Biology - Control in Cells & Organisms

DNA is copied into RNA during protein synthesis. This is because:

• DNA molecules are found in the nucleus but the organelles required for protein synthesis (ribosomes) are in the cytoplasm
• - Because DNA is too large, it can't leave the nucleus so a section needs to be copied into RNA which is small enough to move into the cytoplasm and can attach to the ribosomes.

RNA is similar to DNA but with a few differences...

• The sugar in RNA nucleotides is a ribose sugar not a deoxyribose sugar like in DNA.
• The nucleotides form a single (polynucleotide) strand not a double one.
• The Thymine base is replaced by Uracil - U always pairs with A.

mRNA:

• Is a single nucleotide strand
• Groups of 3 adjacent bases are called codons
• It carries genetic code from the DNA in the nucleus to the cytoplasm.

tRNA:

• A single polynucleotide strand which is folded into a clover shape due to hydrogen bonds between specific base pairs.
• Every tRNA molecule has a specific 3 base sequence at one end called an anticodon.
• They also have a amino acid binding site at the other end.
• It's found in the cytoplasm
• It carries amino acids that are used to make proteins to the ribosomes.

During Transcription an mRNA copy is made in the nucleus

1* Transcription starts when RNA polymerase (an enzyme) attaches to the beginning of the gene of the DNA double helix...

2. The RNA polyermase breaks the hydrogen bonds between the complementary base pairs of the two DNA strands which causes them to separate.

3. One of the strands is used as a template to make the mRNA copy.

3. Free RNA nucleotides line up alongside the template strand and bind to their specific base pairs - this means that the mRNA strand ends up being a complementary copy of the DNA template strand.

4. The RNA polymerase moves along the DNA strand - separating the DNA strand and assembling the mRNA

...once its passed, hydrogen bonds reform and the DNA coils back into a double helix...

5. When RNA polymerase reaches a stop codon, it stops making mRNA & detaches from the DNA.

In Eukaryotic Cells mRNA is edited...

• Introns - sections of DNA that don't code for amino acids.
• Exons - sections of DNA that code for amino acids

During Transcription, intron and exons are copied into the mRNA (called pre-mRNA).

Splicing is the process where the introns are removed and the exons joined which forms the mRNA strands.

The mRNA can then leave the nucleus through the nuclear pore and move into the cytoplasm, where it attaches to a ribosome ready for Translation.

During Translation, amino acids are joined together to make a polypeptide chain (protein).

1. mRNA attaches to a ribosome.

2. tRNA carries amino acides to the ribosome.

3. A tRNA molecule that has an anticodon that's complementary to the first codon of the mRNA attaches by specific base pairing.

4. A second tRNA molecule attaches itself to the second codon on the mRNA in the same way.

5. The amino acids attached to the tRNA molcule are joined together by a peptide bond.

6. The first tRNA molecule moves away from the ribosome, leaving behind the amino acid.

7. This process continues, producing a chain of linked amino acids (a polypeptide chain) until there's a 'stop signal' codon on the mRNA molecule.

8. The protein/polypeptide chain then moves away from the ribosome and translation is complete.

The Genetic Code is...

A triplet code --> 3 bases code for one amino acid. In DNA, the 3 bases coding for one amino acid make up a triplet. In mRNA, the 3 bases coding for one amino acid make up a codon.

Degenerate --> There are more 'codes' than amino acids because

• 64 triplets and only 20 amino acids
• Some amino acids have more than one code
• Some DNA triplets say 'stop transcribing' (and then some RNA triplets say 'stop translating')

Non-overlapping --> The 3 bases that form one triplet are not part of any other adjacent triplet

Universal --> The codes are the same for all organisms.

Introns are non coding sections of DNA (within a gene) and Exon are coding DNA.

Promotors determine what genes are transcribed & how oftn they're transcribed --> they contain RNA polymerase binding sites, which starts transcription.

The 'Transcript' contains non-coding introns, therefore, this is modified after transcription to remove non coding RNA.

In Post Transcription Modification:

Introns are 'cut' out and exons are joined

How does the pacinian corpuscle detect mechanical pressure?

1. The pacinian corpuscle is stimulated.

2. The lamellae are deformed & press on the sensory nerve endings.

3. This causes deformation of stretch-mediated sodium ion channels in the sensory neurone's cell membrane.

4. The sodium ion channels open.

5. Sodium ions diffuse into the cell down their electrochemical gradient, creating a generator potential.

6. If the generator potential reaches its threshold, it will trigger an action potential along the neurone.

Decrease in arterial blood pressure:

1. Detected by baroreceptors in aortic arch & carotid bodies.

2.  Nerve impulses to cardioregulatory centre in Medulla Oblongata.

3. Impulses down sympathetic nerves from accelorator centre of cardioregulatory centre to SAN.

4. SAN stimulates increase in heart rate.

Increase in arterial blood pressure:

1. Detected by baroreceptors in  aortic arch & carotid bodies.

2. Nerve impulses to cardioregulatory centre in Medulla Oblongata.

3. Impulses down parasympathetic nerves from inhibitatory centre of cardioregulatory centre to SAN.

4. SAN stimulates decrease in heart rate.

Decrease in pCO2: Increases pH of blood plasma

1. Detected by chemoreceptors in aortic arch & carotid bodies.

2. Nerve impulses to Medulla Oblongata decreases.

3. Impulses down parasympathetic nerves from inhibitatory centre of cardioregulatory centre to SAN.

4. SAN stimulates decrease in heart rate.

Increase in pCO2: Decreases pH of blood plasma.

1. Detected by chemoreceptors in aortic arch & carotid bodies.

2. Nerve impulses to the Medulla Oblongata increases.

3. Impulses down sympathetic nerves from acceloratory centre of cardioregulatory centre to SAN.

4. SAN stimulates increase in heart rate.

When not conducting an impulse, an axon has a membrane potential called its resting potential.

• In this state, the inside of the membrane is more negatively charged than the outside by about -70mV.
• We say the membrane is polarised.

How is the resting potential maintained?

* Large anions (e.g. negatively charged proteins) are kept inside the axon.

* Facilitated diffusion of Na+ & K+ across the membrane via ion channels --> Na+ diffuse more slowly than K+ so inside of the membrane becomes more negative.

* More Na+ pumped out than K+ pumped in..

Depolarising the Membrane:

1. The energy of the stimulus excites the membrane, causing some of the sodium voltage-gated ion channels (Na+VGIC) in the axon to open.

2. Na+ ions then rapidly diffuse into the axon down the electrochemical gradient.

3. This causes a sudden increase in positively charged ions inside the membrane.

--> The inner surface of the membrane now aquores a positive charge of approx. 30mV compared to the outside.

4. This change in potential difference across the membrane is called depolaristaion 

--> Depolarisation of a small section of a nerve fibre creates an action potenial.

Repolarising the Membrane:

1. Once the potential difference reaches about 30mV, the sodium ion channels close & the rest of/all the K+ ion channels open.

2. K+ diffuse out of the neurone down the K+ conc. gradient.

--> The membrane is starting to return back to its resting potential (-70mV).

Hyperpolarisation:

3. However, the K+ ion channels are slow to close & so too many K+ diffuse out of the neurone which reduces the membrane's potential to about -80/90mV.

--> This 'overshoot' is called hyperpolarisation.

Back to Resting Potential: 'The ion channels are '"reset"

4. The sodium-potassium pump then returns the membrane to its resting potential.

How does the refractory period produce discrete impulses?

1. The refractory period acts as a time delay between one action potential and the next.

2. This makes sure that the action potentials dont overlap, but pass along as discrete (separate) impulses.

3. This also makes sure that the action potentials are unidirectional (they only travel in one direction).

1. Axon at rest. All gated Na+ channels closed but activated.

2. Action potential arrives at one end of axon. Voltage-gated Na+ ion channels open to cause depolarisation here.

3. Depolarisation affects next part of membrane, which also depolarises. Original region begins to repolarise. Na+ ion channels are shut here and inactive.

4. Action potential occurs in next region of axon and the next one...

5. Original region is now fully repolarised and voltage-gated Na+ ion channels are activated again. However, depolarised region is too far down axon to have any affect on it.

How Acetylcholine transmits the nerve impulse across a Cholinergic Synapse:

1. An action potential (or A.P) arrives at the synaptic knob of the pre-SN (-70mV to +30mV)

2. The A.P stimulates a the voltage-gated Ca 2+ ion channels in the pre-SN to open and soCa 2+ ions diffuse down their elecrtochemical gradient into the synaptic knob

3. This influx of Ca 2+ ions causes the synaptic vesicles to fuse with the pre-synaptic membrane so that the vesicles release the neurotransmitter ACh into the synaptic cleft --> This is called Exocytosis

4. ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the post synaptic membrane which causes Ligand gated Na+ ion channels (2xAch on 1 channel) to open

5. Na+ diffuse into the post-SN down the electrochemical gradient which causes an action potential (-70mv to +30mV) if threshold value is reached.

6. ACh is the removed from the synaptic cleft by the enzyme Acetlycholinesterase (AChE), so the response doesn't keep happening --> ACh is broken down into Choline and ethanoic acid which causes the LDNa+IC to close so that th resting potential can be re-established.

What happens to the products of ACh:

Once Acetylcholine has been broken down into Choline and Ethanoic acid by Acetylcholinesterase (which causes LGNa+IC to close) ...

1. Choline and ethanoic acid are transported back into the synaptic knob

2. ATP is then used to synthesise ACh and 'package' it back into the vesicles

1. Once an action potential has reached the muscle cell membrane, it is quickly carried through a system of T-tubules that branch throughout the cytoplasm of the muscle (sarcoplasm).

2. The action potential causes the sarcoplasmic reticulum (which has been actively absorbing Ca2+ from the cytoplasm of the muscle) to release its store of Ca2+ ions into the myofibrils by opening Ca2+ channels on the SR which cause Ca2+ ions to diffuse out down conc. gradient.

3. Ca2+ bind to troponin on the actin filament, which changes shape, moving tropomyosin into the 'groove' to expose the binding sites on the actin.

4. Myosin 'cross-bridges' can now attach to the actin because an ADP molecule attached to the myosin heads means they're now in a state to bind to the actin filament and form a cross bridge.

5. Once attached to the actin filament, the myosin head changes its angle, pulling the actin filament along & releasing a molecule of ADP which then attaches to each myosin head, causing it to become detached from the actin filament.

6. Ca2+ ions then activates the enzyme, ATPase, which hydrolyses the ATP to ADP which provides the energy for the myosin head to return to its original position.