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5.2 Vulva Formation — Test 1
Q1. C. elegans is the favourite model for studying cell lineage because:✓ Its cell lineage is invariant and completely mapped
Q2. In C. elegans vulva formation, the anchor cell acts as the:✓ Inducer of the vulval precursor cells
Q3. The six vulval precursor cells (VPCs) in C. elegans form an:✓ Equivalence group (all competent to form vulva)
Q4. If the anchor cell of C. elegans is killed by a laser early in development:✓ No vulva forms; the VPCs become hypodermis
Q5. If three of the six C. elegans VPCs are killed, a normal vulva still forms because:✓ The remaining VPCs are part of an equivalence group and can substitute
Q6. The anchor cell of C. elegans induces the vulva by secreting which signal?✓ LIN-3 (an EGF-like protein)
Q7. The LIN-3 signal from the anchor cell is received by which receptor on the VPCs?✓ LET-23 (an EGF receptor)
Q8. The VPC directly beneath the anchor cell (P6.p), receiving the most LIN-3, adopts the:✓ Primary (1°) fate
Q9. The VPCs flanking P6.p (i.e. P5.p and P7.p) adopt the:✓ Secondary (2°) fate
Q10. A primary (1°) vulval cell stops its neighbours from also becoming primary by:✓ Lateral inhibition via Notch-Delta signalling
Q11. Overexpression of lin-3 in C. elegans causes:✓ A multivulva phenotype
Q12. The decision between which of two cells (Z1.ppp or Z4.aaa) becomes the anchor cell is made by:✓ Notch-Delta (LIN-12 / LAG-2) lateral signalling
5.2 Vulva Formation — Test 2
Q13. In the anchor-cell decision, the cell that ends up secreting more LAG-2 (Delta) becomes the:✓ Anchor cell
Q14. Evidence that the C. elegans VPCs form an equivalence group includes that, if the anchor cell is destroyed, the VPCs:✓ Contribute instead to hypodermal (skin) tissue
Q15. The maternal SKN-1 protein in C. elegans controls the fate of which blastomere?✓ EMS (which makes pharynx and gut)
Q16. Embryos from skn-1-deficient C. elegans mothers lack:✓ The pharyngeal mesoderm and endoderm derivatives of EMS
Q17. The RAS-MAPK pathway is activated in the primary VPC of C. elegans downstream of:✓ The LET-23 (EGF) receptor binding LIN-3
Q18. The 'equivalence group' concept means the six VPCs:✓ Are developmentally equivalent and any can take any vulval fate
Q19. In C. elegans, the cells farther from the anchor cell (receiving little LIN-3) adopt the:✓ Tertiary (3°) / non-vulval (hypodermal) fate
Q20. Vulva formation in C. elegans is a classic example of:✓ Inductive signalling combined with lateral specification
Q21. Loss-of-function of let-23 (the EGF receptor) in C. elegans would result in:✓ Failure of vulval induction (a vulvaless phenotype)
Q22. The anchor cell signal in C. elegans is described as short-range because:✓ It mainly affects the nearest VPC, with effects falling off by distance
Q23. The LIN-3 / LET-23 vulval induction pathway in C. elegans signals through which conserved intracellular cascade?✓ RAS–RAF–MAPK
5.2 Vulva Formation — Test 3
Q24. A gain-of-function mutation in let-60 (the C. elegans RAS gene) would be expected to cause:✓ A multivulva phenotype
Q25. The lateral signal from the primary VPC that induces the secondary fate in its neighbours acts through which receptor?✓ LIN-12 (the C. elegans Notch)
Q26. The combined use of an inductive (LIN-3) signal and a lateral (Notch) signal in vulva formation ensures that:✓ A precise 3°-2°-1°-2°-3° pattern of fates forms
Q27. The vulval precursor cells are part of a larger set of cells (P3.p–P8.p). Their competence to respond to induction depends on the Hox gene:✓ lin-39
Q28. The C. elegans vulva is a powerful model partly because:✓ Its cells are visible in a transparent body and can be ablated with a laser
Q29. If LET-23 is mislocalised away from the membrane facing the anchor cell, vulval induction would be expected to:✓ Be impaired, because the receptor must face the signal source
Q30. The phenomenon by which the six equivalent VPCs adopt different fates based on their position is an example of:✓ Positional information interpreted by an equivalence group
Q31. A loss-of-function mutation in lin-3 (the anchor-cell signal) would produce:✓ A vulvaless phenotype
Q32. The discovery that the RAS-MAPK pathway controls C. elegans vulva formation was important because:✓ The same pathway, when overactive, drives many human cancers
Q33. The C. elegans anchor-cell/uterine decision and the vulval primary/secondary decision both use Notch signalling, illustrating that:✓ The same signalling pathway can be reused for different decisions
Q34. Overall, C. elegans vulva formation is a model for how a small number of cells achieve a precise pattern through:✓ A combination of induction, lateral signalling and an equivalence group