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Foundation block > All about cells (-6) > Flashcards

All about cells (-6) Flashcards

1
Q

Intermediate filaments

A

Rope-like bundles of proteins (Use: rigid cell shape)

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2
Q

Actin filaments

A

Helical polymers (Use: dynamic cell shape and movement)

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3
Q

Microtubules

A

Hollow polymers (U: Framework for moving objects within cells)

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4
Q

Intermediate filament role (in skin)

A
  • Long and thin, brick like connection, very strong and insoluable. Able to see inficidual strands like rope fibres.
  • Forms bungee cord network in cell to keep everything together
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5
Q

What happens when there is no intermediate filaments in the skin?

A

Having no IF means skin can easily tear causing a blister to form.

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6
Q

Actin filaments cytoskeleton role

A
  • Allows for dynamic movement and is able to break and reshape at moment’s notice.
  • Also able to strengthen plasma membrane and give framework to cell shape
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7
Q

Microtubules role (+ role in mitosis)

A
  • Act as rail tracks to move contents around in cells
  • Spindle microtubules to pull chromosomes apart and astral microtubules to reach back to touch membrane to orient the position.
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8
Q

Collagen’s structure, purpose and location

A
  • 3 separate collagen proteins into 1 triple helix.
  • Interactions between chains give strength
  • Found in connective tissue
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9
Q

Vitamin C + Collagen

A

Cofactor to hydroxylane enzymes which convert prolines to hydroprolines helping with collagen strength.

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10
Q

Dematosparaxis

A
  • Disease that happens when you can’t cut off the pro-collagen at the ends
  • Can’t form fibrils, weak skin
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11
Q

Collagen structure in different parts of the body (tendons, bone)

A
  • Tendons: highly organised for strength
  • Bone: random for support
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12
Q

Ehlers-Danlos syndrome

A
  • Unusally eastic skin, flexible joints and early mobility issues.
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13
Q

Cartillage

A

Frictionless surface between 2 bones

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14
Q

Bone (composition)

A

Specialized connective tissue made of mostly ECM + some cells

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15
Q

Chondroblasts (active)/ Chondryocytes (resting)

A

Forms cartillage skeleton

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16
Q

Osteoblasts

A

Secrete collagen 1, calcium and phospate to mineralise bone on top of cartillage

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17
Q

Osteoclasts

A

Secrete proteases and acid to break down bone. Creates seal to bone surface (no leakage)

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18
Q

Growth plates

A
  • Long bones extend from growth plate.
  • Puberty triggers growth and end of growth plate
  • GP turns to bone
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19
Q

Chondrodysplasia

A

Causes growth plate to turn to bone too quickly (shorter limbs- dwarfism)

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20
Q

What regulates bone density?

A
  • mechanical stress
  • disuse
  • calcium
  • hormones
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21
Q

Hormones controlling bone density?

A
  • ✅ Calcitonin + Oestrogen
  • ❌ Parathyroid hormone (PTH) + Vitamin D
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22
Q

Post-mitotic/ terminally differentiated cells

A

Cells that will never divide again

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23
Q

Quiescent cells

A

Left cell cycle (G0 after G1) and can be signalled to re-enter

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24
Q

What controls the size (growth) of an animal?

A

HORMONES… growth is PROPORTIONAL.

  • also controlled by mechanical stress (muscles) and availability of amino acids
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25
Q

Benefit of post-mitotic cells

A

Lessens the risk of cancer (ex. brain and muscle cancer are very rare)

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26
Q

Cell survival factor

A

Promotes continued life in cells

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27
Q

Cell death factor

A

Promote cell death

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28
Q

What do growth factors do?

A

Regulate cell size

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29
Q

Hypertrophy

A

Increased cell size

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30
Q

Hyperplasia

A

Increased cell number

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31
Q

Apoptosis

A

Controlled cell death of unwanted cells (tadpole tails)

32
Q

Things controlling cell proliferation (3) (not the cause)

A

Hayflick’s number, Senescence, Apotosis

33
Q

Hayflick’s number

A

Fixed # of times animal cells can replicate

34
Q

Senescence

A

Cell aging

35
Q

What happens in primary immune system?

A

Where immune system develops

36
Q

What happens in secondary immune system?

A

Immune response

37
Q

Where do B-cell’s mature and develop

A

Bone marrow;
- Ileal Peyer’s Patches (small intestine) in cattle and sheep
- Bursa of Fabricius in birds

38
Q

Where do T-cells mature?

A

Thymus

39
Q

Encapsulated immune response location

A

Spleen + lymph nodes

40
Q

Unencapsulated immune response location

A

Mucosal lymphad aggregates + Ileal Peyer’s Patches

41
Q

Innate immune system (IIS)

A
  • Fast acting (minutes)
  • Non specific and no memory
  • Ex. barriers, cellular components, soluble factors, etc.
42
Q

Neutrophils

A

IIS
most numerous white blood cell that has multi-lobed nuclei + cytoplasmic granules containing various toxic substances

43
Q

Phagocytes

A

IIS
englufs extracellular pathogens

44
Q

Macrophages

A

IIS
Large mononuclear cells resident in almost all tissues

45
Q

Dendritic cells

A

IIS
Activate T-cells + other immune cells (link between innate + adaptive)

46
Q

Adaptive immune system (AIS)

A

Slow (days), specific and immunological memory
- T-cells and B-cells

47
Q

Lymphocytes

A

AIS
Antigens + Haptens act as keys that when bound to specific antigen receptor elicits a specific immune response.

48
Q

T-cells

A

Destroy infected body cells

49
Q

B-cells

A

Produce antibodies to fight infection

50
Q

Endogenous antigens

A

Tumor or viral antigens

51
Q

Exogenous

A

Bacteria or parasites

52
Q

A-site of ribosome

A

AminoActyl-tRNA binds

53
Q

P-site of ribosome

A

Peptidyl transferase bond forms between amino acids

54
Q

E-site of ribosome

A

Ejected tRNA

55
Q

Ribosome composition

A

80+ proteins and 4 RNA molecules

56
Q

Polyribosome (polysomes)

A

Multiple ribosomes attached to same mRNA to make lots of proteins

57
Q

Tetracycline

A

Blocks binding of Aminoacyl–tRNA to A site

58
Q

Streptomycin

A

Binds to 30s ribosome subunit and blocks transition to chain elongation

59
Q

Chloramphenicol

A

Inhibits peptidyl transferase

60
Q

Cycloheximide

A

Blocks translocation

61
Q

Erthromycin

A

Blocks translocation

62
Q

Aminoacyl-tRNA

A

Uses ATP to join amino acid and tRNA together. When bond is broken, amino acids are strung together

63
Q

How do miRNA control translation?

A
  • Degrading mRNA
  • Binds to mRNA and pauses translation sequence. Eventually, mRNA degreades.
64
Q

Cell check point from G1 to enter S

A

Environment favorable? Enough material?

65
Q

Cell check point from G2 to enter M

A

All DNA replicated + in good condition?

66
Q

Cell check point in M phase

A

All chromosomes properly lined up?

67
Q

What signals a cell to divide? (2)

A

Growth hormones and potential damage

68
Q

What is cyclin and what is it’s purpose?

A

Proteins that accumulate during mitosis + control CDK.

  • Bind to CDK which regulates cell cycle (transcription and splicing)
  • Auto-phosphorylation + phosphorylation of substrates
69
Q

How do cyclin levels drop?

A

Poly-ubiquitin binds to cyclin under growth factor signalling which degrades cyclin and renders CDKs inactive

70
Q

How do stem cells die?

A
  • Telomeres (their ends) become shorter and shorter with each division
  • They become senescent/ stop dividing
71
Q

What do stem cells use to differentiate?

A

Tissue specific transcription factors

72
Q

What transcription factors do we use to control the differentiation of stem cells? (2.5)

A
  • Histone acetylation
  • DNA methylation
  • DNA methltransferase to methylate CpGs
73
Q

DNA methylation (what is it and what’s it purpose?)

A
  • Adding methyl to cytosine
  • Methylation represses transcription
74
Q

Hemi-methylated (and it’s solution)

A

After DNA replication of methylated strand, the new strand isn’t methylated.

Maintenance methylase is used to fix this

75
Q

De-methylation

A

transcription activation and only achieved through DNA repair/ repliaction

76
Q

Where does methylation reset?

A

Epigenetic signals that reset in gametogenesis.

Foundation block (7 decks)

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