BCG LO2: Explain the roles of sub-cellular components
Nucleus:
Nucleosomes: DNA coiled around histones (positively charged octamer attracts negatively charged DNA), condenses to form chromosomes during replication
Chromosomes: short (p) and long (q) arms, two identical chromatids bound at centromere, telomeres (repeat regions which reduce during each replication, regulate cell life)
Nucleolus: rRNA transcription, ribosome subunit assembly and pre-rRNA processing, contains dense fibrillar and granular components
RNA:
rRNA (translation site of ribosomes, forms ribosomes w/ proteins in nucleolus)
tRNA (bound to amino acids, delivered to ribosomes for peptide chain)
mRNA allows info from DNA to be read by ribosome - correct tRNA anticodon selected
Nuclear membrane:
Protects genetic info (DNA never leaves nucleus)
Continuous w/ ER and contains nuclear pores
Endomembrane system:
Nuclear pores:
Protein lined channels closed unless nuclear localisation signals bind to receptors, allowing pores to open.
Transcription changes in response to environmental changes rely on nuclear pores
5-15% total surface in mammals
Allows mRNA to leave the nucleus for translation
Endoplasmic reticulum:
RER - protein synthesis, SER - lipid (+carb) production, liver cells (detoxification), muscle cells (Ca2+ storage)
Golgi apparatus:
Cis -> trans face
Phosphorylation, saccharide and fatty acid addition / cleavage
Exocytosis:
Constitutive - vesicle lined w/ membrane proteins
Regulated - active transport by ligand-receptor complexes
Cytosol:
70-80% water
Contains proteins, mono- and polysaccharides, amino, fatty and nucleic acids, cations
Allows metabolic reactions to occur
Mitochondria:
Maternally inherited circular DNA - produce ATP synthase and other TCA enzymes
Responsible for aerobic respiration (TCA cycle and oxidative phosphorylation)
Bacterial conformation (60S) ribosomes
Endosymbiotic theory - mitochondria formed when bacteria formed symbiotic relationship w/ Archaea: facilitated differentiation, fitness advantage allowed propagation of eukaryotes
Replicate independently of the cell
Double membrane - inner membrane is highly folded (cristae)
Mitochondrial matrix - contains TCA enzymes
Periplasm - intermembrane space, facilitates proton gradient
Electron transport chain:
Complex I
Oxidises NADH, pumps 4 protons, reduces ubiquinone
Complex II
Oxidises FADH2, does not pump protons, reduces ubiquinone
Complex III:
Oxidises ubiquinone, pumps 4 protons, reduces cytochrome C
Complex IV:
Oxidises cytochrome C, pumps 2 protons and reduces O2
2H+ + O + 2e- Oxygen is terminal electron acceptor
10 protons pumped for every 2 electrons (Oxidation of NADH and FADH2
Ubiquinone and Cytochrome C act as shuttles
Proton motive force powers ATP synthase, in reverse orientation to proton pores
Ribosomes:
Responsible for protein translation
Small (40S) subunit holds mRNA binding site
Large (60S) subunit has A (aminoacyl), P (peptidyl) and E (exit) sites for tRNA
Codon - anticodon binding between tRNA and mRNA
Measure of activity (more proteins transcribed, greater ribosomal activity)
Free ribosomes produce intracellular proteins
Bound ribosomes produce specific proteins (lysosomes, extracellular hormones + enzymes)
Highly conserved, phylogenetic marker
Cytoskeleton
Microfilaments (7nm diameter)
Cellular movement - muscle cells use in combination with myosin
Chemokines/cytokines attract cells, microfilaments used to move in direction dictated by signalling molecules
Actin monomers polymerise - create new binding point at cell 'front'
Depolymerisation/hydrolysis at cell 'back' allows movement
Intermediate filaments (8-10nm diameter)
Structural, filamentous proteins allow cell shape and organelle arrangement to be maintained
Microtubules (25nm diameter)
Polymerised a and B tubulin dimers, hollow tubes allow vesicle movement, cell division (centrioles attaching to centromeres) and extracellular appendages (cilia + flagella)
Centrioles
Organisation of short lengths of microtubules
Polymerisation (expansion) allows attachment to and movement of chromosomes through centromere attachment
2 perpendicularly attached centrioles = centrosome
Peroxisomes and Lysosomes
Peroxisomes
H2O2 synthesis and degradation
Detoxify oxidase reactions
Fatty acid degradation for energy release
Self-replicate through fission (think binary fission)
Lysosomes
Highly glycosylated proteins protect membrane from low internal pH
Contain digestive enzymes w/ acidic optimum pH
Active transport proteins pump H+ into vesicle
Bud directly from Golgi apparatus
Prevent signalling cascades
Autophagy, heterophagy, autolysis/apoptosis, fertilisation
Cell Cycle and Cytokinesis
Growth, repair and reproduction
Binary fission used by bacteria: single chromosome replicated - two identical daughter cells produced
Cytokinesis - cell division
Microfilament contraction around cell equator forms cleavage furrow- starting during anaphase and continues in telophase
Interphase
G0 Senescence (metabolism halted)
Become quiescent (dormant), can re-enter the cell cycle, senescent cannot (aging or deteriorating), usually due to damaged or defective DNA
Muscle and nerve cells do not divide (continual G0)
G1 : Gap1
Visual inactivity, high level of metabolic activity (organelle duplication and protein production)
G1 regulation point causes variation in length
S phase - DNA synthesis
Histone production
Phospholipid production
DNA replication, producing
50% of cell cycle
Cyclin production begins
G2 : Gap2
Microtubules and other cytokinetic proteins synthesised
Centrosomes cell poles polymerise microtubules to attach to centromeres of chromosomes
Checkpoint repairs any chromosomal errors
Mitotic phase
Nuclear division of genetic material - genetically identical daughter cells
Prophase
Nuclear membrane breakdown, chromosomal condense, spindle fibres appear
Prometaphase
Spindle fibres attach to condensed chromosomes
Metaphase
Chromosomes align, metaphase plate
Anaphase
Chromosomes divide, chromatids pulled to opposite poles by depolymerising microtubules
Telophase
Nuclear membrane reforms, chromosomes decondense, spindle fibres disappear
Cell Cycle Regulation
Protein concentration changes activated by reactive enzymes
Cyclins, CDKs (Cyclin-independent kinases) and MPF (mitotic promotion factors)
Cyclin accumulates, production begins in late S phase, binds to CDK, forms MPF
Cyclin kinase degrades cyclin, releasing CDK
P53
Prevents DNA replication (G1 -> S) mitosis with unreplicated DNA (disputed)
Stops mitosis after induction by damaged DNA (G2 -> M)
Stops division of tetraploidy cells (M) - if two replications have occurred without cytokinesis
Binds and inhibits cdKs
Activation of inhibitor p21
Anchorage (planktonic -> sessile) and density (high number of cells) dependence
DNA damage/repair
Growth factors
Kinetochore adhesion (Spindle fibre attachment checkpoint)
If cell is forced to stop: senescence can allow DNA repair or apoptosis
If regulatory mechanisms fail, cancer develops
Apoptosis - 'clean': Blebs form, nucleus and organelles break apart into apoptotic bodies which can be engulfed by macrophages and reused.
Necoris - 'messy': release of cellular contents causing immune response (response to injury - viral infections)
Meiosis:
Occurs in somatic cells - 4 genetically different daughter cells
Recombination at chiasmata occurs during Prophase I, sister chromatids overlap
Independent assortment, homologous chromosomes align randomly along metaphase plate
Read: Cell Cycle Regulation by Checkpoints
Kevin J. Barnum and Matthew J. O'Connell
Enzymes:
Catalyse biochemical reactions by lowering the activation energy required:
Strains substrate bonds, reducing energy required to break
Reduces distance between substrate molecules in catabolic reactions, allowing new bonds to form in a collision
Substrate molecules complementary (geometrically or electromagnetically) to active site, competitive inhibitors also complementary
Vmax maintained - enzyme produces equal product to uninhibited
identical L-B y-intercept
Km decreases - less effective affinity for substrate as can also bind competitive inhibitor
reduced L-B gradient
more negative x-intercept
Small conformational changes can occur upon binding
Allosteric sites allow binding of non-competitive inhibitors and coenzymes (apoenzyme -> holoenzyme)
Vmax decreases, due to reduced product production
increases L-B y-intercept
Km maintained, as enzyme has identical effective affinity for substrate despite fewer enzymes able to bind substrate
steeper L-B gradient
identical x-intercept
Uncompetitive inhibitors bind to ES complex, preventing release of products
Gibbs' Free Energy
G = H - TS
Gibbs' Free Energy must be negative for a reaction to be energetically favourable
H = Enthalpy (heat energy given off/taken in) jmol-1
T = Temperature (Kelvin)
S = Entropy
