Gene Expression Flashcards
Totipotent stem cells
Are able to produce any type of body cell
Only live for a very limited time during embryonic development in mammals where they only transfer part of their dna
Pluripotent stem cell
Totipotent cells develop into pluripotent cells in embryos
Pluripotent cells are able to divide in unlimited numbers and produce any type of cell that makes up the body
They are used to treat human disorders
Multipotent stem cells
Found in mature mammals and can divide into a limited number of cell types
Unipotent stem cells
Found in Mature mammals
Can divide into a new cell but can only produce one type
Main sources of stem cells
Adult stem cells, embryonic stem cells and induced pluripotent stem cells
Benefits of using stem cells
To reduce preventable deaths e.g can grow organs to reduce the wait time for transplants
Treat conditions that decrease the quality of life e.g can be used to replace the damaged spinal cord in paralysis
Induced Pluripotent stem cells
Can avoid the ethical issues of extracting pluripotent cells
They are produced from an adult somatic cell which are specialised
Somatic cells are converted to IPS cells by activating genes using protein transcription factors which makes somatic cells unspecialised
They can be made from the patients own body cells which reduces the chance of rejection
Bone marrow transplant
Use multipotent stem cells
Function of transcription factors
Proteins that enter the nucleus from the cytoplasm through nuclear pores
Activators
They promote gene transcription by interacting with RNA polymerase and allowing it to bind to DNA
Repressors
Stop RNA polymerase from binding to dna
Peptide hormones
Bind to the cell membrane and trigger a secondary messenger response which leads to the activation or inhibition of transcription of some genes
Lipid soluble steroid hormones
Can pass through the phospholipid bilayer and interact directly with dna
Oestrogen
Lipid soluble steroid hormone
How does oestrogen reach the nucleus
Diffuses through the cell surface membrane and through the nuclear pore in to the nucleus
Epigenetic regulation
Interacts with dna to control the access of dna so dna alters gene expression without actually changing the genetic code
Chromatin
The combination of dna and histones
Epigenome
Chemical layer surrounding chromatic and interacts with it to change its structure
It can cause chromatin to become:
More condensed= prevents transcription factors from binding to dna
Or less condensed= allows easier access to transcription factors
Epigenetic markers
Groups that do not alter the base sequence
Chromatin becomes more or less condensed when epigenetic markers are attached or removed from dna or histone proteins
Increased methylation
Methyl groups bind to CpG sites on dna and cause chromatin to be more condensed so transcription factors can’t reach dna
Acetylation of histones
Acetyl grpups are added to lysine amino acids on histone proteins which removes a bond between the histone and protein and the dna which causes it to be less tightly wrapped so RNA polymerase and transcription factors can more easily bind and therefore gene expression is stimulated
Inheritance of epigenetic markers
Environmental factors such as methylation can influence the gene expression of their offspring
Abnormal methylation
If methylation is not regulated properly this can affect the regulation of important processes
If increased too much it can decrease the gene expression of tumour suppressor genes so the cells divide uncontrollably
If decreases too much it can increase the expression of proto oncogenes too much
Epigenetic change and treating disease
Epigenetic changes can be reversed
E.g the action of methyl transferase enzyme can be inhibited
Usually adds methyl groups to do dna which can cause disease
RNA interference
Small molecule of double stranded RNA
Binds to the mRNA molecule and breaks it down which prevents it from being translated into a protein
siRNA
Complimentary to the MRNA sequence it inhibits so it targets a specific sequence and breaks it down into smaller fragments
Mirna
Not fully complimentary to the mRNA sequence so it can target multiple sequences
Benign tumours
Not cancerous and don’t spread to invade other tissues
Malignant tumours
Cancerous and spread into other tissues and around the body
Tumour suppressor genes
Inhibit cell division to regulate the rate at which cells divide
Increased methylation of a tumour suppressor gene inihibts this gene
Oncogenes
Capable of transforming a cell into a cancerous cell cause they cause excessive cell division
Mutations of a proto oncogene
Decreased methylation of a proto oncogene causes cell division
Environmental factors that affect cancer
Exposure to radiation
Smoking
Alcohol consumption
Eating a diet high in fat
Genetic factors that affect cancer
Having certain alleles such as the BRCA1 allele can increase the chance of developing breast cancer
Prevention of cancer
Develop more sensitive tests to detect earlier on
Treatment
If we know what gene mutations cause cancer, drugs can be developed to target these specific gene mutations and intensify the treatment
How do transcription factors work
They are activated through a signalling pathway and bind to the promoter region of a gene which can either allow or prevent the transcription of the gene from taking place
What do transcription factors interact with
RNA polymerase either by assisting RNA polymerase binding to the gene or by preventing it from binding
Effect of transcription factors
Either increase or decrease the rate of transcription of a gene
What does oestrogen do when in the nucleus
Attaches to an ERa oestrogen receptor that is held within a protein complex, this causes the ERa oestrogen receptor to under a conformational change
What effect does the new shape of the ERaoestrogen receptor have
Allows it to detach from the protein complex and diffuse towards the gene to be expressed
What does the ERa oestrogen receptor bind to
A cofactor which enables it to bind to the promoter region of the gene, this stimulates RNA polymerase binding and gene transcription
Example of epigenetic links condition
Prader-Willi syndrome is caused by the silencing of an allele on chromosome 15
The severity of the syndrome depends on whether an individual receives the affected dna from their mother - carrier for the defective chromosome so won’t develop the syndrome but in the father they will
SiRNA in the cytoplasm
In the cytoplasm siRNA’s bind to protein complexes which use energy from ATP to seperate the two strands of the siRNA which exposes the nucleotide babes so they are able to pair with bases from an mRNA molecule
RNA interference : mRNA leaves the nucleus
In the cytoplasm single stranded siRNA binds to the target mRNA through complementary base pairing
The mRNA is cut into fragments by the enzyme/protein complex associated with siRNA - cannot be translated and therefore will not produce proteins
