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Unit 4 Flashcards

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Biology 101 flashcards
1
Q

Importance of cell communication

A

Cell specification: Development of cells so they can do their job and cells become the right type of cell needed

Receive signals for cell division

Receive signals for cell death

Cell mating in yeast

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2
Q

What types of cells communicate

A

Single and multi-celled organisms

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3
Q

Quorum sensing

A

communication among bacteria to benefit population
Small signaling molecules used by bacteria to measure population

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4
Q

Importance of quorum sensing

A

resistance to antibiotics
promote motility
Most often- change gene expression to benefit their life cycle

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5
Q

Forms of intracellular signaling

A

Contact dependent signaling
Paracrine
Endocrine
synaptic

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6
Q

Contact dependent signaling

A

signaling molecule presented as a transmembrane protein
Cells have to be in contact with each other

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7
Q

Paracrine and autocrine signaling

A

binding to nearby cells; secreting molecule, released and binding to receptors on neighboring cells

autocrine: signaling molecule comes back to stimulate same cell

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8
Q

Endocrine signaling

A

signaling cell releases molecule enter bloodstream and reaches target cell
Transfer over long distances
hormones

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9
Q

Synaptic signaling

A

Neurotransmitter binds to target cell
Signals within neuron travels long distances because of length of axon

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10
Q

Types of ligands

A

Cell surface-bound

Secreted and bind cell surface receptors

Hydrophobic small ligands diffuse across the membrane and bind to intracellular receptors (inside the cell)

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11
Q

Morphogens

A

Specialized type of ligand

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12
Q

What do morphogens’ effects depend on

A

Depend on how much of them are around
High levels- become cell type A
Medium levels- become cell type B
Low levels- become cell type C

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13
Q

What does the reaction depend on in a cell

A

It can react in different ways depending on combination of signals that a cell receives

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14
Q

How multiple signaling molecules regulate cells

A

Survive
grow and divide
differentiate
die

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15
Q

Why does one signaling molecule have varied responses

A

Different receptors

Different intracellular signals with the same receptor but different intrcellular events

Different responses to different levels or amount of ligand present

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16
Q

Endocrine speed, affininty, concentration of signaling

A

Takes more time with slower responses

Ligand acts at low concentrations

receptors have high affinity for ligand meaning it binds strongly

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17
Q

Synaptic speed, affinity, concentration of signaling

A

Faster response

Ligand acts at high concentrations

Receptors have lower affinity for ligand

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18
Q

What does the speed of signaling responses depend on

A

How far signal travels and how well receptors bind to signaling molecule

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19
Q

Speed of signaling response in altering protein function

A

Fast

Ex: binding event or adding phosphate group

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20
Q

Speed of signaling response in altering protein synthesis

A

Slow

Ex: making protein like Transcription, translation, folding

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21
Q

Molecular switches

A

Protein kinases: add phosphate groups
Protein phosphatase: remove phosphate group

GEF: GTP binding by releasing GDP
turns things on
GAP: binds GDP by GTP hydrolysis
turns things off

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22
Q

What turns proteins on and off for protein kinases and phosphatases

A

Either one

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23
Q

What turns proteins on and off for GAP and GEF

A

GEF turns things on
GAP turns things off

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24
Q

What are G protein-coupled receptors signaling molecules responsible for

A

Taste and smell
neurotransmitters
hormones
light

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25
Q

G protein coupled receptor structure and function

A

7 transmembrane domains
Associate with G protein to relay signal

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26
Q

Trimeric G Protein structure, function

A

3 subunits- a,b,y
Anchored to cytosolic leaflet of membrane
When active can bind other molecules to activate them

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27
Q

Sites where amplification occurs

A

Something activates something else in one step

GPCR activing G protein
AC making cAMP
Enzymes
Phosphorylate kinase
glycogen phosphorylase

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28
Q

Sites where amplification does not occur

A

Have to stay bound to something to stay active

ligand binding receptor
G protein binding cAMP
cAMP binding PKA

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29
Q

4 different ways to turn signaling pathways off

A

Remove receptor from cell surface via endocytosis

Receptor binds to something inside cell so it can’t activate next protein

Turn off proteins that function later in pathway

Activation of receptor activates molecule leading to production of inhibitory protein

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30
Q

When removing the receptor from the cell surface via endocytosis to stop the signaling pathway where can the receptor then go

A

The lysosome to get degraded
Held in the endosome and get recycled

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31
Q

Steps of removing GPCR from membrane via endocytosis

A

1.GPCR kinases phosphorylate intracellular domain of GPCR
2. GRKs acitvated by GPCR leading to its phosphorylation
3. Phosphorylation of GPCR provides binding site for arrestin
4. Arrestin bound to GPCR prevents interaction of receptor with G protein and can’t activate G proteins and leads to endocytosis of receptor

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32
Q

What causes the endocytosis of GPCR

A

Binding of arrestin to modified receptor leading to its endocytosis

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33
Q

What does arrestin do when bound to phosphorylated GPCR

A

prevents interaction of receptor with G proteins so it can’t activate any more G proteins
leads to endocytosis of receptor

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34
Q

What turns off G proteins

A

GAPs lead to hydrolysis of GTP to GDP and make G proteins inactive

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35
Q

What happens when G proteins are inactive

A

they can’t bind to the next molecules in the signaling pathway

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36
Q

Inactivation of cAMP

A

cAMP binds and activates PKA
PKA activates and phosphorylates cAMP phosphodiesterase leading to inactivation of cAMP

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37
Q

What causes the inactivation of cAMP

A

cAMP phosphodiesterase acts on cAMP converting 5’ AMP making it inactive and unable to make PKA

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38
Q

How is CREB inactivated

A

Dephosphorylation: protein phosphatases remove activating phosphate group turning CREB off so it can’t activate transcription of more target genes

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39
Q

GPCRs linked to phospholipase C Pathway

A

1.Ligand binds to GPCR
2. GPCR activates G protein
3. Phospholipase C cleaves phospholipid PIP2 into 2 signaling molecules DAG and IP3
4. IP3 causes Ca2+ release from ER
5. PKA activates by binding calcium and DAG

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40
Q

Intracellular receptor ligands

A

Have to be small and hydrophobic to reach receptors inside cell

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41
Q

Smooth muscle intracellular receptor

A
  1. endothelial cell receives ACh and produces NO to diffuse into muscle cell
  2. NO binds to Guanylul cyclase ad makes cGMP from GTP
  3. Relaxation in smooth muscle cell
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42
Q

Hormones intracellular receptors

A

bind to nuclear receptors, change shape, and interact with other proteins to activate transcription

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43
Q

Tyrosine kinase activity

A

ability to add phosphate to tyrosine amino acids in protein

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44
Q

Insulin signaling pathway

A
  1. Insulin binds to insulin receptor which dimerizes and undergo cross phosphorylation
  2. IRS1 phosphorluates and provides docking sites
  3. PI3K adds phosphate to PIP2 to make PIP3
  4. PIP3 binds to PDK1 activating PDK1
  5. PDK1 phosphorylates and activates PKB causing movement of glucose into membrane
  6. PKB adds Phosphate to GSK3 turning it off
  7. Glycogen synthase stores glucose as glycogen
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45
Q

RTK signaling via Ras

A
  1. Growth factor binds to RTK
  2. Ras binds and activates MAPKKK
  3. MAPKKK activates MAPKK
  4. MAPKK activates MAPK
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46
Q

What is FRET used for

A

Test if G protein and pathway is active

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47
Q

MAPK signaling: scaffolds

A

Scaffold help bring kinases together and speed up signaling
Prevent cross talk between molecules increasing precision of signaling events

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48
Q

PI-3K-Akt signaling pathway

A
  1. Insulin like growth faactor binds to RTK
  2. RTK binds and activates PI3K
  3. PI3K adds phosphate to PIP2 to make PIP3
  4. AKT bound to PIP3
  5. mTOR phosphorylates AKT
  6. Phosphorylates Bad to inactivate and inhibit apoptosis
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49
Q

Rapamycin

A

drug that can turn pathway off so cells die– cancer cells

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50
Q

Tyrosine kinase associated receptors: Cytokine pathway

A
  1. Cytokine binds to cytokine receptor and causes the dimerization of receptors
  2. receptors associated with JAK
  3. JAK phosphorylates itself and the receptor providing a binding site for STAT
  4. STAT gets phosphorylated by JAK and dimerizes with itself and binds to DNA for regulation of transcription
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51
Q

lateral inhibition

A

one cell inhibiting its neighbors from becoming like itself

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52
Q

What proteins from signaling pathways are gene regulatory proteins

A

B- catenin
STAT
Notch

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53
Q

What proteins are ligands from signaling pathways

A

Delta
Wnt

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54
Q

What proteins are effector enzymes from signaling pathways

A

Phospholipase C
JAK

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55
Q

What protein is a second messenger from signaling pathways

A

PIP3

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56
Q

How does FRET work

A

Light excites fluorescent probe proteins to test if molecule is interacting with another molecule

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57
Q

If the pathway is active what will FRET show

A

When light shined on cell, light will be emitted but immediately absorbed

58
Q

How would you know that mutant (inactive) molecule is before the active one

A

If mutant shows signaling event, it is before the others
Ras is independent of molecule so if there was a signaling event still then the molecule is before ras

59
Q

How would you know that mutant molecule is after the others

A

If mutant does not show signaling event,/response, it will be after the others

60
Q

Mitogens

A

signaling molecules activating pathways that stimulate cell division

61
Q

Growth and survival factors

A

Growth factors: stimulate cell growth

Survival factors: signaling molecules that promote cell survival by inhibiting apoptosis

62
Q

Cell cycle phases

A

G1: growth phase

S Phase: DNA replication

G2: growth phase

M phase:
- Mitosis: division of cells
- Cytokinesis: division of cytoplasms

63
Q

G1 phase function

A

Monitor cell conditions to see if cell division is appopriate

64
Q

What is used to see what genes are important for the cell cycle

A

Fission yeast
Budding yeast

They both have temperature sensitive mutatins

65
Q

How can you see what proteins/transitions points are needed in the cell cycle

A

At high temperatures, protein can’t do its job

Depending on what stage of the cell cycle the yeast is in tells what protein is needed to move into the next stage

66
Q

3 checkpoints in cell cycle

A

Start checkpoint: between G1 and S phase

Second checkpoint: between G2 and M phase
Monitor

Third checkpoint: between Metaphase and anaphase stage

67
Q

Start checkpoint

A

between G1 and S phase

Monitor environmental conditions to see if they are favorable to support more cells

68
Q

2nd checkpoint

A

between G2 and M phase
Monitor
- if environment is still favorable
- Ensure DNA was replicated properly in S phase so daughter cells get correct genetic information

69
Q

Third checkpoint

A

between Metaphase and anaphase stage

-ensure chromosomes attached to spindle correctly
-Ensures cell have the correct number of
chromosomes

70
Q

Mechanisms to ensure checkpoints are passed

A

Transcription regulation

Formation of cyclin Cdk complexes

Phosphorylation and dephosphorylation

Protein binding

Proteolysis/degradation

71
Q

Cyclin-dependent kinases (Cdks)

A

Depend on binding of cyclins to be active

72
Q

Cdk activities and amount changes

A

Activities rise and fall throughout cell but amount of Cdks stay the same

73
Q

Cyclins

A

Regulate activity of Cdks
Direct Cdks to molecules that need to get modified

74
Q

Cyclins activity and amount changes

A

protein levels of cyclins rise and fall throughout the cycle due to transcription and degradation and activity changes

75
Q

How to fully activate Cdk

A

Produce Cyclin
Cdk Activating Kinase to phosphorylate cdk so it can start phosphorylating its target protein

76
Q

Regulation of Cyclin Cdk to turn it off

A

Wee 1 Kinase adds inhibitory phosphate group on Cdk to inactivate it until conditions in cell are good

77
Q

Regulation of Cyclin Cdk to activate it again

A

Cdc25 phosphatase removes inhibitory phosphate groups to back to the active Cdk

78
Q

What quickly turns cCdk complex off when there is a mutation

A

P27 is a Cdk inhibitor protein (CKI) produced to turn off cCDK complex by binding to it

79
Q

How to get rid of P27 when not needed

A

SCF complex promotes addition of ubiquitin to CKI (P27) and can go to proteosome to get degraded

80
Q

How mitogens start the cell cycle/division

A

Mitogen activates MAP kinase pathway

MAP kinase phosphorylates and activates gene regulatory proteins to activate early gene expression

81
Q

Myk

A

Binds to DNA and leads to transcription of G1 cyclins

82
Q

How to get active G1-Cdk

A

Myk activates transcription of G1 cyclins

G1 cyclins bind to Cdk

cdk kinase adds phosphate group activating G1-cdk`

83
Q

What happens for G1/S and S cyclins to be made to move into S phase

A

G1-CDK phosphorylates and inactivates Rb (retinoblastoma) turning it off

When Rb is inactive, it turns off and can not bind to E25 so E25 can become active and helps produce G1/S and S cyclins

84
Q

Feedback loops of first checkpoint to ensure the cell can move into the S phase

A

E25 production can lead to more E25
G1/S and S Cdk keep Rb off and inactivated

85
Q

S-Cdk

A

Helps in DNA synthesis by phosphorylating origin recognition complex (ORC) to activate it

86
Q

Cohesins

A

proteins holding sister chromatids together

start organizing for mitosis

87
Q

When and how are centrosomes duplicated

A

During S phase
Triggered by G1/S-CDK complex
Start organizing for mitosis

88
Q

Initiation of mitosis

A

Cdc25 phosphotase is activated to remove inhbitory phosphate group

89
Q

Feedback loops in initiation of mitosis

A

Keep CDC 25 on
Keep Wee1 off

90
Q

M phase steps

A

Prophase: sister chromatids condense and mitotic spindle starts to form outside nucleus

Prometaphase: break down of nuclear envelope

metaphase: chromosomes attach to spindle line up at middle of cell

Anaphase: sister chromatids separate and pulled toward spindle poles due to Kinetocore MT shortening

Telophase: Chromosomes arrive at poles and nuclear envelope reassembles

Cytokinesis: Actin and myosin separate 2 cells by using Rho

91
Q

2 parts of anaphase

A

A. Shortening of kinetochore MT moves chromosomes toward centrosomes

B. Interpolar MT slides using kinesins pushing poles apart from each other and Astro MT pull poles apart

92
Q

What is used to move through third checkpoint

A

APC/C active when bound to Cdc2

93
Q

APC/C

A

Adds ubiquitin chain so they get degraded

degrades
- M cyclins and S cyclins
- Securin

94
Q

Securin

A

when degraded it causes separase to be activated and to separate sister chromatids to move into anaphase

95
Q

How our cells arrest the cell cycle in response to a damage event

A

Damage triggers series of events leading to phosphorylation/activation of p53 causing the production of p21/27 (cdk inhibitory protein) causing cell cycle arrest

96
Q

How our cells arrest the cell cycle in response to excessive Myc

A

Excessive Myc activates Arf (inhibitor protein) binding onto Mdm2 activating p53 causing cell cycle arrest or apoptosis

97
Q

Steps in Checkpoint 1 (G1 to S)

A
  1. Mitogens are released and bind receptors, stimulating cell division

2.Myc protein is produced increasing production of G1 cyclins
3. G1 cyclins associate with Cdk
4. Cdk phosphorylates and inactivates the Rb protein resulting in activation of E2F
5.E2F promotes transcription of G1/S and S cyclins
6. S-Cdk promotes assembly of pre initiation complexes for DNA replication

98
Q

Steps in Checkpoint 2 (G2 to M)

A
  1. M cyclins bind to Cdk
  2. CAK adds activating phosphate group and Wee1 adds inhibitory phosphate so mitosis can proceed
  3. Cdc25 removes inhibitory phosphate group so mitosis can proceed
  4. Positive feedback loops act to inhibit Wee1 and activate Cdc25
  5. M-Cdk also acts to phosphorylate and activate APC/C leading to its own destruction
99
Q

Steps in Checkpoint 3 (Metaphase to Anaphase)

A

1.Cdc20 binds and activates the APC
2. APC promotes activation of separase by causing degradation of securin
3. This causes break up of the cohesin complex and separation of sister chromatids during anaphase

100
Q

Differences between Mitosis and Meiosis

A

Meiosis:
- germ cells
- Half the number of chromosomes as starting cell
Meiosis 1: Homologous pairs of chromosomes line up on spindle and separated in first division
Meiosis 2: sister chromatids line up and separate in 2nd division

Mitosis:
- somatic cells
- Same of chromosomes as starting cell
- Sister chromatids line up on the spindle individually

101
Q

3 types of microtubules

A

Kinetochore microtubules: attach to the kinetochores bound to each sister chromatid, and
shorten during anaphase A.

Astral microtubules:positions the mitotic spindle and involved in pulling the two poles apart
in Anaphase B.

Interpolar microtubules: connect the two poles to each other. The motor protein kinesin
moves along interpolar microtubules to move the two poles apart in Anaphase B.

102
Q

Causes for cell death

A

Organs/tissues have correct structure
dispose of older cells
damaging event
correct number of nerve cells

103
Q

Caspase

A

Enzymes that break down cell components as part of apoptosis

104
Q

the extrinsic pathway of apoptosis (steps)

A
  1. If Killer lymphocytes encounters foreign cell, they express Fas ligand signaling molecule

2.Fas ligand binds to Fas death receptor allowing receptor to interact with FADD adaptor protein

  1. FADD Allows caspase enzymes to be brought in to assemble DISC (death inducing signaling co mplex)
    complex in cell
  2. DISC brings multiple caspase molecules together so they can cleave each other to activate caspase
  3. Initiator caspase: first class to become active and activates executioner caspases

6.Executioner caspase: cleave other molecules (proteins, DNA) in cells leading to apoptosis

105
Q

FADD

A

In extrinsic apoptosis pathway, Allows caspase enzymes to be brought together to assemble DISC (death inducing signaling co mplex) complex in cell

106
Q

Initiator v executioner caspase

A

Initiator caspase: first class to become active and activates executioner caspases

Executioner caspase: cleave other molecules (proteins, DNA) in cells leading to apoptosis

107
Q

apoptosome

A

multiple Apaf1s formed by binding of cytochrome C to Apaf1

108
Q

Anti-apoptotic Bcl2 proteins

A

Inhibit apoptosis by keeping Bax and Bak apart

maintain membrane integrity: Cytochrome C stays inside mitochondria

109
Q

BH3

A

When cell encounters bad event, BH3 proteins are activated and turn off anti apoptotic Bcl2 protein

110
Q

Intrinsic pathway of apoptosis (Steps)

A
  1. When cell encounters bad event, BH3 only proteins are activated and turn off anti apoptotic Bcl2 protein
  2. Inhibiting anti apoptotic Bcl2 protein prevents it from keeping Bax and Bak apart so Bax and Bak associate with each other forming channels
  3. Channels allow cytochrome C to be released from mitochondria
  4. Allows it to bind to Apaf1 changing Apaf1’s structure so multiple Apaf1 can form apoptosome
  5. Apoptosomes can bring initiator caspases together so they can active executioner caspase
111
Q

What gets released when Bax and Bak come together

A

Cytochrome C
Anti-IAPs

112
Q

IAPs

A

inhibit apoptosis In healthy cells, when they encounter caspase, bind and block it to protect cells

113
Q

Anti-IAPs

A

prevent IAPs from binding caspases

Ensures apoptosis proceeds

114
Q

How a cell could be allowed to survive

A

Inactivation of pro apoptotic BH3 -only Bcl2

Increased production of anti apoptotic bcl2 proteins

Inactivation of anti IAPs

115
Q

What characteristic is unqiue to cancer cells

A

prefer only going through glycolysis to use glucose as energy source

Have to take up much more glucose

116
Q

What detects cancerous cells

A

PET scans can detect increased levels of glucose uptake and metabolism

117
Q

Benign v Malignant v Metastiasized tumor

A

Benign tumor: non-invasive; haven’t invaded underlying tissue

Malignant tumor: invasive; invade neighboring tissue pass underlying tissue

Metastasized tumor: cancer cells go farther away and form tumors in new location

118
Q

Why can mutations be present

A

Inheritance
Radiation
Chemical carcinogen
Errors in DNA replication
Defects in DNA repair

119
Q

What processes do mutations alter

A

Cell proliferation
Dna damage response
Cell growth
Alterations in cell survival

120
Q

Angiogensis

A

the process of making new blood vessels to spread cancer cells quicker

121
Q

Cancer cell properties

A

Angiogenesis
Stabilize telomere length
Increased ability to grow/proliferate
Decreased sensitivity to anti-proliferative signals
Less likely to undergo apoptosis

122
Q

Cell senescence and how cancer prevents this

A

Cell senescence: Natural process of a cell no longer dividing

Cancer gets around this:
Keep telomerase active so they don’t shorten
Disable checkpoint so cell cycle proceeds

123
Q

What is cancer accumluated from

A

single cell accumulating at least 3 mutations

124
Q

2 classes of mutations causing gene to become dangerous to cell

A

Overactivity mutation

Underactivity mutation

125
Q

Oncogene with examples

A

genes that experience overactive mutation can become dangerous and can cause cell to become cancer cell

Examples: Myk and cyclin-cdk

126
Q

Mutations that oncogene experiences

A

Deletion or point mutation in coding sequence

Regulatory mutation

Gene amplification

Chromosome rearrangement
-Produce more of protein
-produce more active version of protein

127
Q

oncogene v Tumor suppressor

A

oncogenes cause gain of function effects

Tumor suppressor gene cause loss of function effects

128
Q

How many genes need to be mutated in tumor suppressor gene

A

Both copies of the gene have to be mutated

129
Q

Mechanisms of gene inactivation (2)

A

Change in nucleotide sequence so protein is no longer functioning

Epigenetic changes affect ability of gene to be transcribed

130
Q

2 types of Gene inactivation by epigenetic changes

A

packaging of DNA as heterochromatin making it not accessible for transcription

DNA methylation of C nucleotide to turn gene off

131
Q

P53

A

Important Tumor suppressor genes

Keep things inactive

Components of p53 pathway mutated in all cancer
`

132
Q

Steps to metastasis

A

Tumor has to be able to travel through blood stream , survive and proliferate in new tissue and form tumor

133
Q

How virus can make it more likely to develop cancer

A

Viral genetic info gets integrtated into host genome making it more likely for cell to become cancerous

E6 and E7 interfere with rb and p53 tumor suppressor proteins

134
Q

Overactivity Mutation

A

proteins when active move through the cell cycle

Problem if the mutation is in one copy of oncogene

135
Q

Underactivity Mutation

A

turns off the cell cycle

Problem if mutation in both copy of tumor suppressor genes

136
Q

What proteins type does KIF18B gene encode

A

Kinesin family

137
Q

Effect of KIF18B knock down

A

Decreased colony number
Decreased cell migration
Decreased invasion

138
Q

Overexpression of KIF18B

A

Increase cell imgration, colony number, invasion

139
Q

Knock down of KIF18B on tumor groqth

A

Formation of smaller tumors

140
Q

KIF18B oncogene or tumor supressor gene

A

oncogene promote tumor growth

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