cell mechanics

equation relating energy of a system

ΔU = Q- P ΔV

entropy

ΔS=Q/T

where Q is heat(energy flow)

enthalpy

ΔU = Q-PΔV which can be expanded to a useful equation:

ΔH=Q at constant pressure

Gibbs free energy definition

quantifies if a reaction will occur spontaneously or not

spontaneous or non spontaneous if ΔS<0

non spontaneous

spontaneous or non spontaneous if ΔS>0

spontaneous

spontaneous or non spontaneous if ΔH>0

heat absorbed-non spontaneous

spontaneous or non spontaneous if ΔH<0

heat produced - spontaneous

Gibbs free energy equation

ΔG=ΔH-TΔS

first law of thermodynamics in relation to the cell

ΔU=Q+W

boltzmanns microscopic definition of entropy

S=k ln(Ω)

where Ω is the number of possible configurations of a systemst

ructural requirements of membrane bilayer

semi porous

flexible and deformable

strong enough to withstand external forces and energy fluctuation

surface tension

y = energy/area J/m²

compression energy of bilayer

hypotonic

solution concentration is greater inside the cell, osmosis drives water flow into the cell increasing pressure

isotonic

solution inside is equally concentrated to the outside

hypertonic

solution concentration is greater outside the cell, osmosis drives water out

osmotic pressure equation

P=ΔC RT. where C is change in concentration

flicks laws of diffusion(concentration gradient)

J=-D ∂Φ/∂x where Φ is concentration, D=diffusion constant, J=flux

why do molecules move in the presence of thermal energy

it increases collisions which redirects molecules

cytoskeleton components

spectrin

actin

intermediate filaments

microtubules

cytoskeleton polymerisation

cells move by rapid extension and contraction of cytoskeleton fibres driven by polymerisation and depolymerisation

accessory proteins

control filament length

stages of cytoskeleton polymerisation

nucleation

elongation

steady state

nucleation

individual cells associating e

elongation

once the threshold is hit a linear growth phase is entered

how do the tubular sub units polymerise

alpha and beta tubular sub units involve GTP and GDP (like ATP-ADP) which act as energy converters driving the polymerisation

polymerisation kinetics equation

dn/dt =+KonM-Koff

where Kon/off is the capture/release rate constant, M=concentration of free monomers

Mc(critical concentration)

point at which no net change in filament length

Mc=Koff/Kon

treadmilling

when the growth of the plus end equals the shrinkage at the minus end

properties of polymerisation of filaments

rapid extension and contraction

control of filament length with accessory proteins

chemical to mechanical energy conversion

advantages of polymerisation of filaments

flexibility of response

fmax

(KT/d)ln(M/Mcrit)

f=force

K=boltzmanns constant

T=absolute temp

M=concentration of monomers

Mcrit=Critical concentration

equation illustrating electrons produced by conversion of NADH

NADH—→ NAD^+ + H^+ + 2e^- 

equation illustrating electrochemical gradient driving protons back into matrix through ATP synthase

ADP+Pi+4H^+ ——> ATP+H2O+4H^+

ATP synthase

rotates which acts as a source of potential energy

how ATP synthase produces torque

protons flow through due to electrochemical gradient

electrostatic forces between protons and c ring produce rotational motion

ATP synthase energy consumption

1 rotational step of 120° requires 8×10^-20 J

describe how myosin protein crawls along actin filament

myosin binds to filament

ATP capture releases myosin

hydrolysis of ATP to produce ADP leads to shape change and myosin head moves along filament

myosin protein uses energy of one ATP molecule to move 5nm

motor proteins

transport vesicles within the cell

molecule specific binding of vesicle to the motor so cargo is controlled

different types are differentiated due to different behaviour under same force

bidirectional motion of cargo theory

motors will pull cargo in different directions

overall motion is the balance of the forces

motor protein diseases

Alzheimers-loss of nerve cell function is linked to degradation of kinesin and dynein transporting molecules along the axon

glucose—→ carbon dioxide+water

C6H12O6——> CO2+H2O

when is energy extracted in cell processes

stage 1 glycolysis in cell cytoplasm

stage 2 citric acid/Krebs cycle in mitochondria

glycolysis info needed to know for exam

anaerobic

energy loss stage

energy gain stage

energy loss stage reactions

• Glucose—→ glucose-6-p using P from ATP (so -1ATP)

|___> produced by two separate reactions:
ATP+H2O—→ ADP+H3PO4

Glucose+H3PO4—> glucose-6-P+H2O

• Further oxidation of the carbohydrate:

Glucose-6-P—→ Fructose-6P using P from ATP(so - 1 ATP)

energy gain stage

bisphosphoglycerate*2—→ pyruvate +4ATP (Phosphate from carbohydrate moved to ADP producing 4 ATP total)

citric acid/krebs cycle

• driven by enzymes in mitochondrial matrix

• preliminary step:
  pyruvate—→acetyl-coA+CO2 (turning NAD+ to NADH + H+)

• citric cycle:
  acety-coA+H2O—→Oxaloacetate+CO2 (turning NAD+ to NADH + H+) *3

energy conversion summary

• oxidation of c atoms in sugar release high energy electrons

• hydrolysis of ATP to ADP and Pi is energetically favourable

• cells use enzymes to link energy release from ATP degradation to unfavourable chemical reactions-synthesis, motion

  • 30-36 molecules of ATP produced from 1 glucose, 84 from 1 fatty acid, 40%conversion efficiency

summary energy conversion equations

C6H12O6+6O2+6H2O+36ADP+36P—→6CO2+12H2O+36ATP

NAD+ + 2e- + H+ ←→ NADH

24e- + 6O2 + 24H+ —→ 12H2O

how catalysts aid reactions

oxidation of glucose

glucose+H3PO4—→ glucose-6-P+H2O (ΔG=+3.2)

why are most reactions energetically unfavourable?

so catalysts control which reactions occur, if spontaneous no control

composition of genes

nucleotide units within a polymer molecule (DNA)

4 DNA nucleotides

Adenine

Guanine

Cytosine

Thymine

nucleotide composition

sugar-phosphate-base

Nucleotide pairing

C&G

A&T

genome

the total DNA content of an organismge

genes

formation of nucleotides form a discrete information set for the production of specific protein molecules

where is DNA stored and why

in chromosomes in the nucleus of each cell,

localises genetic decoding, high molecular concentrations and specialised enzymes

DNA replication

double strand is separated by DNA helicase, driven by ATP hydrolase

matching of base sequence through hydrogen bonding adds deoxyribonucleotide monomers to the polymer strand, directed by DNA polymerase

phosphate groups are added to the backbone

large free energy of the reaction provided by the release of phosphate from ATP-ADP

DNA looping

process where proteins cause a segment of the DNA double helix to bend and form a loop, which brings distant DNA sites close together to regulate cellular processes

energy and entropy considerations of DNA looping

requires energy due to strain on structure

entropy reduction

binding proteins help stabilise despite these constraints

gene expression

translation of genetic code to produce proteins

gene expression stages

1. transcription- DNA transformed to RNA Uracil replaces Thymine, controlled by ribosome

   1. protein synthesis directed by RNA molecule- translation

transcription

RNA polymerase begins RNA synthesis once promotor sequence is recognised

polymerase moves along DNA synthesising RNA

polymerase encounters terminator sequence

transcription enzyme

RNA polymerase

mechanics of RNA polymerase

once promotor sequence is recognised it clamps to DNA with movable jaws

after transcription of 10 nucleotides a flap closes to form exit tunnel for the synthesised RNA

at the terminator the nucleotide sequence codes a hairpin into the RNA which releases it from DNA

mRNA

completed RNA destined for protein synthesis. they are passed out of nucleus into cytoplasm

codons

3 letter sequences on RNA used to code for specific amino acid, 64 possible sequences-but only 20 amino acids, this built in safety, if a codon is incorrect it may still code for the same protein

example of biological feedback

principles of feedback for system regulation

negative- output I linked back to input in a way that damps the system to reduce output

positive feedback- output linked back to boost system

control system in coli when glucose is scarce

cell signalling

manifests using molecules, signal transmission is via diffusion and cell receptor molecules are the receiver

this triggers a signalling cascade of molecular interactions that manifest A change

membrane based signalling

membrane houses receptors adapted to recognise and bind to ligands (signal molecules)

example of signalling-circadian oscillator

cyclic response to light/darkness. signals production of hormones in pineal gland cortisol and melatonin. the suprachiasmatic nucleus controls this pattern, a part of the brain linked to stimulation of the optic nerve

cell cycle

process of cell growth DNA replication and division

main cycle phases

S phase- DNA replication takes place 8-10 hours

M phase- 2 DNA copies separated into daughter cells 1 hour

in between G1 and 2 phases- cell grows and checks cycle process

G1 checkpoint

cell control mechanism checks cell status and monitors signals from cellular environment. If cell conditions are not suitable due to chemical cues the cycle is blocked

G2 checkpoint

control mechanism that checks accuracy of DNA copy

cell cycle control system

Timing

synchronicity

directionality-binary on/off switches ensure completion of events

robustness- error checking

flexibility- respond to changes in conditions

does the cycle control system use positive or negative feedback

negative

control based on two families of proteins

Cyclin dependent kinases(cdK)-control major processes of DNA replication, chromosome segregation and mitosis. activity fluctuates, concentration remains constant.

Cyclins- activate Cdk proteins(regulatory molecules) concentration fluctuates.

quality control is initiated at what checkpoints

DNA replication checkpoint- ensure faithful reproduction of genes

Spindle attachment checkpoint- ensure complete attachment of chromosomes

DNA damage checkpoints- ensure damaged genes are not copied

Apoptosis

if damaged cells cannot be repaired they enter a series of molecular interactions which lead to death

activation of p53 by the DNA damage checkpoint

• Mdm2 and p53 molecules phosphorylated

• Mdm2 releases from p53 and becomes stable

• p53 molecule initiates transcription of cdk inhibitor protein-halts cell cycle

• transcription of activator proteins release cytochrome C from mitochondria

steps of apoptosis-an example of positive feedback

• caspases cut up the cell into small pieces

• macrophages (white blood cells) ingest pieces

stages of mitosis(6)

prophase 

prometaphase

metaphase

anaphase

telophase

cytokinesis

prophase

replicated chromosomes condense

outside the nucleus the mitotic spindle assembles between two centrosomes which have replicated and moved apart

prometaphase

• begins with breakdown of nuclear envolope

• chromosomes attach to spindle microtubules via kinetochores

metaphase

• chromosomes aligned at equator of the spindle, midway between spindle poles

• kinetochore microtubules attach sister chromatids to opposite poles of spindle

anaphase

• sister chromatids synchronously separate to form two daughter chromosomes, pulled in polar direction

  • kinetochore microtubules get shorter and spindle poles move apart

telophase

• two sets of daughter chromosomes at poles of spindle decondense

• new nuclear envelope reassembles around each set

  • division of cytoplasm begins with assembly of contractile ring

cytokinesis

• cytoplasm is divided in two by contractile ring of actin and myosin filaments, pinching the cell

• internal vesicles recruited to the cleavage furrow to provide additional membrane required to form the gained surface area of daughter cells

example of anti-cancer drug

paclitaxel inhibits microtubule disassembly so prevents formation of mitotic spindle, cells stall in G2 and enter apoptosis

simple equation describing thee proliferation of cells over time

N=2^t/TD

where TD = cell cycle time

t= time

exponential growth equation

dN/dt=rN

where N=number of cells

r=rate constantlo

logistic growth equation

dN/dt=rN(1-N/K)

K=carrying capacity

what proteins trigger cell proliferation

growth factor proteins

survival factors

proteins secreted by neighbouring cells, they attach to cell surface receptor molecules which down regulates the apoptotic pathway