By expressing the EGF-like ligand LIN-3, the

C. elegans anchor cell (AC) directly triggers vulval development. LIN-3 acts at a distance and has a graded action. The levels of LIN-3 can be controlled by using various genetic techniques.
​Which one of the following options correctly matches Column I and Column II?

Correct option is A

​Explanation:

1. Wild-type worms grown on empty vector RNAi (A →ii)

• Normal LIN-3 levels.
• Standard vulval development pattern:
  (3° - 2° - 1° - 2° - 3°).
• Corresponds to VPC fate I.

2. lin-3 mutant with a stop codon in exon 3 (B → iii)

• No functional LIN-3 protein → No vulval induction.
• All VPCs adopt 3° fate (remain as epidermal cells).
• Corresponds to VPC fate III (Vulvaless phenotype).

3. Wild-type worms grown on lin-3 RNAi (C → iv)

• Reduced LIN-3 levels.
• Insufficient LIN-3 to trigger normal differentiation.
• Most VPCs remain 3° fate → Similar to LIN-3 knockout.
• Corresponds to VPC fate IV.

4. Wild-type worms expressing a multi-copy extrachromosomal array of lin-3 gene (D → i)

• Excess LIN-3 expression → Stronger induction.
• More VPCs adopt 1° and 2° fates → Extra vulval formation.
• Corresponds to VPC fate II.

Information Booster:

Condition A - In wild-type C. elegans grown on empty vector RNAi, there is no knockdown or mutation affecting LIN-3 expression, meaning LIN-3 is present at normal physiological levels. This results in the standard pattern of vulval precursor cell (VPC) differentiation.

Condition B - If C. elegans carries a lin-3 mutant with a stop codon in exon 3, it means LIN-3 protein will not be produced due to premature translation termination. As a result, there will be no LIN-3 signaling from the anchor cell (AC), leading to a failure in vulval precursor cell (VPC) induction.

Condition C- When wild-type C. elegans worms are treated with LIN-3 RNAi, the expression of LIN-3 is significantly reduced due to RNA interference. This leads to a decrease in LIN-3 signaling from the anchor cell (AC), which affects vulval precursor cell (VPC) differentiation.Since RNAi decreases LIN-3 levels, VPCs do not receive sufficient signaling to differentiate properly. most VPCs remain undifferentiated as 3° cells, forming epidermal tissue instead of vulval cells .

Condition D - If wild-type C. elegans overexpress LIN-3 using a multi-copy extrachromosomal array,the levels of LIN-3 increase significantly. This leads to stronger signaling from the anchor cell (AC), which affects vulval precursor cell (VPC) differentiation. more VPCs adopt 1° and 2° fates, leading to excess vulval formation (Muv phenotype).