How Body Clocks Impact Breast Cancer

Volume 30, Number 1, September 2017

Activity

How body clocks impact breast cancer

Martin Rowland

Before attempting the questions in this worksheet, read Tori Blakeman’s article How body clocks impact breast cancer.

Questions 1 to 7 test AO1 skills; other than question 7, they should be accessible to AS/Year 1 A-level biology students.

Questions 8 to 10 test mainly AO2 skills, using stimulus material that you are not expected to have learnt.

Question 10 also includes a test of AO3 skills

Questions 7, 8 and 9 test your general understanding of cell control (a Year 2 A-level biology topic).

Questions

1Shift patterns, such as those required of airline staff and nurses, appear to be risk factors for breast cancer. Explain what is meant by a risk factor. (2 marks)

2Suggest why the body clock mechanism is often referred to as a circadian rhythm. (1 mark)

3The pineal gland, within the suprachiasmatic nucleus (SCN) of the brain, ‘is an evolutionary conserved organ among nearly all vertebrates’. Explain the meaning of an evolutionary conserved organ. (2 marks)

4 Name the environmental factor that controls the activity of the pineal gland. (1 mark)

5 The core biological clock comprises two components. Name these two components. (1 mark)

6 Give one difference and one similarity between a cancer and a tumour. (2 marks)

7 Define each of the following terms:

(a)gene promoter (2 marks)

(b)transcription factor (2 marks)

8Oestrogen is a steroid hormone. During development, oestrogen stimulates cell division in breast tissue. Figure 1 represents the way in which it does this. The numbers in Figure 1 refer to five different steps in the process.

Figure 1

(a)Explain why oestrogen can pass through the cell-surface membrane of a target cell as shown in step 1. (2 marks)

(b)In step 3, a molecule of oestrogen binds to a protein within the cell’s nucleus. This results in the release of an ERα receptor.

(i)Use your knowledge of protein structure to suggest what causes the release of the ERα receptor. (2 marks)

(ii)Suggest one advantage of the ERα receptor normally being bound to a protein.
(3 marks)

(iii)Use information from Figure 1 to describe how the release of ERαreceptors results in gene transcription (steps 4 and 5). (2 marks)

(iv)Eukaryotic promoters often contain a region called a TATA element, which is ‘recognised’ by a specific part of transcription factor molecules. Use your knowledge of DNA structure to suggest why this region is referred to as a TATA element.
(1 mark)

9 Glucocorticoids are a class of steroid hormones, derived from cholesterol. One effect of glucocorticoids is to stimulate the transcription of genes that code for proteins with an anti-inflammatory effect.Figure 2 summarises how glucocorticoids affect their target cells.

Figure 2

Compare and contrast the action of oestrogen, shown in Figure 1, with that of glucocorticoid, shown in Figure 2. (6 marks)

Tip: Question 9instructs you to ‘compare and contrast’. Mark schemes will not allow you to gain full marks for responses to this instruction unless you include at least one similarity (compare) and at least one difference (contrast) in your answers.

10 Use information from Tori Blakeman’s article to answer the following questions.

(a)Name two transcription factors involved in control of the circadian rhythm. (1 mark)

(b) The E-box is a gene promoter. Explain how the information in Tori Blakeman’s article supports this statement. (4 marks)

(c)The per gene encodes a protein, PER, that regulates the p53 gene and the c-Myc gene. Explain how disruption to the control of the p53 gene and the c-Myc gene can increase the likelihood of cancer. (4 marks)

(d)Control of the circadian rhythm is an example of homeostasis. Explain how. (6 marks)

For an animated video representing this control of per and cry, try

Answers

1Any inherited or environmental feature.

That increases the likelihood of developing a disease.

2It is approximately (circa) one day (diem) long.

3It is virtually the same in all current animals/vertebrates.

As it was in a common ancestor (of current animals/vertebrates).

4Light intensity.

5Genes and proteins.

6Similarity: both involve uncontrolled cell division.

Difference: cancer cells metastasise but tumour cells do not.

7(a)A section of DNA upstream of a (target) gene.

Controls transcription of its (target) gene.

(b)A protein that attaches to a specific base sequence on a gene promoter.

Stimulates attachment of RNA polymerase to/transcription of target gene.

8(a)It is lipid-soluble.

(So) the lipoprotein bilayer is no barrier to (simple) diffusion.

(b)(i) Combination with oestrogen causes a conformationalchange in the protein/causes a change in the tertiary structure of the protein.

(So) bonds holding the ERα receptor in place are broken.

(ii) Binding site of ERα receptor hidden (do not credit reference to “active site” of ERαreceptor).

(So) cannot bind to complementary site of promoter.

(So) gene not normally transcribed.

(iii) ERα receptor binds to specific site on promoter.

Allowing binding of RNA polymerase.

(iv) It contains the DNA base sequence thymine-adenine-thymine-adenine.

9 Compare:

Oestrogen and glucocorticoid both enter the cell by (simple) diffusion, since they are steroids.
Oestrogen and glucocorticoid both react with a protein, causing the release of receptor molecules.
The (released) receptor molecules act as transcription factors.

Contrast:

Oestrogen reacts with a protein in the nucleus whereas the glucocorticoid reacts with a protein in the cytoplasm or oestrogen releases receptor molecules in the nucleus whereas as the glucocorticoid releases them in the cytoplasm.
One ERα receptor is released per oestrogen molecule whereas two glucocorticoid receptors are released per glucocorticoid molecule.
Glucocorticoids remain attached to glucocorticoid receptors whereas oestrogen does not remain attached to ERα receptors.

10(a)CLOCK and BMAL1.

(b)It is shown as part of the cell’s DNA.

Proteins bind to it.

Its action is stimulated by (proteins/transcription factors) CLOCK and BMAL1.

(Under the influence of CLOCK and BMAL1) it stimulates expression of the per and cry genes.

(c)p53 is a tumour suppressor gene.

If disrupted, the gene will no longer be able to prevent tumour formation/cell division.

c-Myc is a proto-oncogene.

If disrupted, it might become an oncogene / it might stimulate cell proliferation.

(d)Homeostasis is the maintenance of a stable internal environment.

Over a period of 24 hours, the circadian rhythm controls the concentrations of the proteins CLOCK and BMAL1 / of the proteins CRY and PER in cells.

Rising concentrations of CLOCK and BMAL1 stimulate transcription of cry and per genes and their protein products CRY and PER accumulate in cells.

At a critical concentration in the cell, CRY and PER inhibit transcription of the genes coding for CLOCK and BMAL1.

So the concentrations of CLOCK and BMAL1 fall.

So transcription of the cry and per genes stops, leading to a fall in the concentrations of CRY and PER in the cell.

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