Zoology 2025 Paper II 50 marks Explain

Q7

(a)(i) Explain sigmoidal nature of oxygen dissociation curve for hemoglobin. (10 marks) (a)(ii) Describe differences between adult and fetal hemoglobin and comment on their physiological significance. (10 marks) (b) Discuss the mechanism of action of cytotoxic-T cell. (15 marks) (c) What are homeotic genes ? Explain their role in body axis formation in chick. (15 marks)

हिंदी में प्रश्न पढ़ें

(a)(i) हीमोग्लोबिन के लिए आक्सीजन प्रथक्करण वक्र की सिग्मोइडल प्रकृति की व्याख्या कीजिए । (10 अंक) (a)(ii) वयस्क एवं भ्रूण हीमोग्लोबिन के बीच अंतर का वर्णन कीजिए तथा इनके कार्यिकीय महत्व पर टिप्पणी लिखिए । (10 अंक) (b) कोशिकाविषी-ट कोशिका की कार्यविधि का वर्णन कीजिए । (15 अंक) (c) समापवर्धी जीन क्या हैं ? चुजे में पिंडाक्ष बनने में उनकी भूमिका की व्याख्या कीजिए । (15 अंक)

Directive word: Explain

This question asks you to explain. The directive word signals the depth of analysis expected, the structure of your answer, and the weight of evidence you must bring.

See our UPSC directive words guide for a full breakdown of how to respond to each command word.

How this answer will be evaluated

Approach

The directive 'explain' demands clear causal reasoning and mechanistic detail across all sub-parts. Allocate approximately 40% of time/words to part (a) [20 marks], 30% to part (b) [15 marks], and 30% to part (c) [15 marks]. Structure: brief introduction noting the interconnected themes of molecular function, immune defense, and developmental patterning; then address each sub-part sequentially with diagrams integrated; conclude with a synthesis on how molecular mechanisms scale from protein function to organismal biology.

Key points expected

  • For (a)(i): Cooperative binding, Hill coefficient (n≈2.8-3.0), T-R state transition, and how sigmoidal curve enables efficient O₂ loading/unloading
  • For (a)(ii): HbA (α₂β₂) vs HbF (α₂γ₂), γ-chain substitutions (Ser/Ala at position 136), higher O₂ affinity of HbF, and physiological significance for placental O₂ transfer
  • For (b): TCR-MHC Class I recognition, perforin-granzyme pathway, Fas-FasL mediated apoptosis, and memory T-cell formation
  • For (c): Definition of homeotic genes as selector genes, Hox gene clusters, colinearity principle, and specific role in chick anteroposterior axis formation (e.g., Hoxb-1, Hoxc-6 expression patterns)
  • Cross-cutting: Mention of 2,3-BPG modulation in (a), clinical relevance of HbF in thalassemia/sickle cell, and evolutionary conservation of Hox genes from Drosophila to vertebrates

Evaluation rubric

DimensionWeightMax marksExcellentAveragePoor
Concept correctness22%11Accurately describes cooperative binding mechanism with correct Hill coefficient range; precisely distinguishes γ-chain from β-chain residues affecting 2,3-BPG binding; correctly identifies CD8+ T-cell MHC Class I restriction and dual killing mechanisms; accurately defines homeotic genes vs Hox genes and correctly maps 3' to 5' expression along chick A-P axisBasic understanding of cooperative binding without quantitative detail; knows HbF has higher affinity but misses γ-chain specifics; describes T-cell killing generally without distinguishing perforin vs Fas pathways; defines homeotic genes but confuses spatial/temporal colinearity or misidentifies chick-specific expression domainsMischaracterizes sigmoidal curve as hyperbolic; confuses HbF with embryonic hemoglobin (HbE); describes T-cells as phagocytic or confuses with NK cells; conflates homeotic genes with segmentation genes or describes Drosophila homeobox without chick application
Diagram / labelling18%9Three precise diagrams: (a) sigmoidal ODC with labeled P₅₀, Bohr effect shift, and fetal curve left-shifted; (b) immunological synapse showing TCR-MHC I, perforin release, and target cell apoptosis; (c) chick embryo with Hox expression domains color-coded and aligned to rhombomeres/somites; all fully labeled with molecular componentsTwo adequate diagrams with partial labeling; ODC drawn but missing fetal comparison or Hill plot; T-cell diagram shows contact but not molecular machinery; chick axis sketch without precise Hox domain mappingSingle generic diagram or none; poorly scaled curves without P₅₀; stick-figure T-cells without synapse detail; no developmental axis representation or confused with Drosophila fate map
Examples & nomenclature18%9Uses precise nomenclature: HbA, HbF, HbA₂; cites His146β and His143β for 2,3-BPG binding; names perforin, granzyme A/B, Fas (CD95), FasL; identifies Hoxa, Hoxb, Hoxc, Hoxd clusters; references specific chick genes (e.g., Hoxb-1 in rhombomere 4, Hoxc-6 in brachial region); mentions Indian context (high β-thalassemia prevalence, hydroxyurea use for HbF induction)Generic hemoglobin terminology without subunit notation; mentions 'killer proteins' without naming; knows Hox genes but uses 'homeobox' and 'homeotic' interchangeably; limited or no Indian examplesConfused nomenclature (e.g., 'Hemoglobin F2'); invents terms like 'cytotoxin-T'; misidentifies gene families (e.g., Wnt as homeotic); no applied examples
Process explanation22%11For (a): sequential O₂ binding altering heme-heme interaction, T-state (deoxy) to R-state (oxy) transition with Fe²⁺ movement into porphyrin plane; For (b): stepwise T-cell activation (TCR engagement → Lck/ZAP-70 → PLCγ → Ca²⁺/DAG → granule polarization → multivesicular body release → target cell death pathways); For (c): temporal and spatial colinearity, 3' genes expressed earlier/anteriorly, 5' genes later/posteriorly, with retinoic acid gradient interpretation in chickDescribes cooperative binding as 'helper effect' without structural basis; T-cell killing as 'injection of poison' without pathway detail; homeotic gene action as 'turning on body parts' without mechanistic explanation of transcriptional regulationNo mechanistic detail; describes processes as magic or teleological (e.g., 'HbF exists to help babies'); confuses T-cell with B-cell function; describes homeotic genes as 'creating DNA patterns'
Evolutionary / applied context20%10For (a): evolutionary advantage of cooperative binding for active lifestyle, HbF as evolutionary solution to placental respiration; For (b): evolutionary conservation of perforin in NK cells and cytotoxic T-cells, immune evasion mechanisms; For (c): origin of Hox clusters from ancestral Urbilaterian, duplication events, and applied relevance to chick as model for human developmental disorders; connects to Indian public health (thalassemia screening, hydroxyurea therapy)Mentions 'evolution' superficially without specific mechanisms; notes T-cells fight infection without evolutionary context; knows Hox genes are conserved but cannot articulate duplication history or clinical relevanceNo evolutionary or applied context; misses clinical significance entirely; no connection to model organism value or human disease relevance

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