Brainscape's Knowledge GenomeTM

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


See full index

Microbiology of Disease > Mechanisms of disease one: cell growth and differentiation > Flashcards

Mechanisms of disease one: cell growth and differentiation Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Basic mechanisms to turn a zygote into mature multicellular organism?

A

Cell growth- a bigger organism and more cells

Differentiation- cell become complex an end to growth

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

What are the three main categories of diseases which are related to cell growth and differentiation?

A
  1. DEVELOPMENTAL CONDITIONS
    - related to cell growth and differentiation
    - neural tube defects like spina bifida
  2. NEOPLASIA ( and metaplasia)
    - cancer and tumours
  3. OTHER, E.G- CARDIAC HYPERTROPHY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two main forms of cell growth?

A
  1. Hypertrophy- bigger cell

2. Hyperplasia -more cells

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

What is meant by the term hypertrophy?

A

Hypertrophy- cell growing bigger

  • more proteins more membrane
  • elevated protein synthesis- increased cell size

example: the heart

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

What is meant by the term hyperplasia?

A

Hyperplasia- more cells- caused by cell division or proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is meant by differentiation in terms of the cell cycle?

A
  • exit from the cell
  • a program of cell type specific gene expression
  • cell morphology and function changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does cell growth and cell differentiation have in common?

A

-mechanism which are governing them

-governed by the integration of multiple signals
intra and extracellular signals (checks on cellular physiology, growth and inhibitory factors and cell adhesion)
-signals converge on the promoters of key genes
promoters act as “co-incidence detectors”
express genes

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

What are the three broad classes of extracellular signals?

A

When the ligand binds to the receptors it causes a intracellular cascade.
1. PARACRINE SIGNALLING
produced locally to stimulate proliferation of a different cell type that has the appropriate cell surface receptor.
2. AUTOCRINE SIGNALLING:
produced by a cell that also expresses the appropriate
cell surface receptor.
3. ENDOCRINE SIGNALLING:
like conventional hormones, released systemically for distant effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the extracellular signals in cell growth and differentiation capable of doing?

A

Proteins which:

  1. stimulate proliferation and promote survival
    Mitogens- e.g growth factors and interleukins (EGF, FGF, NGF, PDGF, IGF1, IL2 and IL4.
  2. induce differentiation and inhibit proliferation
    e. g TBFbeta
  3. Can do either
    e. g Wnt ligands
  4. Induce apoptosis
    e. g TNFa and other members of the TNF family
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain the pathway of how the extracellular signals induce gene expression?

A
  1. The growth factor will bind to its receptor
  2. The signal transducers would cause the kinase cascade
  3. This would act on the nucleus causing transcription factor activation
  4. This results in the mRNA changing into a protein.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the different phases of the cell cycle?

A

Interphase: G1, S and G2
Mitotic phase

G1 phase: cell grows in preparation for DNA replication, and certain intracellular components, such as the centrosomes undergo replication
S phase: the cell synthesizes a complete copy of the DNA in its nucleus
G2 phase: cell has grown, DNA has been replicated, and now the cell is almost ready to divide. This last stage is all about prepping the cell for mitosis or meiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does the FACS analysis of cell DNA content look at?

A
  • if a stain is applied FACS can measure the DNA content of every cell in a population.
    Data is used to plot the graph:
    x axis= amount of DNA
    y axis= number of cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

FACS analysis of cell DNA content- Fluorescence microscopy

A 
Blue= DNA 
Red= y- tubulin 
Green= CHEK2 
Yellow= centrioles (y tubulin and CHEK 2 colocalised)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Revise over the stages of mitosis?

A 
-PROPHASE:
nucleus becomes less definite 
microtubular spindle apparatus assembles 
centrioles migrate to poles 
PROMETAPHASE: 
neclear membrane breaks down 
kinetochores attach to spindle in nuclear region 
-METAPHASE
chromosomes will allign in equatorial plane 
-ANAPHASE 
chromatids seperate and migrate to opposite poles
-TELEPHASE 
daughter nuclei form 
CYTOKINESIS 
division of the cytoplasm 
chromosomes decondense
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why are the cell cycle checkpoints important?

A
  • controls (involving specific protein kinase and phosphates) ensure strict alterations mitosis and DNA replication

The different checkpoints:
G1 and S checkpoint: restriction point: DNA not damaged, cell size, metabolite/nutrient stores
2. G2 and M checkpoint: DNA completely replicated DNA not damaged
3. M phase- chromosomes aligned on spindle

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

Cyclin dependant kinases (CDK)

A

Cyclin- regulatory subunit- more than 20 genes- expression induced growth factors
CDK- catalytic subunit- 10 genes
CDK and Cyclin- substrate protein binding to the cyclin

Active cyclin CDK complex phosphorylates specific substrates.

17
Q

Regulation of cyclin CDK activity

A
  • cycles of synthesis (gene expression) and destruction (by proteasome)
    -post trancriptional modification of phosphorylation
    could result in activation, inhibition or destruction.
  • dephosphorylation
    -binding of cyclin dependent kinase inhibitors (CDKIs)
18
Q

How does the retinoblastoma protein (RB) affect gene transcription?

A

RB is a key substrate of G1 and G1/S cyclin dependent kinases.

  1. The retinoblastoma protein which is unphosphorlyated would bind to E2F transcription factor
  2. This binding would prevent E2F transcription factor of its stimulation of the S phase protein expression.
  3. Cyclin D- CDK4 and cyclin E- CDK2 would act to phosphorylate the retinoblatoma protein.
  4. This is lead to the E2F being released.
  5. The released E2F stimulates the expression of more cyclin E and S phase protein
  6. Then DNA rpelication would start.

example of the S phase proteins: DNA polymerase, thymidine kinase and PCNA.

19
Q

Describe the sequential activities in the cycle?

A

Look at slide 23 of the powerpoint:
G1 CDKs are activated in response to environmental signals, late CDKs by preceding kinase activities.
Hyperphosphorylated RB is dephosphorylated by protein phosphatase 1. G1 CDKs hypophosphorylate, and late CDKs hyperphosphorylate.

  • as RBD increases its phosphorylation it would be able to lose its ability to repress E2F.

-mitogens would be acting on signals to the nucleus through transcriptional activation of early genes.
They would increase transcription factors.

20
Q

What are the three different checkpoints of the cell cycle?

A
  1. There will be one at the end of the G1 phase before starting the S phase.
    RESTRICTION POINT:
    DNA not damaged. Cell size and metabolite and nutrient stores
  2. Found at the end of the G2 phase
    Checking if:
    DNA is completely replicated and DNA not damaged.
  3. Found in the mitotic phase
    Chromosomes aligned on the spindle
21
Q

DNA damage triggers cell cycle arrest or apoptosis.

What are three things which can happen when DNA damage is detected?

A
  1. Stop the cycle
    cyclin dependent kinases inhibitors, CHEK2
  2. Attempt DNA repair
    nucleotide or base excision enzymes, mismatch repair.

If the repair is impossible:
Programmed cell death
BCL-2 family, caspases

22
Q

What is the role of TP53?

A
  1. A mutagen will cause damage in the DNA molecule.
  2. This will result in kinase activation where the TP53 molecule would be phosphorylated to form phosphorylated TP53.

The functions of the phosphorylated TP53:

  1. Expression of CK1- cell cycle arrest
  2. Repair not possible. Apoptosis
  3. DNA Repair- excision repair
23
Q

What is the relationship between TP53 and cancer?

A
  • TP53 loss of fucntion mutation are amongst the most frequent in cancer.
    prevent cell cycle arrest- faster growth
    prevent apoptosis- do not die
    prevent DNA repair - more mutation would result in more heterogeneity, more adaptation, cancer progression.
24
Q

How does chemotherapy work?

A
  • chemotherpeutic drugs act on the cell cycle.
  • objective: stop proliferation and induce apoptosis

-S phase drugs causes DNA damage:

Examples of S phase drugs:

  1. 5- FLUOROURACIL - prevents synthesis of thymidine
  2. CISPLATIN: binds to DNA causing damage and blocking repair
25
Q

Chemotherapy and the M phase

A

M phase drugs are able to target the mitotic spindle:

  1. VINCA ALKALOIDS
    - stabilize free tubulin
    - prevent microtubule polymerisation
    - arrest cell in mitosis
  2. PACLITAXEL (TAXOL)
    - stabilises microtubules
    - preventing de polymerisation
    - arrest cell in mitosis

Colchicine is used for immunesupression

Microbiology of Disease (5 decks)

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