Mock Test 4

Mock Test 04: Cell Biology (50 Mixed Questions)

75:00

1. Which lipid movement in the plasma membrane is thermodynamically most unfavorable and requires enzymes? A) Lateral diffusion B) Flexion C) Transverse diffusion (flip-flop) D) Rotation

Ans: C. Moving a polar head through the hydrophobic core requires energy/flippases.

2. Lipid rafts are detergent-resistant membrane microdomains primarily enriched in: A) Phosphatidylcholine B) Cholesterol and sphingolipids C) Cardiolipin D) Phosphatidylserine

Ans: B. The tight packing of cholesterol and saturated sphingolipids creates these rafts.

3. The Na+/K+ ATPase maintains the resting membrane potential by moving: A) 3 Na+ out, 2 K+ in B) 2 Na+ out, 3 K+ in C) 3 Na+ in, 2 K+ out D) 1 Na+ out, 1 K+ in

Ans: A. It is an electrogenic pump, expelling 3 Na+ for every 2 K+ imported.

4. Which glucose transporter is insulin-dependent and found in muscle and adipose tissue? A) GLUT1 B) GLUT2 C) GLUT3 D) GLUT4

Ans: D. Insulin triggers the exocytosis of GLUT4-containing vesicles to the plasma membrane.

5. The MDR1 protein, which confers multidrug resistance in cancer cells, belongs to which transporter family? A) P-type ATPases B) ABC Transporters C) V-type ATPases D) Solute Carrier (SLC) family

Ans: B. MDR1 (P-glycoprotein) uses ATP binding cassettes to pump drugs out of the cell.

6. Aquaporins prevent the passage of protons (H+) to maintain gradients. This is achieved by: A) The NPA (Asparagine-Proline-Alanine) motif B) The KDEL sequence C) ATP hydrolysis D) A magnesium ion block

Ans: A. The NPA motifs interrupt the hydrogen-bonded water chain, preventing Grotthuss proton jumping.

7. Which cytoskeletal protein forms a submembrane meshwork responsible for the biconcave shape of human erythrocytes? A) Keratin B) Tubulin C) Spectrin D) Lamin

Ans: C. Spectrin dimers link with actin to form the cortical cytoskeleton of RBCs.

8. The resting membrane potential of most animal cells is primarily determined by: A) Voltage-gated Na+ channels B) K+ leak channels C) Ligand-gated Ca2+ channels D) Aquaporins

Ans: B. The high permeability of resting membranes to K+ drives the potential near the K+ equilibrium potential.

9. During co-translational translocation, the Signal Recognition Particle (SRP) binds to the ER signal sequence and halts translation. Release of SRP requires: A) ATP hydrolysis B) GTP hydrolysis C) Signal peptidase cleavage D) BiP binding

Ans: B. Both SRP and the SRP receptor are GTPases that hydrolyze GTP to dissociate.

10. Retrograde transport of ER-resident proteins (bearing a KDEL signal) from the Golgi back to the ER is mediated by: A) COPII coated vesicles B) COPI coated vesicles C) Clathrin coated vesicles D) Caveolae

Ans: B. COPI mediates retrograde transport, whereas COPII mediates anterograde (ER to Golgi) transport.

11. N-linked glycosylation in the ER specifically attaches the 14-sugar oligosaccharide precursor to which amino acid residue? A) Serine B) Threonine C) Asparagine D) Glutamine

Ans: C. It attaches to Asparagine (Asn) in the consensus sequence Asn-X-Ser/Thr.

12. The addition of Mannose-6-Phosphate (M6P) tags to newly synthesized lysosomal enzymes occurs in the: A) Rough ER B) Cis-Golgi network C) Trans-Golgi network D) Early endosome

Ans: B. GlcNAc phosphotransferase adds the M6P tag in the cis-Golgi.

13. I-cell disease is a severe lysosomal storage disorder caused by a defect in: A) Hexosaminidase A B) Glucocerebrosidase C) GlcNAc-1-phosphotransferase D) Alpha-galactosidase

Ans: C. This defect prevents the formation of M6P tags, causing lysosomal enzymes to be secreted extracellularly instead of targeted to lysosomes.

14. Proteins imported into the mitochondrial matrix must pass through two translocase complexes. These are: A) TOM and TIM23 B) TOM and SAM C) Sec61 and TIM22 D) TIC and TOC

Ans: A. TOM (outer membrane) and TIM23 (inner membrane) mediate import into the matrix.

15. The classic Nuclear Localization Signal (NLS), such as that found in SV40 Large T-antigen, is rich in which amino acids? A) Acidic (Asp, Glu) B) Basic (Lys, Arg) C) Hydrophobic (Leu, Val) D) Aromatic (Phe, Trp)

Ans: B. The sequence (e.g., PKKKRKV) is rich in basic positively charged residues.

16. Disassembly of the SNARE complex after vesicle fusion is driven by the AAA-ATPase: A) Dynamin B) NSF C) Rab5 D) Sar1

Ans: B. N-ethylmaleimide sensitive factor (NSF) untangles the stable 4-helix SNARE bundle using ATP.

17. Peroxisomal matrix proteins are targeted by a C-terminal PTS1 signal consisting of the tripeptide: A) KDEL B) SKL (Ser-Lys-Leu) C) RGD (Arg-Gly-Asp) D) YXXΦ

Ans: B. The SKL sequence is recognized by the PEX5 receptor for import into peroxisomes.

18. The "dynamic instability" of microtubules is caused by the loss of the: A) ATP cap on actin B) GTP cap on beta-tubulin C) Gamma-tubulin ring complex D) MAP2 coating

Ans: B. Hydrolysis of GTP to GDP by beta-tubulin outpaces addition, leading to rapid depolymerization (catastrophe).

19. Which protein complex nucleates branched actin networks, such as those found at the leading edge of migrating cells (lamellipodia)? A) Formins B) Arp2/3 complex C) gamma-TuRC D) Profilin

Ans: B. The Arp2/3 complex binds to existing actin filaments to nucleate new branches at a 70-degree angle.

20. The drug Taxol (Paclitaxel) is used in cancer therapy because it: A) Depolymerizes actin filaments B) Depolymerizes microtubules C) Stabilizes microtubules, preventing mitotic spindle disassembly D) Inhibits myosin ATPase activity

Ans: C. Taxol binds and stabilizes microtubules, freezing cells in metaphase and triggering apoptosis.

21. Most kinesins are motor proteins that move along microtubules towards the: A) Minus end (cell center) B) Plus end (cell periphery) C) Both directions equally D) Actin filaments

Ans: B. Kinesins are generally plus-end directed motors, while dyneins are minus-end directed.

22. The characteristic "9+2" arrangement of microtubules is found in: A) Centrioles B) Primary cilia C) Eukaryotic flagella and motile cilia D) Bacterial flagella

Ans: C. The axoneme of motile cilia/flagella consists of 9 outer doublets and 2 central singlet microtubules.

23. In the cross-bridge cycle of muscle contraction, the release of the myosin head from the actin filament is triggered by: A) Hydrolysis of ATP to ADP + Pi B) Release of Pi (Power stroke) C) Binding of a new ATP molecule D) Binding of Calcium to troponin

Ans: C. ATP binding causes the conformational change that releases the rigor state cross-bridge.

24. Intermediate filaments completely lack: A) Alpha-helical coiled-coil domains B) Tissue specificity C) Structural polarity (+ and - ends) D) Tensile strength

Ans: C. Because tetramers assemble in an antiparallel manner, the resulting filament has no distinct polarity.

25. Which actin-binding protein enhances filament elongation by replacing ADP with ATP on G-actin monomers? A) Cofilin B) Profilin C) Thymosin-beta4 D) Gelsolin

Ans: B. Profilin acts as a nucleotide exchange factor, recharging actin monomers for plus-end addition.

26. Progression through the mammalian G1 restriction point is primarily driven by which Cyclin/CDK complex? A) Cyclin A / CDK2 B) Cyclin B / CDK1 C) Cyclin D / CDK4/6 D) Cyclin E / CDK2

Ans: C. Cyclin D complexes phosphorylate Rb, initiating commitment to the cell cycle.

27. The tumor suppressor Retinoblastoma (Rb) protein halts the cell cycle by binding to and inhibiting: A) p53 B) E2F transcription factors C) Cyclin E D) MDM2

Ans: B. Unphosphorylated Rb traps E2F. When phosphorylated by CDKs, it releases E2F to transcribe S-phase genes.

28. The Anaphase-Promoting Complex (APC/C) triggers sister chromatid separation by ubiquitinating: A) Cohesin B) Separase C) Securin D) Cyclin D

Ans: C. Degradation of securin frees separase, which then cleaves the cohesin rings holding chromatids together.

29. In response to severe DNA damage, p53 accumulates and induces transcription of p21. p21 functions as a: A) Ubiquitin ligase B) CDK inhibitor (CKI) C) Phosphatase D) DNA repair enzyme

Ans: B. p21 binds and inhibits G1/S and S-CDK complexes, arresting the cell cycle.

30. Unattached kinetochores generate a "wait" signal in the Spindle Assembly Checkpoint by activating: A) Mad2, which inhibits Cdc20 B) Cdc25, which inhibits CDK1 C) Wee1, which inhibits APC/C D) p53, which induces apoptosis

Ans: A. The Mad2/BubR1 complex sequesters Cdc20, preventing the activation of APC/C.

31. During intrinsic apoptosis, Cytochrome c released from mitochondria binds to: A) Fas ligand B) Caspase-8 C) Apaf-1 D) Bax

Ans: C. Cytochrome c binds Apaf-1, causing it to oligomerize into the apoptosome, which activates Caspase-9.

32. Which of the following Bcl-2 family proteins are pro-apoptotic pore-formers at the mitochondrial membrane? A) Bcl-2 and Bcl-xL B) Bax and Bak C) Bid and Bim D) Puma and Noxa

Ans: B. Bax and Bak oligomerize to form MACs (Mitochondrial Apoptosis-Induced Channels).

33. The extrinsic pathway of apoptosis is initiated by death receptors (e.g., Fas) recruiting an adaptor called FADD, which directly activates: A) Caspase-3 B) Caspase-8 C) Caspase-9 D) Cytochrome c

Ans: B. Procaspase-8 is recruited to the DISC complex and undergoes proximity-induced autoactivation.

34. Necroptosis is a regulated form of necrosis dependent on the kinase activity of: A) Caspase-1 B) RIPK1 and RIPK3 C) PI3K and Akt D) JNK and p38

Ans: B. RIPK3 phosphorylates MLKL, which then forms pores in the plasma membrane.

35. Autophagosome formation is marked by the lipidation of which critical protein to phosphatidylethanolamine (PE)? A) Ubiquitin B) Beclin-1 C) LC3 (Atg8) D) mTOR

Ans: C. LC3-I is conjugated to PE to form LC3-II, inserting into the expanding autophagosomal membrane.

36. In G-protein coupled receptor (GPCR) signaling, the G-alpha-s subunit activates: A) Phospholipase C B) Adenylyl Cyclase C) Phosphodiesterase D) Guanylyl Cyclase

Ans: B. It stimulates Adenylyl Cyclase to produce the second messenger cAMP.

37. Phospholipase C (PLC) cleaves PIP2 into two second messengers. These are: A) IP3 and DAG B) cAMP and cGMP C) Calcium and Calmodulin D) PIP3 and PTEN

Ans: A. Inositol trisphosphate (IP3) releases Ca2+ from the ER, while Diacylglycerol (DAG) activates Protein Kinase C (PKC).

38. Receptor Tyrosine Kinases (RTKs) are typically activated by: A) Proteolytic cleavage B) Ligand-induced dimerization and trans-autophosphorylation C) Binding of a heterotrimeric G-protein D) Importin binding

Ans: B. Dimerization brings the kinase domains together to cross-phosphorylate each other on tyrosine residues.

39. The Wnt signaling pathway regulates cell fate. In the absence of Wnt, beta-catenin is: A) Translocated to the nucleus to activate transcription B) Secreted from the cell C) Phosphorylated by the destruction complex and degraded D) Bound to the Frizzled receptor

Ans: C. The APC/Axin/GSK3 complex degrades beta-catenin. Wnt signaling disrupts this complex.

40. The PTEN tumor suppressor directly antagonizes the PI3K/Akt survival pathway by: A) Phosphorylating Akt B) Dephosphorylating PIP3 back to PIP2 C) Inhibiting mTORC1 D) Degrading the EGF receptor

Ans: B. By removing the 3-phosphate from PIP3, PTEN prevents the membrane recruitment and activation of Akt.

41. The Ras protein is a small GTPase that drives proliferation. Oncogenic mutations in Ras typically: A) Prevent GTP binding B) Lock it in the GDP-bound inactive state C) Destroy its intrinsic GTPase activity, locking it in the GTP-bound active state D) Target it for rapid degradation

Ans: C. Mutant Ras cannot hydrolyze GTP, leading to continuous activation of the MAPK pathway.

42. Notch signaling is an example of contact-dependent signaling. Upon binding Delta, the Notch receptor is: A) Phosphorylated by JAK B) Cleaved by gamma-secretase to release its intracellular domain (NICD) C) Internalized into caveolae D) Ubiquitinated by Mdm2

Ans: B. The released Notch Intracellular Domain translocates directly to the nucleus to regulate transcription.

43. Knudson's "Two-Hit Hypothesis" applies to which class of cancer-associated genes? A) Oncogenes B) Tumor Suppressor Genes C) Proto-oncogenes D) Viral integrases

Ans: B. Both alleles of a tumor suppressor gene (e.g., Rb) must be inactivated to lose function and drive cancer.

44. Cancer cells often rely on aerobic glycolysis rather than oxidative phosphorylation, even in the presence of oxygen. This is known as: A) The Pasteur Effect B) The Bohr Effect C) The Warburg Effect D) The Haldane Effect

Ans: C. The Warburg effect allows cancer cells to divert glycolytic intermediates into biosynthetic pathways to support rapid growth.

45. Most human cancers achieve replicative immortality by reactivating which enzyme? A) DNA Polymerase delta B) Telomerase C) Topoisomerase II D) Helicase

Ans: B. Telomerase prevents telomere shortening, allowing cells to bypass the Hayflick limit and avoid senescence.

46. The Hedgehog signaling pathway heavily relies on which cellular structure in vertebrates? A) Primary cilium B) Endoplasmic reticulum C) Lysosome D) Nucleolus

Ans: A. Smoothened and Gli proteins traffic to the primary cilium to transduce the Hedgehog signal.

47. Which enzyme is responsible for producing the second messenger cGMP in response to Nitric Oxide (NO)? A) Particulate Guanylyl Cyclase B) Soluble Guanylyl Cyclase C) Adenylyl Cyclase D) Phosphodiesterase

Ans: B. NO diffuses across the membrane and binds the heme group of soluble guanylyl cyclase.

48. Cell-cell adhesion in adherens junctions is mediated by homophilic binding of: A) Integrins B) Selectins C) Cadherins D) Immunoglobulins

Ans: C. Cadherins (like E-cadherin) bind in a calcium-dependent, homophilic manner to link adjacent cells.

49. The extracellular matrix protein Fibronectin binds to cells via the RGD motif, which is recognized by: A) Cadherins B) Integrins C) Syndecans D) Claudins

Ans: B. Integrins are the primary transmembrane receptors that link the ECM to the intracellular actin cytoskeleton.

50. In the JAK-STAT signaling pathway (used by cytokines), the STAT proteins translocate to the nucleus only after they: A) Are ubiquitinated B) Are cleaved by a protease C) Are phosphorylated on tyrosine residues and dimerize D) Bind to cAMP

Ans: C. JAKs phosphorylate STATs, exposing their SH2 domains to cause dimerization, exposing an NLS for nuclear import.