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Molecular Cell Bio > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

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1
Q

What are the two pathways that stem cells can take?

A

Self renewal and differentiation

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2
Q

What is a totipotent stem cell?

A

Can differentiate into any cell that will become part of the developing embryo or extra embryonic structure (placenta)

ex. cells of the morula

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3
Q

What is a pluripotent stem cell?

A

Can differentiate into any cell that will become part of the developing embryo

ex. embryonic stem cells

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4
Q

What is a Multipotent stem cell?

A

Is restricted into differentiating only into a specific cell type

ex. adult stem cell, lining of gut, hair, blood

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5
Q

What is a cytokine?

A

Proteins that are secreted by certain cells

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6
Q

Are ESCs immortal?

A

Yes, no replicative limit

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7
Q

What are fibroblasts?

A

Cells of connective tissue

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8
Q

How does one create a Chimera?

A

When one injects the stem cells of one organism into the blastocyst of another.

Brown mouse+ white mouse

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9
Q

How does one look for germline transmission in an organism?

A

Back-crossing the chimera with the parental strain, and seeing how the offspring appear

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10
Q

What does the Ectoderm develop in to?

A

Epidermis of skin and derivatives (sweat glands and hair follicles) and nervous system

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11
Q

What does the Mesoderm develop in to?

A

Skeletal system, muscular layer of stomach and intestine

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12
Q

What does the Endoderm develop in to?

A

Epithelial lining of digestive tract and respiratory system, liver and pancreas

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13
Q

What can a Microarray tell us?

A

Whether genes are expressed or not

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14
Q

Where are stem cells located in the gut epithelium?

A

In the crypt, near the paneth cells

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15
Q

What do transit amplifying cells differentiate into?

A

Mucus- secreting cells
Absorptive cells
Hormone-secreting cells (endocrine cells)

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16
Q

What is a niche?

A

A specialized microenvironment

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17
Q

What do paneth cells secrete?

A

The signaling molecule Wnt3a

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18
Q

What is Frizzled?

A

Stem cell’s receptor, it binds to Wnt3a

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19
Q

Describe the Wnt3a pathway and how that controls stem cell fate

A

When Wnt3a is not present, the protein Beta-catenin is degraded by the beta- catenin destruction complex.
Beta- catenin acts like a transcription factor to upregulate expression of genes.
When Wnt3a binds to receptors, it deactivates the destruction complex, allowing the beta-catenin to increase the transcription of stem-cell genes

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20
Q

What does noggin do?

A

It is a BMP antagonist that concentrates near the base of the crypt and block BMP

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21
Q

What does BMP do?

A

Concentrates near villus apex, promotes differentiation

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22
Q

What is an autonomous stem cell niche?

A

When a differentiated stem cell becomes a Paneth cell, and a niche can form on its own

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23
Q

What is an Erythroid?

A

Red blood cells (RBC), platelets

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24
Q

What is a Myeloid?

A

Macrophages (monocytes) (sit in tissue and wait for invaders), Granulocytes (neutrophil)(circulate through blood, help macrophages)

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25
What is a Lymphoid?
Adaptive immunity B cells (generate antibodies) NK and T cells
26
How are myeloids, lymphoids and erythroids created?
Through their respective progenitors
27
What is CD34?
A transmembrane protein only found in the plasma membrane, only expressed in HSC Used in conjunction with magnets in separation columns
28
What is secreted and from where are they secreted needed to maintain HSC potency?
Stem cell factor (SCF) and FLT3 ligands are secreted from mesenchymal stromal cells.
29
Are HCS autonomous or not? Why?
Not. they require other non-blood cell types to maintain themselves
30
What are the three types of Cytoskeleton? List in increasing size order
Actin, Intermediate filaments and Microtubules
31
Describe Actin polymerization
ATP actin binds to + end during polymerization, ATP is hydrolyzed to ADP shortly after. ADP-actin reduces strength between the monomers, resulting in decay on the - end TREADMILLING
32
What are the actin monomers?
Alpha actin- responsible for muscle contraction Beta actin- cytoskeleton structures and cell motility
33
What are the three components of muscle tissue?
z disk (alpha actin) thick filaments (myosin II) thin filament (actin)
34
Describe the steps of muscle contraction
Myosin starts at rest, tightly bonded to actin due to the lack of ATP/ADP binding. Then, the connection is disrupted due to ATP binding to the head of the myosin. Next, the attached ATP gets hydrolyzed, and the myosin moves towards the plus end of the actin. Now that the ATP has been converted to ADP, the ADP-myosin complex can now bind to the actin again. Finally, the power stroke occurs when the ADP is released from the myosin and the myosin binds to the actin, causing a shift downwards.
35
What are muscle contractions initiated by? How does this work?
A rise of cytosolic Ca2+ Neurotransmitters signal to muscle cells to release Ca2+ from sacroplasmic reticulum. Ca is transient, pumped back into SR after contraction, allowing muscle to relax again
36
What are the 4 different types of intermediate filaments?
Lamin Keratin Vimentin Neurofilament
37
How are dimers of intermediate filaments joined?
Head to head coiled dimer NH3 to NH3
38
How are tetramers of intermediate filaments joined? What about 8 of those tetramers?
Head to tail staggered tetramers, and 8 of those tetramers join by lateral association
39
Describe the three layers of the skin that we discussed in class
stratum corneum(Top) - (further development), includes loss of organelles and nucleus, cross linking of keratin Stratum spinosum- the keratinocytes migrate towards the skin, expressing a lot of keratin Basel cell layer- hemidesmosome attachment to basal lamina, rare stem cells and transient amplifying cells
40
What are the steps of Prelamin A processing
1. Farnesylation (adds branched lipid to terminal cysteine) 2. C-terminal cleavage (ZMPSTE24) 3. Methylation (isocysteine methyltransferase) 4. Upstream cleavage (ZMPSTE24)
41
What disease occurs with Prelamin A processing, describe what is is, how it happens and how it affects the patient
A mutation in the lamin proteins keeps the prelamin permanently farnesylated, leads to Hutchinson Gilford Progeria Syndrome. Patents have poor eyesight, nuclear deformation and deformed bone structure.
42
Where do microtubules grow from?
The cell's centrosome
43
What is the difference in the nucleotides that provide energy for polymerization in Actin and Microtubules?
Actin uses ATP and Microtubules use GTP
44
Describe the polymerization of microtubules and how it differs from Actin
GTP- tubulin dimers add to the + end on microtubules, but depolarization also occurs on the + end as well when GTP gets hydrolyzed to GDP (- end is anchored to centrosome)
45
What do microtubules consist of?
alpha and beta tubulin heterodimers
46
What do microtubules do?
Transport macromolecules and situate cellular organelles.
47
What do kinesin and dynein do?
they are crucial in mitosis and vesicle/organelle transport
48
What ends to kinesin and dynein move to on microtubules?
Kinesin moves to + end Dynein moves to -
49
What are kinesins in terms of their individual structure?
They are homodimers. The head region associates with the microtubule, and the tails twist around each other
50
Describe the motor activity of dynein
First, one of the heads, the one that is attached to the tubulin, binds to an ATP molecule. A power stroke occurs when that binding causes the other head, which is bound to ADP to swing around. Next, the ADP molecule is let go from the kinesin, which allows it to bind to the microtubule. Finally, the ATP that was attached before undergoes a hydrolysis reaction, which causes a release from the microtubule.
51
Describe the binding relationships between kinesin and nucleotides
ATP bound: tight binding to microtubule ADP bound: Prevents binding No nucleotide: weak binding
52
What are four important ECM proteins?
collagen Fibronectin Laminen Glycosaminoglycans
53
What is the special amino acid residue present in collagen? Where is it located and what does it do?
Every third amino acid is a glycine, which aids in the flexibility of the peptide chain
54
What is the physical structure of collagen?
A triple helix
55
How is collagen made?
Within the secretory vesicles of fibroblasts, procollagen is packed up. The vesicle then moves towards the plasma membrane, where it fuses and secretes the procollagen. then a protease cleaves the loose ends.
56
What are the three important types of collagen?
Type 1: skin, tendon, vasculature, bone and scar Type 2: cartilage Type 4: Basement membranes (epithelium)
57
What are the three bone cells and what do they do?
Osteocytes- bone cells Osteoclasts- break down tissue Osteoblasts- generate bone tissue
58
How does Osteogenesis Imperfecta (Brittle Bone Disease) happen?
Loss of function mutations in COL1A1 mutations in glycine residues impair the formation of the triple-helix, and collagen fibrils are disrupted
59
What is Ehlers-Danlos Syndrome and how does it occur?
Loss of function mutation in COL5A1. The disease is causes hyperflexibility in skin and joints
60
What is Fibronectin?
A DIMER that mediates the attachment of cells to collagen fibrils
61
How does snake venom work?
The disintegrins within the venom digest the cell attachment, causing muscle to fail. Collagen can't attach to cells
62
What are the subunits of Fibronectin?
Alpha and beta (dimers)
63
Describe Integrin Activation
When alpha and beta bind fibronectin, they activate and dimerize. This activates Focal Adhesion Kinase (FAK) FAK then brings the scaffolding protein Talin to the plasma membrane Talin recruits Vinculin (adapter proteins) and Actin related Protein (ARP213) which promotes actin polymerization (then cell motility)
64
What is the difference between Lamin A and Laminin?
Lamin A: intermediate filament Laminin: ECM protein (makes up basal lamina)
65
How many subunits does Laminin contain and what are they? How many kinds of genes do they contain
3 subunits, alpha beta and gamma. alpha- 5 beta- 4 gamma- 3
66
What is the structure of Laminin?
Triple helix (like collagen)
67
What do basement membranes do?
They protect/ block misbehaving tissues from attacking healthy tissue
68
What do Glycosaminoglycans (GAGs) do?
They lubricate the ECM
69
What are Glycosaminoglycans made of? Whats an example of one?
They are carbohydrate polymers, they they hydrophilic and heavily hydrated. Hyaluronic acid is one and GAGs also make up synovial fluid
70
What are the four different types of Junctions between Epithelial cells?
1. Tight junction 2. Adherens Junction 3. Desmodomes/ Hemidesmosomes 4. Gap Junction
71
What are the two proteins within Tight Junctions?
Claudins and Occludins
72
What is a Tight junction?
They form between epithelial cells through protein- protein interactions, they are watertight and impermeable.
73
What is an Adheren Junction?
They link cadherin to the intracellular Actin Filaments
74
What are the two cadherin proteins (Adheren Junction)
E-cadherin (epithelial) N- cadherin (neuronal)
75
What are the three linker proteins in Adherens Junctions?
alpha actin (muscle z-disk) Vinculin (adapter proteins: integrin) Catenin (like beta-catenin in stem cells)
76
How does cancer metastasis occur?
Cancers (adenocarcinomas) lose expression of the cadherins, allowing them to move.
77
What are Desmosomes?
Cell contact points mediated between cadherins and intermediate filaments
78
What are the 2 cadherin proteins in Desmosomes?
Desmoglein and Desmocolin
79
What are the two attachments proteins in desmosomes?
Desmoplankin and Plankoglobins
80
What happens when a person gets a blister?
Breakage of demosomes severe blistering can be caused by Epidermolysis Bullosa
81
What are the transmembrane proteins in Hemidesmosomes?
Integrins
82
What are the Linker proteins in Hemidesmosomes?
Plectins
83
What do Gap Junctions do?
Allow for the passage of ions and small molecules between adjacent cells
84
How is cell- cell communication mediated
Via connexins in gap junctions
85
How does GCaMP work?
The GFP protein is broken into two parts, and when Ca 2+ is present, it binds the two parts together via M12 and CaM protein, and it glows

Molecular Cell Bio (3 decks)

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