How DNA Codes For Proteins
Characteristics of the Genetic Code:
- Widespread but not universal
- Triplet Code
- Stop Codes
- Degenerate Code
What sorts of polypeptides do genes code for?
What is the Central Dogma of Molecular Biology?
- The gene to be transcribed unwinds and unzips - the length of DNA that makes up the gene dips into the nucleolus.
- Hydrogen bonds between complimentary bases break.
- RNA nucleotides are activated. The activated RNA nucleotides temporarily bind to their exposed complimentary bases.
- This forms the sugar phosphate backbone.
- The two extra phosphoryl groups are released. This releases energy for bonding adjacent nucleotides.
- The mRNA produced is complementary to the nucleotide base sequence on the template strand of the DNA. It is therefore a copy of the base sequence on the coding strand of the length of DNA.
- The mRNA is released from the DNA and passes out of the nucleus, through a nuclear pore in the nuclear envelope, to a ribosome.
- The process of transcription is catalysed by RNA polymerase.
What are the 4 activated RNA nucleotides?
2.1.2 - Ribosomes
What are codons? Why is the sequence of AA's in a protein crucial?
What are the characteristics of a ribosome?
- Free in cytoplasm or bound to RER and are site of translation
- Assembled in the nucleus of eukarytoes
- Ribosomal RNA (rRNA) + Protein = RIBOSOME!
- Made of 2 subunits; the code for the sequence of AA's can fit into grove.
- They move along mRNA, reading code and assembling the AA's in the correct order to make a functioning protein.
Transfer RNA (tRNA)
Made in nucleus and passes into cytoplasm. Lengths of RNA that fold into hairpin shapes. 3 exposed bases at one end = AA can bind. ANTICODON = 3 unpaired nucleotide bases. Each anticodon can temporarily bind with its complementary codon.
- A molcule of mRNA binds to a ribosome. 2 Codons are attatched to the small subunit. The first exposed mRNA codon is always AUG.
- Using ATP energy and an enzyme, a tRNA with methionine and the anticodon UAC, forms hydrogen bonds with this codon.
- A second tRNA bearing a different AA, binds to the second exposed codon with it's complementary anticodon.
- A peptide bond forms between the two adjacent AA's.
- An enzyme present in the small ribosomal subunit catalyses the reaction.
- The ribosome now moves along the mRNA, reading the next codon.
- A third tRNA brings another AA, and a peptide bond forms between it and the dipeptide.
- The first tRNA leaves and is able to collect and bring another of it's AA's.
- The polypeptide chain grows until a stop codon is reached.
- There are no corresponding tRNA's for these 3 codons, so the polypeptide chain is now complete. - UAA, UAC, UGA
Cyclic AMP (cAMP)
CYCLIC ADENOSINE MONOPHOSPHATE
Some proteins have to be activated by cAMP.
It is a nucleotide derivative. It activates proteins by changing their 3D shape so that their shape is a better fit to their complementary molecules - substrates.
Is protein synthesis faster in eukaryotes or prokaryotes and why?
What is the minimum number of different tRNA molcules that are needed for protein synthesis?
Twenty one. One for each of the AA's and one for the stop.
- What are mutagens? Give some examples.
- When might DNA mutations occur?
- Explain how mutations can be associated with MEIOSIS.
- Explain how mutations can be associated with MITOSIS
- Somatic mutations
- 2 main classes of DNA mutation = Point/Substitution and Insertion/Deletion
Point = When one base pair replaces another
Insertion/Deletion = One or more nucleotide pairs are inserted or deleted from a length of DNA. This causes a Frameshift.
- Which has the greater impact on the resulting protein?
- Template Strand > Coding Strand >mRNA copy
Many Genetic Diseases are the result of DNA mutati
- In 70% of cases, the mutation is the deletion of a triplet of base pairs (deleting an AA in a sequence of 1480 AA's)
SICKLE CELL ANAEMIA
- Point mutation
- On codon 6 of the gene for the beta-polypeptide chains of haemoglobin.
- The AA VALINE is inserted in place of GLUTAMIC ACID
- Results from a stutter - an expanded triple nucleotide repeat.
- Normal gene has repeating CAG sequences. If these expand above a threshold number, Huntington's is caused.
- Symptoms manifest in later life - dementia and loss of motor control.
- Some protooncogenes can be changed into oncogenes (a gene that has the potential to cause cancer) by a point mutation.
- Protooncogenes are permanently switched on.
- Such cell division leads to a tumour.
- Eg, RAS gene in human bladder cancer.
Missense - triplet codes for a different AA.
Nonsense - The triplet codes for a stop? Truncated.
Mutations with Neutral Effects
It may produce no change in the organism if:
- The mutation is in a non coding region of the DNA.
- It is a silent mutation - point mutation/degenerative nature.
The effect can also be neutral if the mutation gives no advantage or disadvantage.
- Some people can't smell honeysuckle.
- Some can't taste PTC (Phenylthiocarbamide) tastes bitter and is poisonous in large substances.
- Rolling your tongue
- Detached ear lobes.
Mutations with Harmful or Beneficial Effects
Melanin - The dark skin pigment that protects from UV Light.
Vitamin D - Synthesised from the action of intense sunlight
- Mutations for paler skin in Africa would cause burning and skincancer.
- During migration to temperate climates, sunlight wasn't intense enough to cause enough Vitamin D to be made with dark skin.
- Humans with mutations that lack melanin were advantageous as they could synthesise more vitamin D.
Inuits have maintained some of their skin pigment from the large amount of dietry vitamin D from fish and seal meat and blubber.
Lack of Vitamin D leads to rickets. It also leads to narrowing of the pelvis in women which means difficulties in childbirth.
Environment is never static - same mutation can be beneficial or harmful.