Ablation of the anchor cell in wild-type C. elegans results in a vulva-less phenotype.
What about if the anchor cell is ablated in a let-23 gain-of-function mutant?

Verified step by step guidance

1. Understand the biological context: The anchor cell in *C. elegans* plays a critical role in vulval development by signaling to the underlying vulval precursor cells (VPCs) through the LET-23 receptor tyrosine kinase pathway. Ablation of the anchor cell in wild-type worms results in a vulva-less phenotype because the VPCs do not receive the necessary signal to differentiate.
2. Review the let-23 gain-of-function mutation: A gain-of-function mutation in the let-23 gene leads to constitutive activation of the LET-23 receptor, meaning the receptor is active even in the absence of the anchor cell signal. This can result in inappropriate or excessive signaling to the VPCs.
3. Analyze the experimental scenario: If the anchor cell is ablated in a let-23 gain-of-function mutant, the VPCs will not receive the normal inductive signal from the anchor cell. However, due to the gain-of-function mutation, the LET-23 receptor may still be active, potentially leading to vulval development even in the absence of the anchor cell.
4. Predict the outcome: Consider the role of the gain-of-function mutation in bypassing the need for the anchor cell signal. The VPCs may still differentiate into vulval cells because the LET-23 receptor is constitutively active, mimicking the effect of the anchor cell signal.
5. Conclude the reasoning: The phenotype in this scenario is likely to differ from the wild-type ablation case. Instead of a vulva-less phenotype, the let-23 gain-of-function mutant may still develop a vulva, demonstrating the impact of the constitutively active LET-23 receptor on vulval development.

Key Concepts

Anchor Cell Function

In C. elegans, the anchor cell is crucial for vulval development as it signals to surrounding cells to induce vulva formation. This signaling is mediated through the LIN-3 growth factor, which activates the LET-23 receptor in adjacent cells, leading to the differentiation of vulval precursor cells.

LET-23 Receptor

LET-23 is a receptor tyrosine kinase that plays a vital role in the vulval development pathway in C. elegans. In a gain-of-function mutant, LET-23 is constitutively active, which can lead to abnormal signaling and potentially alter the normal developmental processes, including those initiated by the anchor cell.

Gain-of-Function Mutations

Gain-of-function mutations result in a gene product that has increased activity or a new function. In the context of the let-23 mutant, this means that the receptor is always active, which can lead to excessive or inappropriate vulval cell signaling, potentially compensating for the absence of the anchor cell and affecting the vulval phenotype.