2025 JPJC H2Bio PE P3 (A)

9744 / 03 [Turn over NAME : CLASS : JURONG PIONEER JUNIOR COLLEGE JC2 Preliminary Examination 2025 BIOLOGY Higher 2 9744/03 15 September 2025 Paper 3 Long Structured and Free-response Questions 2 hours Additional Materials: Answer Booklet READ THESE INSTRUCTIONS FIRST Write your class and name in the spaces at the top of this page. Write in dark blue or black pen. You may use an HB pencil for any diagrams or graphs. Do not use staples, paper clips, glue or correction fluid. Section A Answer all questions in the spaces provided on the Question Paper. Section B Answer any one question on the separate Answer Booklet provided. The use of an approved scientific calculator is expected, where appropriate. You may lose marks if you do not show your working or if you do not use appropriate units. The number of marks is given in brackets [ ] at the end of each question or part question. For Examiner’s Use 1 2 3 Section B Total This document consists of 19 printed pages and 1 blank page.

2 JPJC/JC2 H2 Biology/PE/2025 Section A Answer all questions. 1 Following a body injury, bone marrow stem cells migrate to the site of damage, where they undergo cell differentiation to replace damaged cells. In eukaryotes, cell growth and division are tightly regulated processes to ensure proper repair. Cells will only pass specific checkpoints in the cell cycle if certain conditions are met, one of which is the presence of growth factors. Fig. 1.1 shows how this differentiation occurs. Fig. 1.1 (a) (i) Outline how SCFR is produced and transported to the cell surface. ................................ ................................ ................................ ................... [4] 1. gene/c-KIT undergoes transcription in nucleus (to form pre-mRNA) ; 2. post-transcriptional modification s take place [A! RNA splicing, 5’ capping, 3’ polyadenylation (any 1)] to form mature mRNA ; 3. mRNA is translated at ribosomes on rough endoplasmic reticulum (rER) ; 4. biochemical modifications take place in rER ; 5. budding occurs with SCFR/receptor embedded in vesicle membrane / in vesicle ; 6. SCFR/receptor enter Golgi body to be further modified, sorted and packaged ; 7. budding occurs with SCFR/receptor embedded in vesicle membrane ; 8. (compulsory) vesicles with SCFR embedded in vesicle membrane move to and fuse with cell surface membrane (of stem cells) ; MP5&7, award once (ii) Suggest how SCFR is destroyed by a lysosome. ................................ ................................ ................................ ................... [1] 1. The vesicle fuses/binds with a lysosome , the h ydrolytic enzymes break down/hydrolyse/digest SCFR ; A! Accept protease

3 JPJC/JC2 H2 Biology/PE/2025 [Turn over Fig. 1.2 shows an example of how signals from growth factors are transduced to result in cell growth and division. The KRAS protein is a G -protein encoded by KRAS proto- oncogene. Fig. 1.2 (b) Describe the role of the KRAS protein in the transduction of signal fr om growth factors. ................................ ................................ ................................ ............................ [3] 1. Growth factors recognise and bind to the specific binding site of tyrosine kinase receptors (RTK) on the target cell surface membrane, activating the RTK ; 2. The activated RTK binds to KRAS protein and activates it ; 3. A molecule of GTP replaces the GDP on the KRAS protein ; 4. The activated KRAS protein activates (downstream) relay proteins ; 5. to result in the transcription of genes coding for proteins promoting cell growth and division.

4 JPJC/JC2 H2 Biology/PE/2025 (c) Mutations in KRAS proto-oncogene are common in colorectal (colon and rectum) cancer. The oncogene arises from the proto-oncogene by a mutation called G12D. Fig. 1. 3 shows part of the base sequence of the template strand of the KRAS proto-oncogene and the corresponding part of the oncogene. The corresponding parts of the primary structures of the two encoded KRAS proteins involved in GTPase activity are also shown. amino acid position 6 7 8 9 10 11 12 KRAS proto-oncogene 3’ … GAA CAC CAT CAA CCT CGA CCA … 5’ normal KRAS protein leu val val val gly ala gly KRAS oncogene 3’ … GAA CAC CAT CAA CCT CGA CTA … 5’ mutant KRAS protein leu val val val gly ala asp Fig. 1.3 (i) State one possible environmental causative factor that increases the risk of G12D mutation shown in Fig. 1.3. ................................ ................................ ................................ ................... [1] 1. Ionising radiation e.g. X-ray, UV ray ; 2. Chemical carcinogen e.g. tar in cigarette (smoke) ; (Any 1) (ii) With reference to Fig. 1.3, explain how the G12D mutation leads to colorectal cancer. ................................ ................................ ................................ ................... [5] 1. Single Base (pair) substitution (in KRAS proto-oncogene / idea of DNA) ; 2. Thymine replaces cytosine / CTA replaces CCA in the 12th triplet in the DNA ; 3. Instead of GGU, GAU is coded for in the mRNA / codon, resulting in a missense mutation ; 4. Gain of function mutation leading to hyperactive KRAS protein ; 5. Gly replaced by asp, change in amino acid sequence in polypeptide/ primary structure ; 6. Result in change in 3D conformation of (GTPase active site) in KRAS protein ; 7. Can no longer hydrolyse GTP to GDP, thus KRAS protein remains active ; 8. Results in continuous transcription of genes / excessive production of proteins, promoting cell growth and division ; 9. leading to excessive cell cycle progression and uncontrolled cell division , resulting in tumour formation and cancer ; MP1-7 max. 4m R! MP1 & 2 if just state at 12 th amino acid position without idea that it occurred in DNA / gene ;

5 JPJC/JC2 H2 Biology/PE/2025 [Turn over (d) In a genetic study for colorectal cancer, two populations were screened for the G12D mutation. Table 1.1 shows the results of the study. Table 1.1 group total number of individuals number of individuals with G12D mutation without colorectal cancer (control group) 500 2 with colorectal cancer 400 120 (i) Calculate the relative risk (RR) of G12D mutation in the cancer group compared to the control group using the formula provided. risk of G12D in cancer group risk of G12D in control gRR p= rou 1. Relative risk = (120/400) / (2/500) = 75 ; relative risk = ................................ .... [1] (ii) Discuss whether conducting screening tests to detect the G12D mutation is an effective way to screen for colorectal cancer. ................................ ................................ ................................ ................... [2] 1. Effective because there is a strong association/link between G12D mutation and colorectal cancer ; 2. Ineffective because there are people with colorectal cancer who did not have G12D mutation (and their cancer diagnosis will be missed) ; 3. AVP ;

6 JPJC/JC2 H2 Biology/PE/2025 The KRAS oncogene, with G12D mutation, can be detected in stool samples using a technique called droplet digital Polymerase Chain Reaction (ddPCR). ddPCR partitions DNA samples into thousands of individual droplets within which DNA samples are amplified by PCR. Fluorescent -labelled probes specific to the KRAS oncogene are added after which the fluorescence is measured in each droplet. The number of droplets containing the fluorescent signal indicates the amount of KRAS oncogene present in the sample. The method is highly sensitive, detecting even low levels of the KRAS oncogene. (e) (i) Suggest why stool samples are appropriate for the detection of KRAS oncogene. ...................