- Disease that happens when you can't cut off the pro-collagen at the ends - Can't form fibrils, weak skin

- Long bones extend from growth plate. - Puberty triggers growth and end of growth plate - GP turns to bone

F: All about cells Flashcards by Unknown Unknown

Intermediate filaments

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

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Actin filaments

Helical polymers (Use: dynamic cell shape and movement)

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Microtubules

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

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Intermediate filament role (in skin)

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

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

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Actin filaments cytoskeleton role

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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Microtubules role (+ role in mitosis)

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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Collagen’s structure, purpose and location

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

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Vitamin C + Collagen

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

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Dematosparaxis

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

Tendons: highly organised for strength
Bone: random for support

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Ehlers-Danlos syndrome

Unusally eastic skin, flexible joints and early mobility issues.

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Cartillage

Frictionless surface between 2 bones

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Bone (composition)

Specialized connective tissue made of mostly ECM + some cells

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Chondroblasts (active)/ Chondryocytes (resting)

Forms cartillage skeleton

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Osteoblasts

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

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Osteoclasts

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

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Growth plates

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

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Chondrodysplasia

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

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What regulates bone density?

mechanical stress
disuse
calcium
hormones

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Hormones controlling bone density?

✅ Calcitonin + Oestrogen
❌ Parathyroid hormone (PTH) + Vitamin D

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Post-mitotic/ terminally differentiated cells

Cells that will never divide again

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Quiescent cells

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

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What controls the size (growth) of an animal?

HORMONES… growth is PROPORTIONAL.

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

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Benefit of post-mitotic cells

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

Cell survival factor

Promotes continued life in cells

Cell death factor

Promote cell death

What do growth factors do?

Regulate cell size

Hypertrophy

Increased cell size

Hyperplasia

Increased cell number

Apoptosis

Controlled cell death of unwanted cells (tadpole tails)

Regulation of cell proliferation (3)

Hayflick's number, Senescence, Apotosis

Hayflick's number

Fixed # of times animal cells can replicate

Senescence

Cell aging

What happens in primary immune system?

Where immune system develops

What happens in secondary immune system?

Immune response

Where do B-cell's mature and develop

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

Where do T-cells mature?

Thymus

Encapsulated immune response location

Spleen + lymph nodes

Unencapsulated immune response location

Mucosal lymphad aggregates + Ileal Peyer's Patches

Innate immune system (IIS)

- Fast acting (minutes) - Non specific and no memory - Ex. barriers, cellular components, soluble factors, etc.

Neutrophils

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

Phagocytes

IIS englufs extracellular pathogens

Macrophages

IIS Large mononuclear cells resident in almost all tissues

Dendritic cells

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

Adaptive immune system (AIS)

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

Lymphocytes

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

T-cells

Destroy infected body cells

B-cells

Produce antibodies to fight infection

Endogenous antigens

Tumor or viral antigens

Exogenous Antigens

Bacteria or parasites

A-site of ribosome

AminoActyl-tRNA binds

P-site of ribosome

Peptidyl transferase bond forms between amino acids

E-site of ribosome

Ejected tRNA

Ribosome composition

80+ proteins and 4 RNA molecules

Polyribosome (polysomes)

Multiple ribosomes attached to same mRNA to make lots of proteins

Tetracycline

Blocks binding of Aminoacyl--tRNA to A site

Streptomycin

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

Chloramphenicol

Inhibits peptidyl transferase

Cycloheximide

Blocks translocation

Erthromycin

Blocks translocation

Aminoacyl-tRNA

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

How do miRNA control translation?

- Degrading mRNA - Binds to mRNA and pauses translation sequence. Eventually, mRNA degreades.

Cell check point from G1 to enter S

Environment favorable? Enough material?

Cell check point from G2 to enter M

All DNA replicated + in good condition?

Cell check point in M phase

All chromosomes properly lined up?

What signals a cell to divide? (2)

Growth hormones and potential damage

What is cyclin and what is it's purpose?

Proteins that accumulate during mitosis + control CDK. - Bind to CDK which regulates cell cycle (transcription and splicing) - Auto-phosphorylation + phosphorylation of substrates

How do cyclin levels drop?

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

How do stem cells die?

- Telomeres (their ends) become shorter and shorter with each division - They become senescent/ stop dividing

What do stem cells use to differentiate?

Tissue specific transcription factors

What transcription factors do we use to regulate the differentiation of stem cells? (2)

- Histone acetylation - DNA methylation

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

- Adding methyl to cytosine - Methylation represses transcription

Hemi-methylated (and it's solution)

After DNA replication of methylated strand, the new strand isn't methylated. Maintenance methylase is used to fix this

De-methylation

transcription activation and only achieved through DNA repair/ repliaction

Where does methylation reset?

Epigenetic signals that reset in gametogenesis.