Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIO230 > Control of Cell numbers > Flashcards

Control of Cell numbers Flashcards

1
Q

four main phases of the eukaryotic cell cycle

A
  • M phase (mitosis and cytokinesis)
  • G1 (cell growth and partial doubling of proteins and organelles)
  • S (DNA replication)
  • G2 (cell growth and remaining doubling of proteins and organelles)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

three major checkpoints

A
  1. G2/M –> enter mitosis
  2. metaphase-anaphase –> trigger anaphase and proceed to cytokinesis
  3. start checkpoint –> enter cell cycle and proceed to s phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cdks

A

Cyclin dependent kinases

  • protein kinases with targets that control the cell ccle
  • activity allows passage through a checkpint
  • dependent on cyclin binding and other modifications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cdk checkpoints

A

M phase

  • binds to M-cyclin to create M-cdk
  • triggers mitosis machinery
  • degraded to stop mitosis

S phase

  • binds to S-cyclin to create S-cdk
  • triggers DNA replication machinery
  • degraded to stop replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cyclins in yeast and vertebrates

A

VERTEBRATES

  • different cyclin
  • sometimes the same Cdk

YEAST

  • different cyclin
  • always the same Cdk (Cdk-1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how is cdk activated

A

inactive –> t-loop blocks the active site
low/ no activity –> t-loop a part of the cyclin
full activity –> CAK comes in and phosphorylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

S-cdk and M-cdk

A

S-Cdk promotes DNA replication

M-Cdk phosphorylates multiple targets required to start mitosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what turns cdk off?

A

targeted degradation of cclins

  • e.g. anaphase promoting complex (APC) targets M-cyclin to the proteasome allowing the completion of mitosis
  • E3 adds a polyubiquitin tail causing degradation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CKI

A

Cdk inhibitor proteins

  • regulate Cdk activity by clamping on the protein and inactivating it
  • the active site is distorted and the ATP binding site is blocked
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cdk regulation by phosphorylation

A

Wee1 kinase phosphorylates cdk on a different spot, causing inhibitory phosphorylation

Cdc25 phosphatase removes the inhibitory phosphate

  • see lecture 10 for summary slide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rb

A

Retinoblastoma protein

  • tumour suppressor
  • inhibits cyclin synthesis and blocks G1 progression and S phase
  • without it, E2F is always active and DNA proliferation goes on uncontrolled
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

mitogen activation of the cell

A

mitogen signaling induces Myc transcription via a Ras-MAP kinase signaling cascade
- increases cyclin synthesis and CKI degradation by regulating transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Myc

A

an oncogene

- overactivity leads to cancer due to excess cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

temporal feedback promoting M phase

A

M-cyclin + Cdk-1 –> inactive M-Cdk –> CAK + Wee1 –> M-Cdk has both inhibitory and activating phosphates –> Cdc25 is activated by polo kinase –> active M-Cdk

positive feedback for Wee1 and Cdc25 phsophorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

p-53

A

tumour suppressor

  • loss of p53 leads to cancer
  • stops cell cycle in response to DNA damage

DNA damage –> phosphorylation of p53 –> Mdm2 can’t bind –> active p53 binds to regulatory region of p21 gene –> transcription of clamp protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

apoptosis

A

programmed cell death

  • sculpts fingers and toes
  • kills dangerous cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

necrosis

A

accidental cell death

- can lead to a damaging inflammatory reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how does apoptosis avoid inflammatory reactions?

A
  • shrinking the cell
  • collapsing the cytoskeleton
  • fragmenting the NA
  • signaling to macrophages for cell removal by engulfment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is apoptosis triggered?

A
  • cysteine proteases cleave target proteins at SPECIFIC aspartic acid residues
  • synthesized as procaspase precursor molecules (ready to be activated)
  • procaspases are cleaved and activated by other caspases
  • leads to an amplified cascade of caspase activity
20
Q

individual caspase activation

A

procaspases activated by cleavage

  • two cleavage sites
  • one multiprotein complex made of small and large subunits
  • caspase-8, -9, -10
  • results in cleavage of cytosolic protein and nuclear lamin
21
Q

detecting fragmented DNA in a gel after induction of apoptosis

A
  • Terminal deoxynucleotidyl transferase mediated dUTP Nick End Labeling (TUNEL)
  • cells have phospatidylserine in the outer leaflet instead of the inner
  • time is dependent on stimulus
22
Q

what activates caspase cascades

A

extrinsic signals (e.g. via death cell receptors)

  • Fas (death) ligand binds to Fas receptor
  • assembly of DISC (death inducing signaling complex)
  • activation and cleavage of procaspase-8, -10, or both
  • activation of executioner caspases

intrinsic (e.g. triggered from within)

  • apoptotic stimulus causes release of cytochrome c
  • activation of Apaf1, dATP –> dADP
  • assembly of apoptosome triggered by release of dADP in exchange for dATP
  • recruitment and activation of procaspase-9 which cleaves and activates executioner procaspases
23
Q

extracellular inhibitors for apoptosis

A

decoy receptors act by competitive inhibition

  • have a ligand-binding domain but not a death domain
  • out-compete functional Fas death receptors
24
Q

intracellular inhibitors for apoptosis

A

examples of competitive inhibition

- e.g. mimic of an initiator caspase that lacks a proteolytic domain

25
Q

Bcl2

A

inhibits channel formation in the outer mitochondrial membrane
- stops BH123 proteins from being released by apoptotic stimulus

26
Q

IAPs

A

inhibitors of apoptosis

  • block caspase activity in the cytoplasm
  • bind to caspases
  • stopped by anti-IAPs to activate apoptosis
27
Q

cells can choose to induce or prevent apoptosis

A
  • default state kills off cells if they leave their protective environment
  • survival factors are used to control proper cell numbers in body tissues
28
Q

molecular machinery and pathways linked to cancer

A

oncogenes and tumour suppressors often function in the same pathway

29
Q

basic bio of cancer

A

cancer develops from a cell gaining a mutation allowing it to survive and divide forming a tumour
- clonal origin of cancer

30
Q

carcinoma

A

epithelial cell cancers

31
Q

sarcoma

A

connective tissue or muscle cell cancers

32
Q

leukemia

A

blood cell cancers

33
Q

tumour (neoplasm)

A

uncontrolled growing mass of abnormal cells

- not all tumours are cancers and not all cancers have tumours

34
Q

benign vs malignant tumours

A

benign

  • growing mass is self-contained
  • still has cell-cell adhesion and basal lamina

malignant

  • aggressive tumor that has broken free and invaded surrounding tissue
  • destroys surrounding area
35
Q

how are tumours categorized?

A

by stage

- metastatic tumour: cancer invading other tissues

36
Q

cancerous cell DNA

A

DNA is disrupted

  • large scale chromosomal abnormalities
  • point mutation (can’t be detected by karyotypes)
37
Q

what causes mutations leading to cancer?

A

chemical mutagens

- can be either natural or man-made

38
Q

the Ames test

A
  • mix test compound, histidine-dependent salmonella, and homogenized liver extract
  • plate out on agar medium lacking histidine
  • nothing should grow if there’s no mutagen

experiment must be done with and without the liver extract

39
Q

oncogenes

A

cancer arises from a gain of function mutation

  • normal form of the gene is a proto-oncogene (e.g. Ras, Myc)
  • mutations are dominant
40
Q

tumour suppressor genes

A

cancer arises from a loss of function mutation (p53, Rb)

- mutations are recessive

41
Q

Philadelphia chromosome

A
  • example of producing an oncogene
  • Bcr gene on chromosome 22 (ser-thr kinase) + Abl gene on chromosome 9 (tyrosine kinase)
  • translocation fuses the two
  • transcription and translation creates an oncogene causing chronic myelogenous leukemia
42
Q

producing tumour suppressor genes

A

inactivating mutation event + inheritance/environment

43
Q

how do mutations cause cancer

A

abnormal cell cycle

  • leads to more cells in the tumour
  • missed checkpoints permit further chromosomal aberrations

abnormal cell death
- loss of control of cell number

abnormal cell differentiation
- cells may live longer and acquire additional mutations

abnormal cell-cell interactions
- low cell adhesion contributes to metastasis

44
Q

gleevec

A

drug treatment for chronic myelogenous leukemia targeting Bcr-Abl

  • binds to Bcr-Abl
  • cannot bind to substrate protein
  • no signal
  • no lelukemia
45
Q

multi drug treatments vs sequential treatments

A

multi-drug treatments more effective

  • sequential ones may allow for uncontrollable cancer resistant to both drugs
  • simultaneous creates a cell resistant to only one drug
  • side effects may aggregate

BIO230 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions