Brainscape's Knowledge GenomeTM

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


See full index

CTO 2 > 3. Cell differentiation > Flashcards

3. Cell differentiation Flashcards

1
Q

Define differentiation

A

Differentiation - a process by which unspecialised cells become cell specific types (in embryos / in tissue homeostasis)

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

Approximately how many types of cell tissues there are in a human?

A

~ 200 main types

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

What makes cells different from one another?

A
  • different macromolecules
  • different metabolites
  • different morphologies and behaviours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Housekeeping vs specialised proteins?

A
  • Housekeeping proteins - proteins found in most cell types for shared essential cell functions (ex ATP synthase)
  • Specialised proteins - proteins specific to a particular cell type (ex insulin synthesising protein in beta cells in the pancreas)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the main embryonic germ layers from which all tissues differentiate?

A
  • ectoderm
  • mesoderm
  • endoderm

Trophectoderm (embryo tissue which forms placenta)

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

Why is differentiation considered progressive?

A
  • forms intermediate (transient) states (progenitor / precursor cells)
  • has a terminal differentiation point - final cell from
    => progressive specialisation, not immediate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What drives specific cell differentiation?

A

Differentiation is driven by interplay between cell’s lineage and its environment

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

During which process of embryo development are the germ layers formed?

A

Gastrulation

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

What is haematopoiesis?

A

Haematopoiesis - formation of blood components - differentiation of blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What genetic mechanism drives cell differentiation?

A

Selective activation / inactivation of particular genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Can the nucleus of a differentiated cell support development of a new organism?

A

Yes - nuclear transfer experiment - sheep Dolly (first cloned mammal)

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

What is gene constancy?

A

Gene constancy - all cells in a multicellular organism have a full complement genes (full genome)
=> cells differentiate because of gene activity rather than gene content (differential gene expression)

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

How is gene expression controlled?

A

By control of gene transcription - transcription factors (TF) - genes can individually be switched on/off - different gene expression patterns in different cells

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

What is the DNA signal sequence which is a recognition site / binding site?

A

TATA box - binds TATA binding proteins - transcription factors (TFIID)

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

What is the role of TATA box?

A

TATA box controls where transcription starts - binds TF
(doesn’t control when transcription starts)

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

What is an enhancer?

A

Enhancers - short regulatory nucleotide sequences recognised by TF that enhance the rate transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a promoter?

A

Promoters - rather long regulatory nucleotide sequences that initiate transcription - polymerases bind

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

Explain promoters vs enhancers

A

Promoters - long sequences / initiate transcription
Enhancer - short sequences / increase transcription rate

Enhancers activate promoters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are transcription factors (TF)?

A

Transcription factors (TF) - proteins which activate/repress polymerase function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the methods by which TFs can initiate transcription?

A
  • can act directly (directly recruit RNA polymerase to TATA box)
  • can act via chromatin modification (indirectly recruit RNA polymerase: histone acetyl transferase / chromatin-remodelling complex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the two indirect methods of TFs for recruiting RNA polymerase for transcription initiation?

A
  • Histone acetyl transferase (HAT): acetylations loosens histone interactions with DNA - genes more accessible for transcription
  • Chromatin-remodelling complex: chromatin modifying enzymes promote RNA polymerase binding and function by remodelling chromatin and making it more accessible
22
Q

What controls gene’s transcriptional activity in a cell?

A
  • binding sites in enhancer sequences of DNA for the gene
  • presence of appropriate TFs for the gene
23
Q

Give two examples of TF in differentiation

A
  • MyoD - TF which activates expression of genes for muscle myosin II protein - in muscle cell differentiation - recognition site: E box
  • GATA1 - TF which activates expression of several target genes (for α+β globin, erythropoietin receptor, heam biosynthesis enzymes, spectrin) - in RBC differentiation
24
Q

Can one TF target several genes transcription?

A

Yes - MyoD activates transcription of many genes acting in muscle cell differentiation + represses non muscles genes

25
Q

What’s the effect of MyoD knockout?

A

MyoD knockouts produce undifferentiated muscle cell precursors - myoblasts

26
Q

How can MyoD expression pattern be investigated?

A

Modify embryos with MyoD mRNA staining (in situ hybridisation) - observe MyoD expression patterns where stained (muscle cell differentiation sites)

27
Q

Can TF force other lineage cells to differentiate into lineage to which the TF is specific?

A

Yes - ex: fibroblasts (skin precursors) transfected with MyoD containing plasmid - differentiated into muscle cells

28
Q

What are the correct steps in genetic analysis of TF function?

A
  1. Analysis of expression pattern (where it is expressed in developing body?)
  2. Analysis of loss-of-function (is the TF required for differentiation?)
  3. Analysis of gain-of-function (can the TF force other lineage cell differentiation into its own - is it sufficient for full differentiation?)
29
Q

How TFs recognise their binding sites?

A

TF - high specificity - specific am. a. in recognition site - bind specific base sequence

30
Q

How are TFs categorised?

A

TFs are categorised into families - based on 3D structure of their DNA binding domains where binding sites are located

31
Q

Usually, do TFs work on their own or in combinations?

A

In combinations - groups of TFs at binding sites

32
Q

What are the possible TF combination interactions for transcription enhancing?

A

When several TFs for the same gene regulation:
- either TF may be sufficient / doesn’t matter which binds for transcription
- all TFs required together for transcription

33
Q

What are the possible TF combination interactions for transcription repressing?

A

When several TFs for the same gene regulation:
- repressing TF may prevent binding of activating TF (picture)
- recruit proteins that tighten chromatin - gene less accessible

34
Q

What regulates TFs and how?

A

What:
- envronmental signals (signals from other cells: hormones, growth factors)
- developmental history (earlier TFs regulate later TFs)
How:
- controlling their activity by PTMs
- controlling their gene expression

35
Q

How are TFs regulated by cell signalling?

A
36
Q

How are TFs regulated by PTMs?

A

PTMs - ex: phosphorylation - phosphate alters protein conformation -> activate / inhibit TF

37
Q

How growth factors can control TF activity?

A

Growth factors regulate TF activity by phosphorylation -> target gene activity changed
Growth factor signal activates protein kinase cascade:
1) phosphorylation of MAP-kinase-kinase kinase (activated) ->
2) phosphorylates MAP-kinase kinase (activated) ->
3) phosphorylates MAP kinase (activated) ->
4) MAP kinase enters nucleus and phosphorylates TFs - activates TFs for target gene

38
Q

Explain how epidermal growth factor activates cyclin genes

A

Epidermal growth factors - mitogen (promotes cell proliferation)
1) Growth factors signal initiates kinase cascade - phosphorylates MYC (TF) on serine (Ser-62) + threonine -> changes MYC conformation to stable active
2) Activated MYC drives cyclin gene transcription

39
Q

Explain how hormone erythropoietin (EPO) regulates GATA1 activity

A

1) Hormone erythropoietin (EPO) secreted from kidneys
2) EPO binds to receptors - kinase cascade
3) GATA1 (low activity) phosphorylated - conformational change -> high activity
3) GATA1 increases DNA binding
4) Stimulates blood progenitor proliferation and RBC differentiation

Low O2 conditions (ex: hipoxia) stimulate EPO secretion - more RBCs - higher efficiency

40
Q

Why control of TFs is important for orderly progression of differentiation?

A

TF regulate gene expression which drive differentiation -> cell fate:
Different TFs regulate different steps in differentiation

41
Q

Explain how leaf progenitor cells differentiate into epidermis and stomata?

A

Default pathway - epidermis cells
Some progenitor cells induced for stomata (guard cells) differentiation by SPCH, MUTE, FAMA TFs

42
Q

What is a gene regulatory network (GRN)?

A

Gene regulatory network (GRN) - a set of genes which interact to control a specific cell function

43
Q

How is MyoD initially activated in muscle differentiation gene regulatory network?

A

By co-regulation of Pax3 and Myf5 TFs (work in combination) - for initial MyoD levels - later MyoD activates its own expression
Pax3 + Myf5 - transient process

44
Q

How is MyoD regulated in muscle differentiation?

A

Autoregulation - MyoD activates further MyoD expression - becomes independent of Pax3 and Myf5 regulation (cell memory)

45
Q

How do growth factors stop MyoD expression?

A

1) Growth factors promote cell division -> cdk produced
2) Cdk phosphorylate MyoD and Myf5 -> proteolytic degradation -> muscle cell differentiation inhibited -> myoblast proliferation enhanced (growth factor response - cell division achieved)

46
Q

What is RNA interference?

A

RNA interference (RNAi) - post transcriptional gene silencing - degrade mRNAs

47
Q

How is Pax3 degraded during muscle differentiation?

A

Via RNA interference (RNAi):
- Pax3 only for early muscle development - must be down-regulated for later stages to proceed
- Pax3 mRNA degraded by microRNA (miR-1) - double stranded RNA - bound to an enzyme

48
Q

Explain Waddington’s developmental landscape

A

Represents cell specialisation - binary fate decisions (which valley will roll into - increasing specialisation - decreasing potency to develop into any other cell type

49
Q

Explain pancreas cell differentiation progress

A

Binary cell fate choices: specific cells from the gut can choose 1/3 cell lineages - pre-pancreatic - Ngn3 TF needed for all endocrine cells (if Ngn3 missing - no endocrine cells developed - all exocrine) - Ngn3 needed for general endocrine precursor development but not for a specific cell type in endocrine cells

50
Q

What decides pre-pancreatic fate in foregut?

A
  • Pre-pancreatic region affected by TFs - loops formed - comes closer to notochord - receives signalling - Fgf2 TF turned on -> further pancreas development
51
Q

Explain erythroid/myeloid cell fate choice

A

Common myeloid progenitor - binary cell choice -> GATA1 / PU.1 TFs
GATA1 / PU.1 autoregulate and inhibit each other -> different blood cells differentiate - ANTAGONISTIC interactions

52
Q

What are master regulators of organogenesis, give example

A

Master regulators - TFs which are essential for the development of all organ - without it nothing formed - if injected into wrong location - organ still formed
Example:
- Pax6 in eye development
- same TF in many animals - was present in a common ancestor
- MyoD in muscle differentiation
- Shh in anterior-posterior axis development

CTO 2 (8 decks)

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