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BIOL112 Flashcards

1
Q

How big are eukaryotes

A

5-100 micrometres

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2
Q

How do archea function at extreme conditions

A

They have specific adaptations to withstand temperature stresses such as temperature resistant enzymes

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3
Q

What are extremophiles useful for

A

1)PCR
2)Biofuels
3)Biomining
4)Carotenoid production
5)Detergents

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4
Q

How does prokaryotic flagella function

A

ATP is used to pump hydrogen ions through the motor turning the flagellum (like atp synthase but active)

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5
Q

Whats the difference between gram postive and gram negative

A

Poistive has thick peptidoglycan wherease neative has thin
Positive has simple cell wall and negative has complex double layer
Positive has teichoic acids and negative has lipopolysaccharides

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6
Q

Uses of bacteria

A

Medical: e.g insulin production and drug screening
Agricultural: introducing new genes to plants
Environmental: removing pollutants
Industrial: lactic bacteria develops flavour and others can improve storage length of wine

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7
Q

what modes of nutrition are there

A

Photo/chemo autotrophs

Photo/chemo heterotrophs

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8
Q

What shapes of viruses are there

A

Filamenous (long)
Spheroid (capsomere)
Enveloped (membrane envelope)
Tailed spheroid (bacteriopahge)

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9
Q

What are some uses of microscopy

A

Frequency of cell types in a sample, Host-pathogen interaction, Abundance of proteins after stimulation, colocalisation of proteins, localisation of proteins or microbes in cells

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10
Q

Name 6 types of microscopy

A

Brightfield (stained and unstained)
Flourescence
Phase-contrast
ifferential-interference-contrast
conofocal (optical sectioning)

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11
Q

Ways to get better images in light microscopes

A

Deconvulation (algorithms remove out of focus light to sharpen image)
Super resolution (gets light from individual florescent molecules recording their position (breaks resolution limit)

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12
Q

How to electron microscopes maginify

A

Using magnetic objectve and projective lenses

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13
Q

How do you keep cell samples flat and not wrinkled in an EM microscope

A

using a copper grid

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14
Q

How do you see a protein with an electron microscope

A

using cryoTEM

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15
Q

What are samples in SEM coated with

A

Gold to protect from electron beam damage

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16
Q

What is cell fractionation used for

A

Protein enrichment/characterization/translocation

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17
Q

How does the cell break down its own cell debris

A

using lysosomes

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18
Q

What are the holes in plant membranes and walls called and what do they do

A

Plasmodesmata and they are used for exchange and communication between plant cells

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19
Q

How do people think the mitochondira come about in eukaryotes

A

Via endoymbiosis (prokaryote absorbing aerobic bacterium)

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20
Q

What enzymes are responsible for flip-flopping in cell membranes

A

flippase and floppase

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21
Q

How does cholesterol affect fluidity

A

At low temperature it increases the distance between phopsholipids increasing fluidity but in high temperature it does the opposite

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22
Q

What is the lipid bilayer to membrane proteins

A

A solvent

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23
Q

Why is freeze-fracture EM used

A

to split the membrane under pressure to show that the inside and outside layer of the membrane are different

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24
Q

What is the glycocalyx

A

a thin layer of carbohydrate present on the plasma membrane with a varitey of functions such as absorption and protection

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25
Q

How could removing CCR5 stop HIV infections

A

prevents the HIV virus from attatching to these receptors and entering the cells

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26
Q

How are eithelial cells fastened together

A

By desmosome junctions to withstand stresses and strains

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27
Q

What does the epithelium protect against

A

Mechanicla injury, microbes and fluid loss

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28
Q

What types of epithelium are there

A

Simple (single layer), stratified (multi layer)
and they can have different shapes
Cuboidal and columnar

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29
Q

What types of connective tissue are there

A

Dense (bone ect) and loose (holds glands and epithelia together)

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30
Q

What types of vertebrate muscle are there

A

Skeletal (voluntary movement)
Smooth (involuntary movement)
Cardiac (same as smooth but has intercalated disc for electrical signals in heart)

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31
Q

What cells are responsible for nourishing, insulating and replenishing neurons

A

Glilial cells (gila)

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32
Q

What is the smooth edoplasmic reticulum and what does it do?

A

It produces phospholipids, fat and steroids and metabolises carbohydrates
In hepatocytes it breaks down glycogen into glucose
It detoxifies lipid soluble drugs

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33
Q

What is the sarcoplasmic reticulum

A

A network of tubular sacs in muscle cells that stores and regulates calcium ions (controls contraction) and electrical signals
They surround myofibrils like a membrane

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34
Q

What are the Z, H, A and I lines?

A

Z - Dark lines between actin and myosin filaments
H - Middle bit with only myosin that shortens in contraction
A - Length of total myosin
I - length of actin including Z line

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35
Q

How do calcium ions expose myosin binding site on the actin

A

They attatch to the tropomyosin complex changing the shape of the tropomyosin

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36
Q

Describe actin-mysoin interactions

A

Myosin head binds to atp and moves into a high energy configuration
When it binds to an exposed actin binding site it moves back to its low energy configuration releasing adp + pi and dragging the actin along it then unbinds and repeats

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37
Q

What classes of protein synthesis take place in the RER

A

Secreted proteins
Glycosylated proteins
Lysosomal enzymes
Membrane bound proteins

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38
Q

What do signal peptides do

A

They attatch to a signal-recognition particle (SRP) which binds to a translocation complex on the RER binding the ribosome to the RER and released the protein produced into the RER for packaging

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39
Q

What are polyribosomes

A

An mRNA molecule that is being simultaneously translated by multiple ribosomes (common)

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40
Q

What side of the golgi accepts the ER transport vesicles and which releases it

A

Recieves on the cis face and releases from the trans face

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41
Q

What does the golgi apperatus do

A

It mediates the flow of proteins from RER and their destinations (either secreted or to an organelle)

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42
Q

What does the mannose 6-phosphate receptor do

A

binds to the phosporylated lysosomal enzyme and tells the golgi that it is a lysosomal enzyme that must be transported to the lysosome (it is recycled in its pathway)

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43
Q

What is glycosylation

A

Principle modification of protwins in the golgi

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44
Q

How does cystic fibrosis affect cilliated and goblet cells

A

Goblet cells produce dry mucus that is harder to remove and there are less cilliated cells to remove them

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45
Q

What are lysosomes and what do they do

A

A vesicular structure that contains 60 hydrolytic enzymes that activate in acidic conditions. They digest targets by fusing with it and pumping hydrogen ions into the lysosome to activate the enzymes

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46
Q

what are lysosomal storage diseases

A

Non funtional lysosomal enzymes resulting in build up of insoluble metabolytes causing the lysosome to enlarge

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47
Q

What is exocytosis

A

Vesicles that fuse to the interior of the cell membrne to expel their contents out of the cell

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48
Q

What is endocytosis - phagocytosis

A

Pseudopodium elongate and engluf the target and wrap around it to absorb it into the cell creating a vacuole containting the target (protozoa feed like this)

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49
Q

What is pinocytosis

A

Plasma membrane being pinched off to absorb extracellular fluid

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50
Q

What is receptor-mediated endocytosis

A

Macromolecules binding to specific cll surface receptors triggering endocytosis. This can cause them to be transferred to lysosomes or golgi for processing.
This is also how viruses enter the cell

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51
Q

Where did mitochondira come from in theory

A

Anaerobic cell ingests aerobic bacteria and over time becomes adapted to the internal environment of the cell

52
Q

Why and how do mitochondira move around the cell

A

They move via the microtubules of the cytoskeleton and are found in locations of high ATP consumption

53
Q

What can ATP do

A

Can phospohyorlyate trnasport proteins
Can phosphorylate motor proteins
Can phosphorylate key reactants

54
Q

How do mitochondria obtain the energy for ATP synthesis

A

High energy electrons of orgnnic molecules

55
Q

How many molecules of NADH , ATP and FADH2 are produced in one cycle of the krebs (one Acertyl CoA)

A

3 NADH
1 ATP
1FADH2

56
Q

What is the electron transport chain

A

A collection of multiprotein complexes in the mitochondria inner membrane
Electrons from NADH and FADH2 loose energy as they go down the chain (energy used to pump hydrogen ions across the membrane)

57
Q

What is the difference between FADH2 and NADH

A

FADH2 picks up slightly lower energy electrons and joins the electron transport chain at a different point

58
Q

How many ATP molecules are produced roughly per 10 Hydrogen ions

A

~3 ATP per 10 H+

59
Q

What are some mitochondrial poisons

A

Cyanide (blocks electron transport chain)
2,4-Dinitrophenol (makes membrane leaky to H+ and cooks you from the inside)

60
Q

Where does the light dependant reactions (reaction type 1) in the cholorplast take place and where does the calvin cycle (reaction type 2) take place

A

LDR - thylakoid membrane
Calvin - Stroma

61
Q

What pigments do thylakoid membranes contain

A

Chlorophyll a and b and carotenoids

62
Q

What does chlorophyll do when isolated and exposed to a photon and how does this change in a group

A

photoelectric effect and energy is released as heat when alone

In groups the energy is passed onto bordering molecules until it reaches a primary electron acceptor known as a reaction center

63
Q

In the light reaction there are two different photosystems what are they and what is the difference between them

A

In photosystem 1 water is not split and the electrons are replaced in the p700 (700nm optimal) reaction center by electrons from the electron transport chain that originated in the P680 (through plastoquinone, cytochrome complex ad plastocyanin)

In photosystem 2 water is split and Electrons from the water are used to replace the electrons lost in the p680 reaction center (works best at 680nm)

64
Q

What happens to electrons that leave photosystem 1

A

They are fed into NADP reductase via an electron transport chain (through ferrodoxin)

65
Q

How can photosystem 1 get its electrons

A

from photosystem 2 or from a cyclic electron flow through cytochrome complex

66
Q

What is used up in the calvin cycle

A

3 molecules of CO2
9 ATP
6 NADPH

67
Q

What is the cytoskeleton made up of

A

Actin microfilaments
Intermedidate filaments
Microtubules

68
Q

What are the functions of the cytoskeleton

A

Muscular movement, molecule transport and normal embryonic development

69
Q

What is the structure of microfilaments and what are their functions

A

Two intertwined actin strands (individual molecules are Globular but a olymer of actin molecules is filamentou) and 7-9nm wide
Functions:
Cell shape maintenence and change
Muscle contraction
Cytoplasmic streaming
Cell motility
Cell division (contractile ring around cell boundary to pinch off)

70
Q

What is the stucture of microtubules and what is it’s functions

A

Hollow tubes with a wall made of 13 tubuln molecules 25nm in diameter
Functions:
Cell shap maintenence
Cell motility
Chromosomal movements
Organelle movement

71
Q

Why do microtubules move

A

Dymnamic instability

72
Q

What is the difference between prokatrotes flagellla and eukaryote flagella

A

Pro:
protrudes through cell wall
Spins due to motor protein
Euk:
(9+2) of microtubuled
Whipping movment

73
Q

What are the microtubule motor proteins

A

Kinesin nd dynein
Kinesin moves cargo to the + side of the microtubuke and Dyenins trnansports it the other way (uses ATP to move along microtubule)

74
Q

What are intermediate filaments and what are their functions7

A

Fibrous proteins supercoiled into cabkes
Functions:
Cell shape maintenence
Nuclear anchorage
Nuclear lamia formation

75
Q

How many types of intermediate filaments are there

A

Each cell type expreses different intermediate filaments

76
Q

What types of cell junctions are there

A

Impermeable junctions E.g tight junctions
Adhesive Junctions E.g Adherens junctions
Communicating junctions E.g Chemical synapses

77
Q

What purpose do tight junction proteins serve

A

They prevent molecule from leaking between adjacent cells (e.g pathogen preventions or keeping stomach acid getting into the blood

78
Q

Describe the physiology of a tight junctions

A

Transmembrane proteins:
Junction adhesion molecules (JAM)
Caludins
Occludin

Connecting to cytosolic proteins that act as scaffolding, signalling and polarity

79
Q

Name the anchoring junctions and a breif description of them

A

Adherens junction:
Connects cells to actin filament
Demosomes connect cells to intermediate filaments
Focal adhesion: connect ECM to actin filaments
Hemi-desmosomes: connect ECM to intermediat filaments

80
Q

Descrobe the Cadherin/catenin complex (adherens junction)

A

Beta catenin inside cell connected dto E cadherin outside cell which is attatched to another E cadherin outside the cell attatched to another Beta catenin inside a different cell

81
Q

Up to what size can molecules pass through gap junctions

A

1500 Molecular weight

82
Q

What are the channels in gap junctions made of

A

12 connexin molecules (6 from each cell)

83
Q

Why do cells divide

A

To create new organims (e.g bacteria)
For growth (e.g children)
For cell replacement where there is wear and tear or programmed cell death

84
Q

What basic requirements do cells need to divide effectively

A

DNA must be duplicated
Chromosomes must be physically seperated into daughter cells
Daughter cells must physically divide

85
Q

What is the point of no return in the cell cycle

A

Once it reaches S phase it can no longer stop cell division

86
Q

Describe the G2 phase of interphase

A

Nuclear envelope intact
Chromosomes replicated
Centrosomes replicated
Microtubules extending radially

87
Q

Descripe prophase

A

Chromatin fibres condense (discrete chromosomes)
Nucleoli disappear
centrosomes seperate
Mitotic spindles start to form

88
Q

Describe prometaphase

A

Nuclear evelope breakdown
Microtubules attatch to chromosomes at kinetochores
Microtubules interact with opposite pole microtubules

89
Q

Describe metaphase

A

Centrosomes at opposite poles
Chromosomes align on metaphase plate
sister kinetochores attatch to microtubules

90
Q

Describe anaphase

A

Centromeres seperate
Sister chromatids move to poles
Chromatids become chromosomes
Poles seperate further

91
Q

Describe telophase

A

Elongation of cell by microtubules
Daughter nucleoli form at poles
Nuclear envelopes form
Chromatin decondenses

92
Q

What families of microtubules are there

A

Astral (basically an anchor)
Kinetochore
Non-kinetochore

93
Q

What causes movement in cell division

A

Astral motors - dyenin (pull astral microtubules and shortens the microtubule by depolymerising the end)
Kinetochore motor - dyenin also depolymerises the microtubules at the end
Non-kinetochore polar motors - use ATP to push microtubules away in opposite directions ins meta and anaphase (makes microtubules longer)

94
Q

How are chromatids seperated

A

The proteins holding sister chromatids together are inactivated
Kinetochore microtubules have dyenin motor proteins to move chromosmes to the poles
Microtubules shorten at the ends (depolymerisation)
Non-kinetochore microtubules elongeate the clell in anaphase

95
Q

How does cytokinesis occur

A

microfilaments form a ring at the cell furrow (centre)
The ring contracts (actin and myosin responsible)
Cell is pinched in two

96
Q

Why is regulation of cell division important

A

Development
Injury
adaptive responses

97
Q

What are the two main ways cell division is regulated

A

External signals e.g growth factors
Internale signals (produced by the cell e.g cyclin dependent kinases)

98
Q

How do Mitogens (growth factors) promote cell growth

A

they bind to receptors in the membrane and a chain of relay molecules transports the signal to activate the cellular response

99
Q

How were internal signals discovered

A

Cells of different stages of the cell cycle were fused resulting in one of the cells entering mitosis that wasn’t already there

100
Q

What are the three checkpoints of the cell cycle

A

G1 check - is cell big enough and has it recieved externak signals
G2 check - Is cell big enough, is DNA replcated, is environmrnt favourable,
M (metaphase ) check - are all chromosomes attatched to spindles

101
Q

What regulates the G1 and G2 checkpoint

A

G1 - SPF (Cyclin E + cdk2)
G2 - MPF(Cyclin B + cdk1) (triggers mitosis)

102
Q

How and when is MPF formed

A

cdk1 is already in the cell and when the need for MPF is present the cyclin is produced to bind it before it is removed

103
Q

what protein regulates the M checkpoint

A

Anaphase promoting complex (APC)

104
Q

What are the trends of cancer from 1975

A

Increase in incidence due to longer lifespans (more common)
But decrease in mortality (especially in women)

105
Q

Why is it so hard to cure cancer

A

There are lots of causes and no one cure for all of them

106
Q

What classifications of cancer is there

A

1) Carcinoma - epithelial cell cancer common (80-90%)
2) Sacroma - connective and supportive tissue cancer (rare 1%)
3) Myeloma - cancer of plasma cells of bone marrow
4) Lymphoma - tumours of the lymphatic system formed from maturing WBCs
5) Leukemia - Blood cancer (cancer of bone marrow producing nonfunctional blood cells)
6) Mixed classifications - cancers in germ and stem calls causing a wide range of effects

107
Q

How do cancerous cells differ in growth

A

They are not anchorage dependant (dont need a surface)
They aren’t density dependant (they will grow on top of each other)

108
Q

What mutation can cause cancer

A

decativation of tumor supressor genes or activation of an oncogene

109
Q

What are the stages of cancer progression

A

1)initiation (first mutation)
2) clonal expansion
3)primary tumor
4) secondary mutation
5) malignant cancer
6) Invasion of lympth/ blood
7)metastatic tumours

110
Q

What are some characteristics of malignant tumors

A

1) Excessive proliferation
2) Unusual chromosome numbers (usually aneuploidy)
3) deranged metabolism - more nutrient demands and aerobic glycolysis used for ATP primarily
4) Reduced neighbouring cell attatchment
5) Invaseive phenotype (enters blood/lympth)
6) Proliferation (metastasis)

111
Q

Is cancer genetic

A

Yes but in most cases not inherited (e.g retinoblastoma inherited)

112
Q

How do oncogenes cause cancer

A

They mutate and cause an excess of growth stimulation

113
Q

How are oncogenes found

A

Human tumor DNA extracted and added to mouce cells, mouse DNA from cell culture introduced to bacteriophage, phages added to bacteria and human oncogene DNA detected via probe against alu sequence (human only not mouse)

114
Q

Why dont cancer cells need growth factors

A

Hyperactive RAS protein (due to oncogenes) issues growth signals on its own

115
Q

How does the diploid nature of cells affect tumor suppressor genes

A

Tumor supressor gene mutations are recessive (need both chromosomes mutated for a cancer to form)

116
Q

How is a retinoblastoma formed

A

mutation in the retinoblastoma protein Inherited dominantly despite being recessive because it needs to be activated by mitotic recombination. This protein inhibits G1-S transition so if mutated allows cells to pass through to S phase

117
Q

What does p53 do?

A

It recognises genome damage and stops the cell cycle until It can be fixed or causes the cell to permanenelty enter a non-replicative state (or apoptosis)

It is constantly produced but degrades when there is no genetic damage and is only stable in presence of genetic damage

118
Q

How does p53 detect genetic damage

A

Protein kinases pass a signal to p53 causing it to activate and it is a transcription factor when activated and triggers exression of cell cycle inhibiting proteins such as p21

119
Q

What does p21 do and what causes it to be expressed

A

it inhibits cyclin E-Cdk2 to arrest cell cyle at G1 and is caused by p53 detecting genetic damage

120
Q

why may apoptosis be needed?

A

Activated by p53 when DNA is beyond repair
Regulated by caspases (proteins)

121
Q

What is the difference between apoptosis and necrosis

A

In apoptosis cell contents do not leak out and are contained in vesicles

122
Q

What is the difference between intrinsic and extrinsic apoptosis

A

Intrinsic is caused by signalling within the cell
Extrinsic is medicated in response to external stimuli

123
Q

How does intrinsic apoptosis happen?

A

Bax protein forms a pore in mitochondrial membrane and cytochrome C released into cytoplasm causes cell death (foreign as mitochondria is prokayotic) (stimulated by Bid protein)

124
Q

How does extrinsic apoptosis happen

A

Fas ligand on killer lymphocyte activates fas death receptor and forms Death-inducing-signalling complex which activate caspases to regulate cellular disintegration

125
Q
A

BIOL (5 decks)

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