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University > MCO 22-33 > Flashcards

MCO 22-33 Flashcards

1
Q

What happens in G2

A

2 centrosomes become visible

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2
Q

How are chromosomes made visible

A

By FISH (fluorescent in situ hybridisation)

  • cells are fixed and permeabilised by detergent
  • Incubated with fluorescent primers
  • Primer become hybridised and “painted”
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3
Q

What happens in prophase

A
  • Centrosomes move to opposite poles of the cell
  • Chromosomes condense and become long
  • Nuclear membrane disintegrates
  • Spindle fibres attach to chromatids
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4
Q

What happens in metaphase

A
  • Chromosomes line up along the metaphase plate

- metaphase has diagnostic value, you can compare the lined up chromosomes

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5
Q

What happens in anaphase

A
  • Sister chromatids are separated into separate chromosomes

- cleavage furrow forms

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6
Q

What happens in telophase

A
  • Chromosomes uncoil
  • Nuclear membrane forms around the daughter nuclei
  • Spindle fibres break down
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7
Q

What is the controller of mitosis

A

cyclin

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8
Q

Experiment that identified cyclin

A
  • Some sea urchin eggs which were growing but not dividing and some which were growing and dividing were taken
  • They were then placed separate lanes during different times
  • An electric current was run through to separate proteins
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9
Q

What is cyclins partner called

A

cyclin dependent kinases (CDK)

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10
Q

How are cyclin/CDK complexes controlled

A

By destructive phases which reduces concentration

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11
Q

Why are there different cyclin/CDK complexes formed in different stages

A

To phosporylate different targets and perform different functions

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12
Q

How many cyclin and CDKs are there

A

At least 4 of each

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13
Q

Can the cycle survive on one cyclin and one CDK

A

Yes, cell grows slowly

  • Low concentrations of cyclin/cdk fuse to G1 targets, they have a high affinity
  • High concentrations of cyclin/cdk fuse to G2 targets, they have a low affinity
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14
Q

When are sorting signals needed in protein sorting

A

When proteins doesn’t reside in the cytosol

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15
Q

What can sorting signal be

A
  • short peptides
  • 3 dimensional domains (secondary/tertiary structures)
  • other molecules
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16
Q

Modes of transport

A
  • Gated transport (nuclear import)
  • Trans-membrane transport
  • Vesicular transport
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17
Q

Process of nuclear import

A
  • Importins bind the nuclear localisation signals (NLS) on the cargo protein to the FG-nucleoporins
  • Transient interactions with FG-nucleoporins allows movement of protein into the nucleus through repeated binding and dissociation steps
  • Importin receptors disengage from cargo and the NLS is not cleaved off
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18
Q

How do importins know when to let go of cargo

A
  • Importin binds to a GTPase switch called Ran
  • Ran can either bind to GTP or GDP
  • Depending which one it binds to there is a different conformational change
  • Ran GDP conformation only exists in the cytosol
  • Ran GTP conformation only exist in the nucleus
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19
Q

what determines asymmetric distribution of Ran-GTP and Ran-GDP

A

Ran specific GEF and GAP

GEF- exchanges GDP to GTP
GAP- hydrolysis of GTP to GDP

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20
Q

Why is the NLS not cleaved after import

A
  • NLS maybe a functional domain
  • It is needed again
  • Re-import in need after every mitosis
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21
Q

what does ran-GTP do and what does it bind to

A

Binds to importins and displaces the imported protein

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22
Q

What does ran GDP do

A

it is generated and ran falls of the importin

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23
Q

Why does the cell cycle need breaks

A

to provide an opportunity to repair

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24
Q

What is genome instability

A

cell cycle runs at full speed, where there is little time to proof read

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25
Q

Hereditary retinoblastoma

A
  • A child receive one normal and one defective Rb allele
  • somatic mutation inactivates the normal allele
  • Typically both eyes are affected
26
Q

sporadic retinoblastoma

A
  • A child recieves 2 normal alleles
  • There are 2 separate mutations which inactivate each allele
  • Typically 1 eye affected
27
Q

Role of Rb gene

A
  • it is a tumour suppressor gene and regulates the restriction point
  • slows down entry into s phase by inhibiting cyclin/CDK complexes
28
Q

Role of p53

A
  • another tumour suppressor protein which decides if the cell cycle stops, repairs and restarts. or kills damaged cells
  • p53 can arrest cells in G1 by activating genes that inhibit cyclin/CDK complexes
29
Q

Apoptosis stages

A

cell shrinks, nucleus condenses, cells blebs, releasing apoptotic bodies which are then phagocytosed
Intracellular constituents are not released into the extracellular environment

30
Q

what is Necrosis

A

cells that die through tissue damage and swell, intracellular constituents are released into the environment

31
Q

What are the effectors for apoptosis

A

caspases which cleaves proteins of the nuclear lamina and cytoskeleton.
Caspases are kept inactive by trophic signals

32
Q

Triggers for apoptosis

A

external: lack of tropic signals, stress, recognition of virally infected cells
integral: recognition of irrpairable DNA

Developmental: highly regulated non random cell death

33
Q

role of the quiescent phase (G0)

A
  • cells in G0 have the opportunity to differentiate into different tissue
  • Other differentiated cells can be stimulated to re-enter the cell cycle and replicate, this requires mitogenic signals
  • once cells pass the restriction point they are committed to the cell cycle
34
Q

How does G0 protect cancer

A
  • cells in G0 divide slowly so radiotherapy doesnt work

- cells dont replicate there DNA so chemotherapy doesnt work, which depends on the incorporation of toxic nucleotides

35
Q

How do mitogenic signals work

A
  1. EFG binds to EGFR
  2. Activated EGFR recruits adaptor molecule which recruits Ras
  3. mRas recruits Raf to the membrane and a signal is passed via intermediates to MAPK
  4. MAPK stimulates early response genes c-FOS and c-JUN
  5. c-FOS and c-JUN are transcription factors that induces expression of delayed response genes, inducing G1 cyclins and CDKs
36
Q

What can go wrong with mitogenic signals

A
  • a mutation may cause something to be permanently activated causing unregulated proliferation
  • viral subversion which produces molecules that mimics c-FOS and c-JUN
37
Q

How do proteins enter the excretory pathway

A
  1. N-terminal signal sequence targets the surface of the ER
  2. Leads to the docking of a ribosome nascent chain complex onto the ER membrane
  3. The signal sequence is removed once the protein is in the ER
38
Q

Role of ER

A
  • lipid synthesis
  • Protein translocation (proteins are N-glycosylated)
  • Quality control
39
Q

Role of the golgi

A
  • protein and lipid modification

- Protein packaging and sorting

40
Q

how do transport vesicles form

A
  • recruit proteins to the site where the membranes will form
  • bend the membrane to form vesicle
  • cut the vesicle free
  • send vesicle to target location
  • fusion
41
Q

As all organelles in the ER are interconnected what does this mean

A

Once in the ER proteins dont need to cross anymore membranes to be secreted

42
Q

when are sorting signals need once in the ER

A

Needed when enzymes are heading to intracellular destinations. None are needed if they are travelling to the plasma membrane

43
Q

Targeting hydrolytic enzymes to lysosomes

A
  • Lysosomal enzymes have a M6P (target signal)
  • M6P binds to M6P receptor which recruits clatherin
  • clatherin bends the membrane
  • dynamin cuts the budding vesicle
  • vesicle loses the clathrin coat and fuses with the late endosome and release M6P
  • late endosome fuses with the lysosome, delivering cargo enzymes
  • receptors are recycled to TGN
44
Q

How do lysosomal proteins acquire M6P

A

Lysosomal hydrolases have a 3D signal patch which puts a phosphate on mannose to end up with M6P

45
Q

Role of GAGs

A

GAGs form hydrated gels and provide turgor, support and a medium for cell migration. They are negatively charged attracting cations causing large amounts of water to be sucked into the matrix

46
Q

cytoskeleton components

A
  • microtubules
  • actin
  • intermediate filaments
  • associated proteins
47
Q

cell - cell junctions

A
  • cell adhesion molecules (CAMS) are part of the cadherin family
  • cadherins of the same type interact weakly, but many act
  • selective recognition ensures cadherins of the same type interact with each other, so they can be segregated and sorted
  • cause coordinated contractions
48
Q

cell-extracellular junctions

A

focal adhesion - integrins allow the cytoskeleton to grip to ECM molecules

49
Q

in cell-extracellular junctions what must integrin do so cells can migrate

A

integrins must be able to switch from an active state to an inactive state. it does this by changing its confomation at both ends

50
Q

what is anchorage dependence

A

when integrins activate intracellular signalling pathways to control a cells behaviour

51
Q

Tight junctions

A

maintain cell polarity by blocking the mixing of apical and basal membrane proteins
-use claudins and occludins to interlock cells preventing lateral diffusion

52
Q

Gap junctions

A

use connexins from adjacent plasma membranes to create channels between cells

53
Q

what are the determinants of fate

A
  • induction: where signal from one group influence the developmental fate of another, from morphogens
  • Asymmetrical cell division: significant molecules are differently distributed
54
Q

cortical rotation

A

results in asymmetry of mRNA

55
Q

Gatrulation

A

lays down germ layers and body axis

56
Q

body axis

A
  • anterior end
  • posterior end
  • dorsovental axis
  • mediolateral axis
57
Q

2 types of smooth muscle

A

visceral - several fibres 1 ANS motor neuron synapse
multiunit - each fibre has one ANS motor neuron

smooth muscle are short fibres, non overlapping and tapered

58
Q

skeletal muscles

A

long, fast contractions, striated (overlapping)

59
Q

cardiac

A

branched, many gap junctions, connected to neighbouring fibres

60
Q

2 types of neuron tissues

A

neuron

neuroglia: dont generate impulses, supporting role to neurons

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