BIOSCI107 · Biology for Biomedical Science: Cellular Processes and Development
Gene Expression, Cell Division & Cancer
Topic 2 finishes with the flow of genetic information and how cells divide. It covers transcription and RNA processing (cap, tail, splice), translation (read 5′→3′, protein built N→C), and protein sorting; then the cell cycle, mitosis and meiosis with their checkpoints (MPF at G2); and finally how mutations in proto-oncogenes and tumour-suppressor genes cause cancer. Assessed in the 30% mid-semester test (paper Teleform MCQ) — with a recurring 'use a codon table' item and reliable questions on mitosis vs meiosis, checkpoints and mutation types.
What this chapter covers
- 01Central dogma DNA → RNA → protein; transcription (initiation/elongation/termination), RNA polymerase II at the promoter (TATA box), RNA uses uracil
- 02RNA processing in order: 5′ cap, 3′ poly-A tail, splicing (spliceosome removes introns, joins exons); alternative splicing
- 03Translation: mRNA read 5′→3′, protein made N→C; ribosome A/P/E sites; peptide bonds catalysed by rRNA (ribozyme); stop codons UAA/UAG/UGA
- 04Protein sorting: signal peptide + SRP direct the ribosome to the rough ER; post-translational modifications
- 05The cell cycle: interphase (G1, S, G2) + M phase; G0 exit; mitosis (2n→2n identical) vs meiosis (2n→1n, variable)
- 06Meiosis I separates homologous chromosomes (crossing-over, independent assortment); meiosis II separates sister chromatids
- 07Checkpoints (G1, G2, M) and MPF = cyclin + Cdk driving entry to mitosis
- 08Mutation types (silent, missense, nonsense; frameshift indels) and cancer genes (proto-oncogenes 'accelerator', tumour-suppressors 'brakes')
Chromosome number after mitosis vs meiosis
- +1(a) Mitosis produces two genetically identical daughter cells with the SAME chromosome number as the parent — sister chromatids separate at anaphase but ploidy is unchanged. So each mitotic daughter has 24 chromosomes. [+1]
- +1(b) Meiosis is a reductional division (2n → 1n): meiosis I halves the number by separating homologous pairs, and meiosis II separates sister chromatids without further DNA replication. So each of the four meiotic products has 24 ÷ 2 = 12 chromosomes. [+1]
- +1(c) An event unique to meiosis I is the pairing (synapsis) of homologous chromosomes into tetrads, with crossing-over between non-sister chromatids — this never happens in mitosis. (Independent assortment of homologous pairs at metaphase I is an equally valid answer.) [+1]
Key terms
- RNA processing
- The modifications a pre-mRNA undergoes before it leaves the nucleus, in the order taught: 5′ capping (a modified guanosine), 3′ polyadenylation (a poly-A tail), and splicing at the spliceosome (introns removed, exons joined). Alternative splicing lets one gene yield several proteins.
- Translation (N→C, 5′→3′)
- Protein synthesis at the ribosome: mRNA is read 5′→3′ while the polypeptide is built from its N-terminus to its C-terminus. The ribosome has A (incoming tRNA), P (growing chain) and E (exit) sites; peptide-bond formation is catalysed by the large-subunit rRNA (a ribozyme).
- Meiosis I vs meiosis II
- Meiosis I is the reductional division — homologous chromosomes pair, cross over and separate, halving the chromosome number. Meiosis II resembles mitosis — sister chromatids separate — but with no preceding DNA replication, yielding four haploid cells.
- MPF (maturation-promoting factor)
- The cyclin + cyclin-dependent kinase (Cdk) complex that acts at the G2 checkpoint to trigger entry into mitosis by phosphorylating target proteins. Cyclin levels fluctuate through the cycle and cyclin is degraded after mitosis; Cdk is constant.
- Frameshift mutation
- An insertion or deletion of 1 or 2 nucleotides that shifts the reading frame from that point on, scrambling every downstream codon — usually catastrophic, especially near the 5′ end. Indels of 3 nucleotides keep the frame (one amino acid added or lost).
- Proto-oncogene vs tumour-suppressor gene
- Two opposing classes of cancer gene. Proto-oncogenes normally stimulate proliferation; over-activation (too much accelerator) makes them oncogenes (e.g. Ras, Myc). Tumour-suppressor genes normally restrain proliferation; loss of function removes the brakes (e.g. TP53/p53, BRCA1/2, APC). Cancer typically needs several such mutations.
Gene Expression, Cell Division & Cancer FAQ
How do I answer the 'use a codon table' question?
This recurring test item gives you a template DNA strand and asks you to work forward: transcribe it to mRNA (remember RNA uses uracil and is read 5′→3′), then translate codon by codon using the supplied codon table, comparing wild-type to mutant. Classify the change — silent (same amino acid), missense (different amino acid), nonsense (premature stop), or frameshift (1–2 nt indel) — and predict the effect on the protein. The table is always provided, so the skill is doing the decoding carefully and getting the reading frame right, not memorising codons.
What is the difference between mitosis and meiosis outcomes?
Mitosis makes two genetically identical daughter cells with the same chromosome number, for growth and repair. Meiosis makes four genetically different haploid cells (gametes) with half the chromosome number. The halving and the variation both come from meiosis I: homologous chromosomes pair, cross over (prophase I) and assort independently (metaphase I), then separate. Meiosis II simply separates sister chromatids, like a mitosis without prior DNA replication.
How do mutations cause cancer?
Through two gene classes acting in opposite directions. A proto-oncogene normally promotes proliferation; a mutation that over-activates it (an oncogene) is like jamming the accelerator. A tumour-suppressor gene normally restrains the cell cycle; a loss-of-function mutation removes the brakes. Cancer generally requires several such mutations accumulating (for example the colon-cancer sequence APC → Ras → p53), which is why it is more common with age and carcinogen exposure.
Can AI help me with gene expression and cell division in BIOSCI 107?
Yes, for study. Sia can decode a practice codon-table problem with you, drill the mitosis-vs-meiosis outcomes, and quiz you on checkpoints and mutation types. Use it to prepare for the mid-semester test — it does not sit the test for you, and the test is an AI-free lane under the course's academic-integrity policy. Confirm the rules on Canvas.
Exam move
Split this chapter into two skills. First, the information flow: be able to draw transcription → RNA processing (cap, tail, splice, in that order) → translation, remembering the directionality traps (mRNA read 5′→3′, protein built N→C, RNA uses uracil). Practise the codon-table decode as a procedure — transcribe, translate, compare, classify — so the recurring test item is routine. Second, the division block: build a two-column mitosis-vs-meiosis table (ploidy, number of divisions, where homologues vs sister chromatids separate, source of variation), and memorise the three checkpoints and MPF (cyclin + Cdk). For cancer, learn the accelerator/brakes framing (proto-oncogene vs tumour-suppressor) and the mutation types (silent/missense/nonsense/frameshift). This is test-only material (Topics 1–3); drill it before the mid-semester test and confirm the Teleform format on Canvas.
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