

A
  • microtubules
  • actin filaments (aka microfilaments)
  • no intermediate filaments
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19
Q

True or false: plant cells have dynein

A

False

  • plant cells only have myosin and kinesin
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20
Q

True or false: plants have centrioles and centrosomes

A

False, because they have no cilia or flagella

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21
Q

What is a MTOC on plant cells and where are they located?

A

MTOC - microtubule organizing center

  • on nuclear envelopes/plasma membrane in plants
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22
Q

What are the 4 microtubule arrays (organization/distribution of microtubules) in plants?

A
  1. Cortical array - in the cortex region, only array present in interphase. These microtubules are located just beneath the plasma membrane, running parallel to the cell surface. Cortical microtubules are involved in guiding the deposition of cellulose microfibrils during cell wall synthesis and determining cell shape.
  2. Pre-prophase band of microtubules
  3. Mitotic spindle
  4. Phragmoplast - important in cell division as well
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23
Q

What is plasmodesmata? What are they important for?

A
  • Cytoplasmic connections between adjacent cells.
  • important in moving small (more passively) and large (more selectively) molecules
  • important for cell-cell communication
  • found in most cell types
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24
Q

What is meant by “plant cells are supercellular organisms”?

A

All plant cell cytoplasms are connected.

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25
Q

What organelles do plant cells have that animal cells don’t?

A
  • central vacuole
  • tonoplast

-chloroplast

-plasmodesmata

-cell wall

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26
Q

When do plasmodesmata form and how?

A

Form during cell division

  • ER trapped in cell wall.
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27
Q

What is the size exclusion limit for plasmodesmata?

A
  • 1 kDa
  • anything smaller than 1 kDa can travel through
  • macromolecules can selectively move
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28
Q

What happens when a 30 kDa protein (for example) wants to move through plasmodesmata?

A

A signal opens a gate and allows movement.

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29
Q

What is a vacuole?

A

Fluid-filled compartment surrounded by the tonoplast membrane

  • usually takes up ~30% volume of the cell, but can take up to 95%
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30
Q

What are the functions of the vacuole?

A
  1. Storage- ions, organic acids, sugars, proteins
  2. Digestion - like lysosomes in animal cells, have hydrolases, nucleases, proteases - degradation
  3. pH and homeostasis - <5.5 pH
  4. Defense - toxic compounds - pests + pathogens (vacuoles break open to defend plant)
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31
Q

What are the 2 types of vacuoles?

A
  1. Lytic vacuole (involved in storage, digestion, pH/ion homeostasis, defense)
  2. Protein storage vacuole, e.g. found in seed cells.
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32
Q

After cargo travels through the golgi to the TGN, what are the 3 fates of the cargo?

A

Either go to plasma membrane, lytic vacuole, or protein storage vacuole.

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33
Q

True or false: all plant cells have a primary and a secondary cell wall

If false, give an example of cells that have a secondary cell wall

A

False

  • all have a primary cell wall synthesized outside the plasma membrane (extracellular)
  • some cells have a secondary wall (synthesized after the primary wall, cells that are rigid have a secondary cell wall, e.g. xylem cells)
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34
Q

What is present in the secondary cell wall that provides strength?

A

Lignin

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35
Q

What is middle lamella?

A

Thin layer rich in sticky polysaccharides called pectins. glues adjacent cells together

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36
Q

What is turgor pressure?

A

Internal hydrostatic pressure of plant cells

  • when turgor pressure is low (low water), plant “flops over”
  • opposite in high turgor pressure (cellular turgor pressure is important in maintaining leaf shape)
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37
Q

What prevents the cell from bursting?

A

Primary cell wall

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38
Q

What are the 4 components of the cell wall?

A
  • made of polysaccharides + protein
  • cellulose microfibrils provides strength
  1. Cellulose microfibrils
  2. Hemicellulose
  3. Pectin
  4. Proteins
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39
Q

Describe cellulose microfibrils

A

Polymers of glycosyl subunits

  • bundled together by beta-1,4 linkages, which allows for getting 1000 subunits (bundled together)
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40
Q

Describe hemicellulose

A

Crosslinks adjacent cellulose microfibrils through hydrogen bonding

  • hydrogen bonding is reversible (easily broken, allows plant cells to grow)
  • linear polymer of glucose and another sugar, e.g. xyloglycan (a type of hemicellulose)
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41
Q

Describe pectins

A

Determine the porosity of the wall (amount of pores)

  • pectins also bind proteins

-Pectins are composed of chains of galacturonic acid, which are linked by various bonds.

-these polysaccharides are hydrophilic

  • When pectins interact with water, they form a gel-like substance, which contributes to the thickening and gelling properties of fruit preserves and jellies.
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42
Q

Describe proteins in cell wall

A

Role in wall stability and loosening.

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43
Q

Explain roles of expansin and hemi-cellulose during plant growth

A

Expansin breaks hydrogen bonds between cellulose and hemi-cellulose

  • loosens the cell wall, allows for plant growth
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44
Q

Difference between cellulose and hemicellulose?

A

cellulose = repeating units of glucose

hemicellulose = various sugars (xylose, mannose, glucose, and galactose, among others.)

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45
Q

What synthesizes cellulose microfibrils? Be specific

A

Cellulose synthase in the plasma membrane

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46
Q

What does cellulose synthetase hydrolyze?

A

Glucose surrounding cell

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47
Q

What guides cellulose synthetase movement?

A

Microtubules

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48
Q

True or false: numerous rosettes can produce a single cellulose microfibril

A

True

Each rosette synthesizes its own cellulose chains, which then join others in the formation of the microfibril.

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49
Q

Where is hemicellulose and pectin made?

A

Made in Golgi stacks

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50
Q

Where are proteins like expansin made?

A

Made in the rough ER

  • traffic through Golgi- deposited in vesicles at the trans Golgi network
  • vesicles fuse with plasma membrane and deposited in wall
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51
Q

Describe root cell-elongating

A

Cellulose microfibrils and microtubules are arranged like a slinky (perpendicular to direction of expansion) . Makes it so root can’t grow sideways, only upwards.

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52
Q

What 3 things contribute to lengthwise growth?

A
  • turgor pressure
  • cell wall loosening
  • orientation of cellulose
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53
Q

True or false: coordinated cell elongation can result in complex plant movements.

Give an example

A

True

  • allows stem to loop around stick
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54
Q

True or false: mitosis is very conserved between animals and plants

A

True

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55
Q

Describe cytokinesis in plant cells

A

Cytoplasm divides by the formation of a cell plate that eventually becomes the cell wall.

  • cell plate matures -> new cell wall
  • pre-prophase band of microtubules -> transient band of microtubules that predicts the plane and position of the new cell wall. Touches the plasma membrane - leaves a footprint on the plasma membrane (will be the attachment point of the cell wall).
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56
Q

What does the pre-prophase band of microtubules specify?

A

The plane of cell division.

  • cell plates touch the points where the pre-prophase band had left on the plasma membrane.
  • PPB is not part of the spindle apparatus. it is associated with the microtubule cytoskeleton and is involved in determining the position of the cell division plane.
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57
Q

Where do the chromosomes align during metaphase of plant cell division?

A

Metaphase plate at where the pre-prophase band was.

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58
Q

Describe the phragmoplast

A
  • double-band of microtubules (on either side of forming cell plate)
  • delivers Golgi-derived vesicles to the developing cell plate
  • plus end of microtubules is toward the center of the phragmoplast
  • kinesin motors moving vesicles to the + end of microtubules
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59
Q

What direction does the phragmoplast move during phragmoplast development?

A

Outwards toward the periphery of the cell

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60
Q

The epidermis has…

A

Closely packed cells of epithelial tissue (top layer of skin)

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61
Q

What is the dermis?

A

A type of connective tissue

  • much looser
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62
Q

what are cell interactions required for ? (6)

A
  • Intercellular communication (signal transduction)
  • Survival
  • Tissue strength
  • Organ function
  • Immune system function
  • Embryonic development
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63
Q

how do cells interact with e/o?

A

selective interactions of cells of same or diff type

cells recognize surface of other cells

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64
Q

how were early cell-cell interactions studies?

A
  1. remove developing organ from chick embryo
  2. dissociating organ’s tissue to form suspensions of single cells
  3. determine ability of cells to reaggregate in culture
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65
Q

what happens when 2 diff cell types mix together?

A
  1. cells aggregate to form mixed clump
  2. cells rearrange themselves over time (cell adhere to same type)
  3. once homogenous, it differentiates to diff structure to form embryo
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66
Q

what is the first step of acute inflammation?

A

Nearby damaged tissue activates endothelial cells (becomes more adhesive to neutrophils)

P and E selectin gets temporarily activated

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67
Q

what is the second step of acute inflammation?

A

Carbohydrate residue (Psgl-1) on Neutrophil binds to selectins

Neutrophil starts rolling on cell wall until inflamed site reached

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68
Q

what is the third step of acute inflammation?

A

Platelet Activating factor (PAF or IL-8) binds to receptor on endothelial cell

G protein coupled receptor activates on Neutrophil –> activation of integrin proteins

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69
Q

what is the fourth step of acute inflammation?

A

Integrin activation binds IgSF molecules (ICAMs) to endothelial surface.

causes neutrophil to stop rolling + change conformation to squeeze past endothelial cells to damaged tissue

(transendothelial migration)

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70
Q

what is metastasis

A

spread of cancer

cancer cells growing and proliferating in unregulated manner

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71
Q

what reduces metastasis>

A

E-cadherin (better binding = less spreading)

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72
Q

Name the 4 integral membrane proteins responsible for cell-cell interactions

A
  1. Selectins
  2. Immunoglobulin super family (IgSF)
  3. Members of integrin family
  4. cadherins
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73
Q

what do protein kinase do

A

activates or inhibits target protein via phosphorylation

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74
Q

what do G proteins do>

A

activates or inhibits protein targets via physical interaction

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75
Q

What are the Selectins and what are their roles?

A
  • family of integral membrane glycoproteins
  • recognize + bind to sugars
  • Role: catch leukocytes + mediates interactions between leukocytes and cell walls @ inflamed sites
  • bonds become stronger under mechanical stress
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76
Q

are selectins Ca dependent or independent

A

dependent

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77
Q

what are the 3 types of selectins

A
  1. E-selectin: on endothelial cells
  2. P-selectin: on platelets and end on endothelial cells
  3. L-selectinL on all types of leukocytes
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78
Q

What do Immunoglobulin super family (IgSF) and an example

A
  • Has Ig domains that connect to integrin or another IgSF
  • ICAMs
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79
Q

Are IgSFs Ca independent or dependent

A

independent

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80
Q

what are ICAMs

A

intercellular adhesion molecules

integrins are some proteins that act as receptor for ICAMS

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81
Q

What are Cadherins and what do they do?

A
  • Role: adhesion or transmits signals. binds similar cadherin on neighbouring cell
  • responsible for cells to sort themselves when blended together
  • molds cells into cohesive tissues in embryos; holds them together as adults
  • Found: cell surfaces or part of interceullular junctions
    (ie. sypnases, adherens junction, desmosomes)
82
Q

are cadherins Ca dependent or independent

A

dependent

83
Q

ingetrins act as receptors for what?

A

ICAMs

84
Q

what are the 3 types of junctions?

A
  1. Tight Junction
  2. Adherens junction
  3. Desmosomes
85
Q

Where are tight junctions?

A

apical

86
Q

what do tight junctions do?

A

regulate passage of solutes between membranes of cells

can interact with actin and microtubules

87
Q

what are tight junctuons responsible for controlling? (2)

A
  1. Gate function: controls passage of molecules between cell plasma membranes (ie. ions, proteins, water)
  2. fence function: controls diffusion of integral membrane proteins between apical and basolateral membranes of one cell

(makes sure Protein A does not invade Protein B)

  • conects to actin cytoskeleton and microtubules
88
Q

What do adherens junction do?

A

connects external enviroment to actin cytoskeleton (forms band across/around cells)

contributes to tissue strength (like glue)

  • provides pathday for signals from cytoplasm to nucleus

have cadherins

88
Q

what is an example of a tight junction protein?

A

Claudins

mutation in Claudin1 leads to dehydration

89
Q

what do desmosomes do

A

protein rich area

  • cadherins here interact w/many proteins to form cytoplasmic plaque on inner surface
  • intermediate filament cytoskeleton anchors 2 cells together
  • strength to cell sheets
90
Q

What are keratin intermediate filements?

A
  • part of desmosomes
  • on epithelial cells
  • forms heterodimers (2 diff keratins) to form long cable
  • contribute to cell strength
  • mutations causes skin fragility
91
Q

where are Keratin 5 and 14 located and what do they do?

A

basal

not specialized (undergrads)

92
Q

where are keratin 1 and 10 located and what are they?

A

suprabasal (more on top)

specialized (professors)

93
Q

what are gap junctions>

A
  • communication cells (intercullular channels)
  • transmits small soluble signalling molecules through cytoplasm of one membrane to the other
  • made of connexin proteins
  • 6 connexin sibunit form transmembrane channel
  • central pore = connexon
94
Q

how many connexons to form a gap junction?

A

2

95
Q

what does hemidesmosome do?

A

anchors cell to the basal part

  • has dense cytoplasmic plaque w.keratin filaments
  • keratin filaments linked to ECM via integrins
96
Q

what are focal adhesions

A

anchors cell to the bottom but are dynamic

  • important for cell locomotion
97
Q

what do integrins do

A

transmembrane linkers

  • joins cytoskeleton to ECM or other cytoskeleton
98
Q

what is FAK

A

Focal Adhesion Kinase (central regulator of cellular responses to extracellular cues)

  • tells cells to stick to surface, move around, communicate, proliferate, or survive
  • cell to ECM
99
Q

What is SRC kinase

A
  • phosphorylates proteins to cause cell growth, proliferation, differentiation, adhesion or migration.
  • messenger of cells
100
Q

what is in a Hemidesmosome

A
  • keratin intermediate filaments attach
  • has integrin proteins
101
Q

what is in focal adhesion?

A
  • actin cytoskelton attached
  • has integrin proteins
102
Q

what is attached to tight junctions?

A

actin and microtubules

103
Q

what is on the lateral membrane?

A
  • tight junction
  • adherens junction
  • desmosomes
    -gap junction
104
Q

what is on the basal membrane?

A
  • hemidesmosomes
  • focal adhesions
105
Q

what is the Glycocalyx (cell coat)? (where it is and role)

A
  • carbohydrate projections from integral proteins to membrane

Roles:
- mediate cell-cell and cell-substratum interactions

  • provide mechanical projection to cells
  • barrier
106
Q

what is the ECM (where it is, what its made of and role)

A

Extracellular matrix

  • basement membrane extending past plasma membrane
  • can surround muscle and fat cells
  • made of secreted proteins
  • includes epithelial tissues (skin, kidney, intestine)
  • sends critical signals for survival, orientation and differentiation)
107
Q

what is a chondrocyte

A
  • connective tissue (cartilage) acting as cushion + support
  • produce + maintain ECM
108
Q

can RBC get close to chondrocytes?

A

no. Chondrocyre layer is too thick so RBC cannot get to it

109
Q

what is talin?

A
  • cell adhesion
  • formation + regulation of focal adhesions
  • connects integrins to actin cytoskeleton
110
Q

what does binding of a talin do? What does no binding of Talin do?

A
  • Talin binding to beta subunit of integrin opens alpha and beta subunits
  • ACTIVE CONFORMATION
  • no binding = inactive
111
Q

What is inside-out signalling of integrins?

A
  • activation of integrin proteins (internal) leading to strength enhancement of interactions between cell surface and extracellular ligands
112
Q

what is Outside-in signalling of integrins

A
  • binding of substrate (by integrin) send signals to FAK creating signalling cascade to nucleus
  • important for survival
113
Q

what are RGD binding sites? (where does it bind to and what do they do?)

A
  • binding sites (domains) on integrins
  • binds integrins to RGD peptide
    (Arg-Gly-Asp)
  • not all integrins have it
  • allows integrins to contract other proteins
114
Q

what are the 4 different ECM protein examples? And what do they ALL interact with?

A
  1. Collagen
  2. Proteoglycans
  3. Fibronectin
  4. Laminins
  • all interact with integrins
115
Q

describe the structures of Collagen I. (what its made of and where it is produced)

A
  • made of triple helix of 3 alpha helical chains

produced by:

  • fibroblasts (in connective tissues) in dermis below basement membrane
  • smooth muscle cells + epithelial cells
116
Q

Fibrous glycoproteins are found where?

A

only in ECMS

  • very strong
  • part of collagen I
117
Q

what does collagen do?

A
  • provides insoluble framework (determines mechanical properties of matrix ie. whether its transparent or how strong)
118
Q

how are layers of collagen in corneal stroma layered

A

uniform and alternate layers (highly organized) so provide strength + transparency

119
Q

what does proteoglycans do? (what does it bind to, what does binding result in?)

A

Binding:
- binds many cations (which binds a lot of water) to form porous hydrated gel

Results in:
- increased resistance to crushing + compression

120
Q

what is proteoglycans made of. what does it bind to

A
  • core protein (carrying covalently attached glycosaminoglycans or GAG -ve)

Binds to:
- ECM
- cell surface receptors (integrins)

121
Q

what is fibronectin consist of and where does it bind to?

A

Consists of:
- 2 similar polypeptides joined by disulfide bond (DIMERS)

Binding:
- ECM
- Cell receptor surface

122
Q

what happens if cells dont migrate on fibronectin?

A

dies

123
Q

what does fibronectin do?

A
  • cell adhesion
  • helps cell migration (highway)
124
Q

what are laminins made of and how are they organized? Where do they bind to>

A

made of:
- glycoproteins (3 diff proteins linked by disulfide bond) TRIMERS

Organized:
- in cross-like shake

Bind:
- cell-surface receptors
- laminins
- proteoglycans

125
Q

what are laminins involved in?

A
  • migration, growth and differentiation (specialization)
126
Q

as differentiation proceed does chromatin become more open or closed>?

A

more closed for more cell types

127
Q

what is heterochromatin

A

tightly, compacted/condensed DNA

128
Q

what is Euchromatin

A

loose, less condensed/accessible DNA

129
Q

what is chromosome consist of

A

chromatin fibers, histones

130
Q

what does Histone (H1) DO

A

LINKER

131
Q

describe the structure of a nucleosome

A

8 Histones (octamer) linked by H1

132
Q

what are the roles of histones

A

helps mediate DNA transcription, compaction, replication, recombination and repair

133
Q

how do you alter character of nucleosome?

A

histone modification

134
Q

what can histone modifications (epigenetic marks) do? what does it include?

A
  • serve as docking sites to recruit non-histone proteins

includes:
- phosphorylation
- acetylation
- methylation
- ubiquitination

135
Q

What is DNA or histone methylation? where is it methylated on?

A
  • methyl group added to 5’ Carbon
  • closes chromatin

methylated on:
- arginine and lysine residues

136
Q

what does HATs do?

A

Histone acetyl transferases

  • acetylates histones on lysines
  • opens chromatin
137
Q

what does HDACs do?

A

Histone deacetylases

  • deacetylates histone
  • closes chromatin
138
Q

what does HP1 do? what histone and lysine does it involve to activate?

A

heterochromatin protein 1

  • closes chromatin if methylated or deacetylated
  • Histone 3 (H3)
  • Lysine 9 (K9)
139
Q

what does H3K27ac do?

A

acts as a bookmark for transcription so that we know which cells were “on”

140
Q

what is a Barr Body?

A

The second and inactive X chromosome of females.

  • remains condensed
141
Q

how does the second X chromosome (in females) become inactive?

A
  • becomes inactive due to Xist (non-coding RNA)
  • Xist silences gene or entire chromosome
  • binds to gene rich area of chromosome b4 covering entire things
142
Q

what is totipotent?

A
  • can form everything (extraembryonic tissue)
  • can differentiate to anything
  • fertilized egg (zygote)
143
Q

what is pluripotent?

A
  • not able to produce everything required for embryo (no extraembryonic tissue)
  • baby not formed bc pregnancy not supported
  • only forms embryo
144
Q

what is multi-potent?

A
  • more limited differentiation
  • only form tissue type
145
Q

what are the steps in human therapeutic cloning or stem cell therapy? (5 steps)

A
  1. somatic cells removed from patient
  2. Somatic cell nucleus donated to enucleated egg
  3. Nucleated oocyte develops to blastocyst
  4. Embryonic stem (ES) cells from blastocyst removed and grown in culture
  5. Induce ES cells to differentiate and transplants them back to patient
146
Q

stem cells are what? what are they capable of?

A
  • they are undifferentiated

capable of
1. self-renewal

  1. commitment
147
Q

what is self-renewal

A

production of cells with similar capacity to profilerate and differentiate

(AKA SC dividing into 2 SC)

148
Q

What is commitment

A

production of cells committed to differentiate

CANNOT create SC

(SC –> progenitor–> differentiated cell)

149
Q

what is a progenitor

A

SC –> Progenitor –> differentiated cell

  • partially differentiated
150
Q

what does sperm have instead of histones

A

protamines (act like histones but easily removed by DNA)

151
Q

What are protamines joined by?

A

disulfide bonds

152
Q

what does Glutathione do?

A

reduces disulfide bonds in protamines (removed them) allowing sperm chromatin to uncoil

153
Q

what is plasticity

A

ability of partially differentiated adult stem cells to change its genetic program and differentiate into another cell

154
Q

what can the microenvironment do to cells?

A

can reprogram cells

155
Q

can cells from different species contribute to organ development

A

yes

156
Q

can adult SC do self renewal?

A

yes

157
Q

what is transdifferentiation

A

differentiated cells change to become a diff type of cell w/o going back to SC state

specialized –> specialized

158
Q

what is signal transduction

A

info from extracellular molecules translated to internal cellular signal

159
Q

what is receptor based signalling

A
  • target cells has receptor that binds specific signals (called ligands)
  • receptors are transmembrane
  • receptors are cytosolic (ligand must cross membrane on its own)
160
Q

describe and explain the main mechanisms for cell stimuli

A
  1. Autocrine/paracrine: signalling cells and target cells are the same or neighbours
  2. Cells secrete autocrine signals to stimulate own receptor signal transduction
  3. Endocrine Signalling: signal carried through body via blood to target cells (eg. estrogen, testosterone, prolactin)
  4. Juxtacrine signalling: both ligand and receptor membrane bound in close proximity
161
Q

what are some extracellular messengers?

A
  1. Amino Acids (epinephrine)
  2. Gas, NO and CO
  3. Steroids (cholesterol) eg. estrogen, testorone)
  4. protein ligands
162
Q

what are the steps of cell signalling?

A
  1. Extracellular signalling molecule (first messenger) gets bind to transmembrane receptor
  2. Effector produces second messenger

3.Second messenger causes conformational change and activates target protein

163
Q

what are second messengers

A
  • non protein molecules that amplify signal inside cell
164
Q

what does kinases do?

A

add phosphate groups

makes them active

165
Q

what does phosphatases do

A

removes phosphate group

deactivates

166
Q

describe the signalling pathway

A
  1. Protein Kinase 1 phosphorylates Protein Kinase 2
  2. Protein Kinase 2 phosphorylates Protein Kinase 3
  3. Protein kinase 3 phosphorylates transcription factor
  4. transcription factor delivers message
167
Q

what controls signal transduction

A
  1. timing of docking protein activation
  2. Ligand specific receptor
  3. Presence/absence of docking sites
  4. inhibitory proteins
168
Q

Describe the prolactin-Jak-STAT pathway

A
  1. Prolactin (Ligand) binds to prolactin receptor
  2. Binding causes conformational change (brings dimers together)
  3. Jak2 phosphorylated
  4. Jak2 phosphorylation cascades to STAT molecules (binds STAT molecules together)
  5. transcription initiation
169
Q

what is SH2?

A

domain on Stat5 that glues 2 stat molecules together

170
Q

what does STATs do

A

signal transducer and “activators” of transcription

171
Q

what type of signalling is a G protein coupled receptor (GPCR)

A

Second messenger based

172
Q

How is a G protein turned on/active?

A
  • GTP bound to G protein
173
Q

How is a G protein turned off/inactive?

A
  • GDP bound to G protein
174
Q

How do you interchange G protein active to inactive and inactive to active states?

A

active to inactive:

hydrolysis

Inactive to Active:

Release GDP, Bind to GTP (nucleotide exchange)

175
Q

what does G proteins work with to relay signals?

A

Heterotrimeric G proteins

(has α, β, and γ subunits linked by lipid groups)

176
Q

what is the first 3 steps of receptor mediated activation of effectors by heterotrimeric G proteins

A
  1. Ligand binds to receptor; conformational change; affinity for G protein increases
  2. Gα (GTP + α subunit) release GDP and released by GTP
  3. nucleotide exchange cause conformational change in Gα subunit. Gα attaches to effector
177
Q

what is steps 4 and 5 of receptor mediated activation of effectors by heterotrimeric G proteins?

A
  1. Effector produces cyclic AMP (cAMP) as second messenger (which activates cascade effect)
  2. GTP hydrolysis induces conformational change in Gα
    (GTP–>GDP)
178
Q

what are steps 6, 7, and 9 of receptor mediated activation of effectors by heterotrimeric G proteins?

A
  1. Conformational change causes Gα to dissociate from effector and back to Gβγ dimer (Inactive heterotrimeric G protein)
  2. Receptor phosphorylation allows G protein coupled receptor kinase (GRK) to bind to it
  3. Phosphorylated receptor bound by arrestin (inhibits ligand bound receptor from activating G proteins) TURNED OFF
179
Q

what does arrestin do?

A
  • terminates activation of receptors
  • facilitates degradation of 2nd messengers
180
Q

what is adenylyl cyclase?

A
  • effector that catalyzes cAMP from ATP
  • produce cAMP (a second messenger)
  • broken down by phosphodiesterase
181
Q

what are the 3 ligands that activates adenylyl cyclase?

A

ACTH, epinephrine, and glucagon

182
Q

What is the response of a liver cell to glucagon or epinephrine

A

the reaction cascade occurs as hormones binds to GPCR

183
Q

What happens when Gα subunit activates

A

activates adenylyl cyclase with produces cAMP molecules

184
Q

How do you activate Protein Kinase A (PKA) and what does it do?

A

cAMP diffuses into cytoplasm and binds to PKA

PKA amplifies G protein coupled receptor (GPCR)

185
Q

how do you amplify signal

A

Binding of a single hormone molecule activates multiple G proteins, each leading to adenylyl cyclase activation, producing numerous cAMP messengers.

186
Q

how do you regulate transcription?

A

Phosphorylated cAMP response element-binding protein (CREB) binds to CREs on DNA

187
Q

what is Gluconeogenesis regulation

A

CREB affects genes that help make glucose in the liver.

188
Q

what group is phosphatidylinositol from

A

head group

189
Q

what is a phospholipid?

A

lipid with a phosphate group

190
Q

what is a phosphoglyceride?

A

phospholipid build on glycerol backbone

191
Q

what does phosphatidylinositol interact with

A

phospholipase-c

192
Q

what is smooth muscle contraction stimulated by

A

acetylcholine (neurotransmitter)

193
Q

what does breakdown of phosphoinositides do?

A

generates second messengers

194
Q

what happens when acetylcholine bind to a smooth muscle cell?

A

receptor activates a heterotrimeric G protein

it then activates effector PLCβ

PLCβ catalyzes and splits PIP2 into IP3 and DAG

195
Q

What is DAG and what does it do?

A

Second messenger

recruits + activates effector proteins that have DAG binding C1 domain (protein kinase C)

196
Q

What does protein kinase C do

A

important in cellular growth, cellular metabolism, cell death , immune response, muscle contraction

197
Q

Describe the IP3 receptor and what happens when the receptor is bound?

A

tetrameric Ca channel

opens channel allowing Ca to diffuse into cytoplasm

198
Q

where does IP3 go>

A

diffuses into cytoplasm and binds to IP3 receptor at SER

199
Q

what messengers are Ca

A

second messengers bc bind to various target and triggers diff responses

200
Q

how do you visualize calcium levels in a cell

A

Fluorescent calcium binding compounds (fura2)

201
Q
A