- Development of vulva in C. elegans is initiated by the induction of a small number of cells by short range signals from a single inducing cell. With reference to this, following statements were put forward.
A. When the anchor cell was ablated early in development no vulva formed.
B. In a dominant negative mutant of let-23, a primary vulva formed but the secondary vulva formation did not take place.
C. A cell adopting a primary fate inhibits adjacent cells from adopting the same fate by lateral inhibition involving LIN-39 and also induces the secondary fate in these cells.
D, A constitutive signal from the hypodermis inhibits the development of both the primary and secondary fates but it is overruled by the initial signal from the anchor cell.
Which of the above statements is true?
(1) A and B (2) A and C
(3) A and D (4) B and DVulval development in Caenorhabditis elegans is a model for studying how a single inducing cell and short-range signaling specify distinct cell fates during organogenesis. This process is tightly regulated by the anchor cell’s inductive signals and involves complex interactions among vulval precursor cells (VPCs).
Analysis of Statements Regarding Vulval Development
A. When the anchor cell was ablated early in development no vulva formed.
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Supported by experiments: the anchor cell secretes LIN-3 (EGF-like) which induces vulval precursor cells, so its removal prevents vulva formation.
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This confirms the anchor cell’s essential role as an inducer.
B. In a dominant negative mutant of let-23, a primary vulva formed but the secondary vulva formation did not take place.
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LET-23 is the EGFR receptor that mediates the primary fate induction by the anchor cell signal. Mutations affecting LET-23 can disrupt secondary fate induction by Notch signaling from primary cells to neighbors.
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This statement aligns with known genetic data where primary vulval fate occurs improperly or secondary fate is impaired when let-23 function is compromised.
C. A cell adopting a primary fate inhibits adjacent cells from adopting the same fate by lateral inhibition involving LIN-39 and also induces the secondary fate in these cells.
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Primary VPC (usually P6.p) induces lateral inhibition and secondary fate in adjacent cells (P5.p and P7.p) mainly via Notch (LIN-12) signaling, not directly LIN-39.
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LIN-39 is a Hox gene required for VPC competence but not the key lateral inhibition mediator.
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So this statement is partly inaccurate in its details.
D. A constitutive signal from the hypodermis inhibits the development of both primary and secondary fates but it is overruled by the initial signal from the anchor cell.
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Hypodermal cells provide an inhibitory environment, establishing competence boundaries that are overridden by the LIN-3 signal from the anchor cell for vulval induction.
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This statement reflects the balance of inductive and inhibitory signals in development.
Correct Pairing of Statements
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Statement A is definitely true.
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Statement B accurately reflects the phenotype seen in let-23 mutants.
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Statement C contains inaccuracies regarding the role of LIN-39 in lateral inhibition.
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Statement D is consistent with known inhibitory regulation.
Thus, the most correct pairing is:
(1) A and B
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1 Comment
Bhawna Choudhary
November 16, 2025A and B is correct