Ablation of the anchor cell in wild-type C. elegans results in a vulva-less phenotype.

What phenotype is to be expected if the anchor cell is ablated in a let-23 loss-of-function mutant?

Key Concepts

Anchor Cell Function

In C. elegans, the anchor cell is crucial for vulval development as it signals to surrounding cells to form the vulva. This signaling is mediated through the induction of a specific cell fate in the vulval precursor cells. When the anchor cell is ablated, it disrupts this signaling pathway, leading to a vulva-less phenotype in wild-type organisms.

let-23 Gene and Its Role

The let-23 gene encodes a receptor tyrosine kinase that is essential for vulval induction in C. elegans. In wild-type organisms, let-23 is activated by signals from the anchor cell, promoting the development of vulval precursor cells. A loss-of-function mutation in let-23 impairs this signaling, preventing the proper formation of the vulva even in the presence of the anchor cell.

Phenotypic Outcomes of Genetic Mutations

Phenotypic outcomes in genetics refer to the observable traits resulting from the interaction of an organism's genotype with its environment. In the case of the let-23 loss-of-function mutant, the expected phenotype upon ablation of the anchor cell would likely be a vulva-less phenotype, similar to the wild-type scenario, since the signaling pathway necessary for vulval development is already compromised.