2025 EJC JC2 Biology Prelim P3 (A)

©EJC 2025 9744/03/J2H2PRELIM/2025 [Turn over EUNOIA JUNIOR COLLEGE JC2 Preliminary Examinations 2025 General Certificate of Education Advanced Level Higher 2 CANDIDATE NAME CIVICS GROUP 2 4 - REGISTRATION NUMBER H2 Biology Paper 3 Long Structured and Free-response Questions 9744/03 17 September 2025 2 hours Additional Materials: 12-page Answer Booklet READ THESE INSTRUCTIONS FIRST Write your name, civics group and registration number on all the work you hand in. Write your answers in dark blue or black pen. You may use an HB pencil for any diagrams or graphs. Do not use paper clips, highlighters, glue, or correction fluid/tape. Section A Answer all questions on the Question Paper. Section B Answer one question on the 12-page Answer Booklet provided. Write your answer to each part of the question on a fresh sheet of paper. The use of an approved scientific calculator is expected, where appropriate. The number of marks is given in brackets [ ] at the end of each question or part question. At the end of the examination, ensure that you submit both the Question Paper and Answer Booklet. This document consists of 12 printed pages. For Examiner’s Use Section A 1 2 3 Section B 4 OR 5 Total 75

2 ©EJC 2025 9744/03/J2H2PRELIM/2025 Section A Answer all questions on the Question Paper. 1 Fig. 1.1 is a diagram showing the transcription of part of the CALD1 gene that codes for a protein known as caldesmon. The part of the CALD1 gene shown is a section of exon. Structure A represents an enzyme involved in transcription. Fig. 1.1 (a) (i) Name the enzyme labelled A in Fig. 1.1. [1] ....................................................................................................................................... [1] RNA polymerase; (ii) Name the bond that forms between the nucleotides in the primary transcript. [1] ....................................................................................................................................... [1] Phosphodiester (bond); Table 1.1 shows the codons that correspond to some amino acids. Table 1.1 amino acid codons Phe UUU UUC Trp UGG Met AUG Thr ACU ACC ACA ACG Arg AGA AGG Val GUU GUC GUA GUG Gly GGU GGC GGA GGG (iii) State the amino acid sequence that is coded for by the sequence of nucleotides on the primary transcript shown in Fig. 1.1. [1] [starting from UUU] Phe–Thr–Arg–Gly–Val R: starting from AUG: Met–Trp–Arg–Thr–Phe (wrong direction)

3 ©EJC 2025 9744/03/J2H2PRELIM/2025 [Turn over (iv) Explain why one of the strands of DNA is not transcribed. [3] 1. Non-transcribed strand is not the template strand / only the template strand is transcribed; 2. If non- template strand is transcribed, the mRNA sequence codes for a different sequence of amino acids (A: different sequence of codons / different primary transcript for RNA); 3. Thus resulting in a non -functional polypeptide (A: polypeptide with a different function / structure / 3D conformation); 4. Translation would be a waste of energy / translation will not occur; 5. AVP; e.g. if non-template strand is transcribed as well, ds RNA will form which cannot be translated Caldesmon is a large protein with a number of binding sites to attach to other proteins. Caldesmon exists in two different forms, H-caldesmon and L-caldesmon. H-caldesmon helps to regulate contraction and relaxation in smooth muscle cells. L-caldesmon is found in some non-muscle cells, where it also acts as a regulatory protein. • Caldesmon is coded for by a gene known as CALD1. • CALD1 has 17 exons. • The primary structure of H-caledesmon has a repeating sequence in the middle of the amino acid chain that is not present in L-caldesmon. (b) (i) Researchers have discovered that a gene mutation is not the cause of the two different forms of caldesmon. Explain what is meant by a gene mutation. [2] 1. A gene mutation is a change in the sequence of base pairs in a DNA molecule; (A: change in DNA/base/nucleotide sequence) 2. Which codes for / results in an altered / different polypeptide; (A: altered amino acid sequence / primary structure of polypeptide/protein) I: change in RNA base sequence, types of mutations (ii) Researchers now known that the two different forms of caldesmon are the result of events occurring directly after transcription of DNA. Changes occur to the primary transcript that is formed by DNA transcription. Explain how the smooth muscle cells and non- muscle cells can produce different forms of caldesmon from the same primary transcript. [2] 1. Different forms of caldesmon are produced via alternative splicing; (R: DNA splicing, mutation occurring during gene/RNA splicing) 2. Which involves the removal of introns; (R: introns described as bases/nucleotides/codons) (R: different number of introns removed / some introns remain) and joining of different combination of exons;

4 ©EJC 2025 9744/03/J2H2PRELIM/2025 3. Thus, producing different types of mature messenger RNA (A: mRNA without “mature” as long as not referring to primary transcript); (iii) Suggest how the two different forms of caldesmon can still have similar functions, even though they have a different primary structure. [1] 1. Despite having different primary structures, H-caldesmon and L-caldesmon may still have similar (R: same) tertiary structure / 3D conformation/shape OR Binding sites of H-caldesmon and L-caldesmon still have similar 3D conformation; 2. Hence, binding sites (R: active site) are still complementary to attach to proteins; 3. Removed amino acids are not structural amino acids / not part of binding sites; (Note to marker: accept “non-essential amino acids”) 4. R-group interactions within caldesmon are still the same / similar; 5. AVP: e.g. caldesmon has more than one binding site and only one/few changed; 6. AVP: e.g. same type of binding site, but a different number Caldesmon was recently reported in the scientific literature to be involved in gastric cancer progression, invasion, and migration. Tumour cells can become invasive through increased mobility and decreased adhesion, which can lead to metastasis from the primary tumour site. This process is triggered through changes in gene expression mediated by signalling pathways, including the PI3K-AKT pathway. Fig. 1.2 shows the PI3K-AKT signalling pathway, in which: • KRAS and RHEB are G-proteins. • PI3K, AKT, RAF, MEK, and ERK are all protein kinases. • Sharp arrows (↓) represent activation, while blunt arrows ( ┴ ) represent inhibition.

5 ©EJC 2025 9744/03/J2H2PRELIM/2025 [Turn over Fig. 1.2 (c) (i) Other than signal amplification , describe one advantage of the PI3K -AKT signalling pathway using one example shown in Fig. 1.2. [2] 1. There are multiple checkpoints for regulation / several steps in the signalling pathway can be regulated/controlled; 2. For instance, inhibition by PTEN (A: other examples, MTORC1 / AKT etc) OR 3. Ability of a signal molecule/ligand (growth factor) to elicit cellular responses such as gene expression (A: other examples of cellular response) upon binding to cell surface receptor; 4. without the need to move into cell; (ii) Using Fig. 1.2, describe a phosphorylation cascade that results in cell cycle progression. [2] (RAFMEKERK) 1. Phosphorylation cascade is the sequential activation of kinases within a signalling pathway; 2. Where RAF phosphorylates and activates MEK; 3. and then MEK phosphorylates and activates ERK;

6 ©EJC 2025 9744/03/J2H2PRELIM/2025 (d) Describe the role of second messengers. [2] 1. Second messengers bind to a downstream protein kinase/relay protein 2. This indu