1. Totipotent cells can divide and produce any type of body cell. What happens to a totipotent cell to result in cell specialisation ?
Answer
Only part of their DNA is able to be translated.
2. What are induced pluripotent stem cells ?
Answer
They are made from body cells that have already differentiated, but by using appropriate protein transcription factors, they can be reverted back into pluripotent cells.
3. What effect does increased methylation of DNA have on gene expression ?
Answer
It suppresses gene transcription.
4. Induced Pluripotent Stem Cells (iPSCs) can be produced from adult somatic cells by inducing the expression of specific transcription factors. These reprogrammed cells then have similar characteristics to embryonic stem cells. Suggest how transcription factors can lead to a somatic cell becoming a pluripotent stem cell.
Answer
Transcription factors move from the cytoplasm into the nucleus, where they bind to the promoter regions of specific genes. This binding initiates the transcription and expression of genes required for a cell to become pluripotent.
5. It is hoped that patient-specific iPSCs will be used in the treatment of degenerative diseases. What advantage would these cells have over using embryonic stem cells ?
Answer
Embryonic stem cells would not be genetically identical to the patient. Patient-specific iPSCs, however, would be genetically identical, meaning they would not be recognized as foreign. As a result, they would not trigger an immune response and therefore would not be rejected.
6. One of the transcription factors used to induce pluripotency activates a proto-oncogene and uses retroviruses to provide the transcription factor gene in order for this transcription factor to be expressed. Other methods have been investigated to avoid this, but have had very low success rates of inducing pluripotency. For scientists, what would be the concerns of using viruses to activate a proto-oncogene?
Answer
If a proto-oncogene mutates once it is activated, it could lead to tumour formation. Similarly, if a retrovirus inserts a gene within a proto-oncogene or a tumour suppressor gene, this could also result in tumour formation.
7. When a doctor suspects that a woman may have breast cancer, the initial step is to take a biopsy. The biopsy contains a small sample of cells from the affected breast tissue. If the cells are cancerous, the number of oestrogen receptors (ER) present in the cells is one indicator of a certain type of breast cancer. This also helps in determining whether hormone treatment will be of benefit to the patient. Women with a high ER are referred to as having ER-positive breast cancer. Only certain types of cells such as breast, ovary and womb respond to the hormone oestrogen. Explain why.
Answer
Only these cells have receptors complementary to oestrogen, so only these cells will respond. The transcription factors then initiate transcription of specific genes.
8. Name the region of the DNA that the oestrogen-receptor complex binds to for transcription to be initiated.
Answer
Promotor region.
9. Using the information above suggest the cause of cancer in ER-positive breast cancer sufferers.
Answer
They have more oestrogen receptors. In some cases, these receptors are mutated and can stimulate cell division even without being bound to oestrogen. As a result, oestrogen binding leads to increased transcription of genes that promote cell division, causing cells to divide rapidly and form tumours.
10. There is also another receptor, the progesterone receptor (PR). The number of these receptors is also found. Women with high levels of both receptors (ER and PR) respond better to hormone treatment and are referred to as double-positive women. Double-positive breast cancer cells were investigated, providing them with enough oestrogen and progesterone to stimulate both receptors. When these receptors were then taken out of the cancer cells, scientists discovered that they were physically stuck together. The scientists discovered that when both receptors are together they stimulate the transcription of different genes from those that are stimulated by ER on its own. It was seen that over 400 genes were controlled differently in this way. The overall effect was that the cancer cells stopped growing as quickly. Suggest the reason why the presence of both receptors (ER and PR) and their sticking together caused a different outcome for tumour cell growth.
Answer
When ER and PR receptors bind together, they form a different tertiary structure. This altered structure is complementary to different promoter regions, leading to the transcription of different genes. Because not all of the same genes are expressed, the pattern of gene expression changes, resulting in slower cell growth compared to when the receptors act independently.