Update - September 2011

Hey guys,

I'm taking a break while I start my degree but I've actually been encouraged into developing this into a proper website - which is something I think I'll persue. I'm dreadful at web programming though, and if anyone would like to lend me your services, get in touch. :3

But yeah, watch this space. ^-^

In the meantime, email if you want to arrange any tutoring? (:

BIO5 Notes are well on their way! :D

I'm getting them all done at once, then there's gonna be a bit bulk upload. I'm going to change the tagging system tooo. At some point. So, instead of clicking either CHEM2, Unit 2, or Chemistry, they'll just be Chemistry Unit 2 AQA, etc.

I am absolutley bricking it for final exams, but hey yo, as the ramones would say. The BIO5 notes will be finished by study leave. I've done all about hormones, the oestrous cycle, feedback, behaviour, etc. Need to do nerves. Have done a learge bit of the DNA stuff. Need to get on with the techniques. I'll hopefully put it together into a kind of key-facts booklet.

Anyway. In the next few posts, you're getting CHEM1 notes. I hope they're useful. To any AS's reading this, whenever it is, please feel free o email if you're stuck, and arrange some tutoring if you're in the leicester area. (:

Author's noteeee...

So HI.

Firstly, how did January go for everyone? I hope it went well. Went okay for me. B's all round in chemistry, averaging a B overall. Got a B in BIO4, which I'm retaking. Hmm.

Anyway, on to Juneee... is anyone bricking it as much as me? My BIO5 notes are well on their way, I've found some useful resources too. If anyone wants to arrange to meet up and revise, then email me from the link at the top.

-Nin (:

Recapping Control of Gene Expression. ^-^

So, I have a mock test on all the genetics stuff this afternoon. Just going over stuff now. How are all of you guys going? Comment me and tell me how your unit four, or ones went in january. If you're retaking, or you're a first year flapping about Unit 2, take my email from the top of this page, or just comment by using the link at the bottom, where it says the number of comments, and drop me a line. If you're in the Leicester area, I can help you out. If not, email'll do. xD I'm happy to try. (:

So yeah. Gene Expression.

Totipotent Cells are undifferentiated cells, such as embryonic stem cells, that are not yet defined in their function. In animals, stem cells are totipotent. Plants have far more types of totipotent cells (Think of how you can make cuttings of plants, and grow an entirely new plant, given the right conditions?)

Cells loose totipotency, as, with age, different genes are swtiched on/off. When certain genes are switched of, they are not translated to produce polypeptides, meaning cells only have specific genes, the proteins produced serving only to aid their function.

Totipotent cells can be used to treat human disorders such as Parkinson's Disease, Alzheimers, Osteoarthritis, MS... all my growing new tissues from stem cells, and growing a culture of the needed type of cell after speciailisation. (That is TOTALLY spelt wrong.)

Oestrogen:

1. The DNA binding site on a Transcription Factor (the thing that stimulates transcription), can sometimes be inhibited
2. Oestrogen is lipid soluble and passes through the cell surface membrane easily
3. It binds with the receptor of the transcription factor.
4. This changes the same of the whole molecule, including the DNA binding site.
5. The Inhibitor is subsequently, removed.
6. The Transcription factor can now join to the DNA, initiating transcription (production of mRNA from DNA)

SiRNA:

1. An enzymes cuts up a piece of double stranded mRNA.
2. This makes little double stranded fragements, called SiRNA.
3. One strand of the SiRNA binds with a enzyme.
4. The enzyme is brought to the mRNA, due to the free bases of the SiRNA binding to a complimentary region on the mRNA.
5. The enzyme cuts of the mRNA into smaller fragments, seperating the sequence of triplet codons, meaning not all of the amino acids needed for the proteins are coded for, meaning the correct protein cannot be translated, as the amino acid sequence determines the strucutre, and it is not present in full.

Small Interferring RNA. (SiRNA)

Quick recap of oestrogen first - transcription stimulated by transcription factor, which has to bind to a specific region on the DNA. Can be inhibited. Oestrogen dissolves through phospholipid bilayer, as it is lipid soluble. Combines with receptor of transcription factor (complimentary). Changes the shape of DNA binding site, releasing inhibitor. Transcription factor can now join with DNA and stimulate transcription.

SO. The transcription factors can be inhibited. Oestrogen bind to the transcription factor on the receptor. Changes molecule shape, including DNA binding site. Releases inhibitor, and can now bind to DNA.

Righto. :P

So, now on to how SiRNA effects gene expression.

Small interferring RNA are little sections of RNA, double stranded. It prevents gene expression my breaking down mRNA.

1. Enzyme breaks down double stranded chains of mRNA into smaller sections, called SiRNA.
2. One strand of the SiRNA combines with an enzyme.
3. This one strand then pairs with the complimentary section of bases on a single stranded chain of mRNA.
4. The enzyme then cuts the mRNA down into smaller sections.

The effect this has? With a broken chain of the mRNA, there is not the correct sequence of triplet codons, meaning incorrect amino acids are produced/not all of the amino acids necessary are produced - meaning the protein outcome will not have the same teritary structure, and therefore, shape, and possibly will not function in the same way. The gene is not expressed.

How this can be used? Use of SiRNA to block the genes that cause some diseases, or to identifiy the role of particular genes by eliminating them, and study the effects/missing chracteristics.

Regulation of transcription and translation. OESTROGEN

1. Oestrogen is lipid soluble, so it can diffuse through the phospholipid bilayer easily. 
2. Oestrogen binds to the receptor molecule on a transcription site.The are complimentary. 
3. This binding changes the shape of the transcription factor, causing the inhibitor (of where the DNA goes) to detatch. 
4. DNA can join with transcription factor, and transcription is stimulated. 

Totipotency and cell specialisation.

What are Totipotent Cells?
Totipotent cells are undifferentiated, non specialised cells. Initially, cells can become any type of cell (muscle, epithelial, etc.). Totipotent cells do not yet have a function.

Which cells in plants and animals are totipotent?
Fertilized egg cells.Embryonic Stem cells. Meristematic Cells in plants.

How do cells loose totipotency and become speicialised?
Cells become specialised because some genes become switched off/left on. This means that not all of the cells code for the same proteins, and therefore, have different constitutions, and have different functions due the the varying frequencies of the avaliable proteins.

How can stem cells treat human disorders?
Stem Cells can treat human disorders as they are undifferentiated. A factor can be used to force the cells to differentiate into particular cells - giving the avaliability to re-grow tissues that have been damaged, either by accidents, or via degenrative disease. For example, nerve cells being produced can combat the prgressions of diseases such as Parkinson's, Alzheimers, MS, and strokes. 

Cell Division

The rate of cell division is controlled by two things:

Proto-oncogenes :- stimulate cell division
Tumour Supressor Genes :- slow cell division.

Proto-oncogenes code for GROWTH FACTORS. They attatch to a receptor protein on the cell surface membrane, and 'switch on' the genes for DNA replication via relay proteins.
However, the mutated form of a proto-oncogene is a oncogene. Oncognes could either code for a growth factor that is produced in excessive amounts, or just permanently activate the receptor protein, leaving the DNA constantly switched on for replication.

Cells would divide too quickly/too much, meaning a tumour/cancer would occur.

Tumour supressor genes inhibit cell division. It maintains the rate of cell division, and therefore, prevents the growth of tumours. If the tumour supressor gene mutates, it becomes inactive. Most of these mutated cells die, but a small frequency of cells continue to exist and thrive. Being strutually different to other cells in the body, the mutated cells, if built up, on that small chance, can form a tumour.
A tumour that exists without spreading is almost harmless, called Benign. Malignant tumours are cancer. The tumour spreads throughout the body via the blood, existing and affecting multiple locations.

Gene Mutation.

Mutation: Change in quantity or structure or DNA of an organism.

Nonsense mutation:
The mutation creates a stop codon. I.e. The mutation changing one base. Say the recognised stop codon is AUG. And, currently, your codon is ACG. If the C was swapped for a U, this would now be a stop codon, do the polypeptide chain would stop being produced at that point. Final protein would be different, and nto function the same.

Mis-sense Mutation: 
If the codon ends up coding for a different amino acid. Say ACC codes for Alanine, and ACG codes for
Glutamine. If the final C on the initial codon was swapped for a G, the codon would now produce Glutamine, not Alanine.The amino acids determine the tertiary structure - so the shape of the protein is likely to be changed, possibly making it non-fucntional.

Silent Mutation:
The Mutation changes a bases, but the codon still does for the same amino acid as previously. This is due to the genetic code being DEGENERATE. 

These are all SUBSTITUTION

Deletion of Bases:
A single base is deleted from the code. Although initially thought to be a mild effect, this usually causes what is known as a frame shift. Meaning - where the one base has been removed, the entire chain left shifts over by one place to the left. This changes all of the codons after that point, so the nearer to the begining of the chain, the worse off it is.

Genetic mutation is RANDOM. Mutagentic factors can affect this however. So, high energy radiation, and chemicals that alters the DNA structure, or interferes with transcription.

Translation, Assmebling a polypeptide.

Also, little note about splicing: the introns are removed because they would interfere with translation. 

Translation:

1. A ribosome attatches to the start codon on the mRNA. 
2. tRNA, which has an amino acid on one end, and an anticodon on the other. The anti codon in complimentary to the mRNA and joins with it. 
3. Another tRNA joins next to the last, complimentary to the mRNA triplet codon there. 
4. By the means of an enzyme, and ATP, the two amino acids on the top of the tRNA's are joined by a peptide bond. 
5. The ribosome moves on to the next codon in the sequence of the mRNA - another tRNA joining to it, aligning the amino acids in order for these to also be joined via a peptide bond. 
6. This process continues until a stop codon is reached. At this point, there will be a full polypeptide chain formed - the ribosome, mRNA, and final tRNA all detatch. 

Unit 1 Recap: 

Secondary stucture - the polypeptide is coiled or folded 

Tertiary structure - secondary structure is folded 

Quaternary structure - different polypeptide chains linking. 

In Translation, mRNA's function is to act as a template on which the polypeptide is formed.

tRNA acts as a carrier for the amino acid. Without tRNA to carry the amino acid AND attach to the mRNA on opposite sides, the amino acids could not line up.