All about cells (-6) Flashcards
Intermediate filaments
Rope-like bundles of proteins (Use: rigid cell shape)
Actin filaments
Helical polymers (Use: dynamic cell shape and movement)
Microtubules
Hollow polymers (U: Framework for moving objects within cells)
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
What happens when there is no intermediate filaments in the skin?
Having no IF means skin can easily tear causing a blister to form.
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
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.
Collagen’s structure, purpose and location
- 3 separate collagen proteins into 1 triple helix.
- Interactions between chains give strength
- Found in connective tissue
Vitamin C + Collagen
Cofactor to hydroxylane enzymes which convert prolines to hydroprolines helping with collagen strength.
Dematosparaxis
- Disease that happens when you can’t cut off the pro-collagen at the ends
- Can’t form fibrils, weak skin
Collagen structure in different parts of the body (tendons, bone)
- Tendons: highly organised for strength
- Bone: random for support
Ehlers-Danlos syndrome
- Unusally eastic skin, flexible joints and early mobility issues.
Cartillage
Frictionless surface between 2 bones
Bone (composition)
Specialized connective tissue made of mostly ECM + some cells
Chondroblasts (active)/ Chondryocytes (resting)
Forms cartillage skeleton
Osteoblasts
Secrete collagen 1, calcium and phospate to mineralise bone on top of cartillage
Osteoclasts
Secrete proteases and acid to break down bone. Creates seal to bone surface (no leakage)
Growth plates
- Long bones extend from growth plate.
- Puberty triggers growth and end of growth plate
- GP turns to bone
Chondrodysplasia
Causes growth plate to turn to bone too quickly (shorter limbs- dwarfism)
What regulates bone density?
- mechanical stress
- disuse
- calcium
- hormones
Hormones controlling bone density?
- ✅ Calcitonin + Oestrogen
- ❌ Parathyroid hormone (PTH) + Vitamin D
Post-mitotic/ terminally differentiated cells
Cells that will never divide again
Quiescent cells
Left cell cycle (G0 after G1) and can be signalled to re-enter
What controls the size (growth) of an animal?
HORMONES… growth is PROPORTIONAL.
- also controlled by mechanical stress (muscles) and availability of amino acids
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)
Things controlling cell proliferation (3) (not the cause)
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
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 control the differentiation of stem cells? (2.5)
- Histone acetylation
- DNA methylation
- DNA methltransferase to methylate CpGs
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.
