Vulval development in C. elegans is dependent on the response of some of the central epidermal progenitor cells in the region of the developing vulva to a chemical signal from the gonad. Signaling from the gonad is blocked by action of the vulvaless mutant let-23 so that none of the central progenitor cells form vulval structures. In the vulvaless mutant, n300, the central progenitor cells do not form.
Which gene is likely to act earlier in the vulval developmental pathway?

Verified step by step guidance

1. Understand the biological context: Vulval development in C. elegans involves a signaling pathway where the gonad sends a chemical signal to central epidermal progenitor cells, triggering them to form vulval structures.
2. Identify the role of the let-23 gene: The let-23 gene encodes a receptor that receives the gonadal signal. In the vulvaless mutant let-23, this signaling is blocked, so the progenitor cells receive no signal and fail to form vulval structures.
3. Analyze the phenotype of the n300 mutant: In the n300 vulvaless mutant, the central progenitor cells themselves do not form, indicating a defect earlier in development than just signal reception.
4. Compare the positions of the genes in the developmental pathway: Since let-23 affects the response to the signal but the progenitor cells are present, and n300 mutants lack the progenitor cells entirely, the gene mutated in n300 likely acts upstream of let-23, controlling progenitor cell formation.
5. Conclude that the gene mutated in n300 acts earlier in the vulval developmental pathway than let-23 because it affects the presence of progenitor cells, which is a prerequisite for the signaling step mediated by let-23.

Key Concepts

Genetic Pathway Hierarchy

Genetic pathways involve a sequence of gene actions where upstream genes regulate downstream genes. Genes acting earlier influence the activation or repression of subsequent genes, determining developmental outcomes. Identifying which gene acts first helps understand the order of molecular events in development.

Role of let-23 in Vulval Development

The let-23 gene encodes a receptor tyrosine kinase essential for receiving the gonadal signal that induces vulval cell fate. Mutations in let-23 block this signaling, preventing vulval formation, indicating let-23 acts at a critical signaling step in the pathway.

Phenotypic Effects of Mutations in Developmental Genes

Mutations can disrupt gene function at different stages, leading to distinct phenotypes. A mutation causing absence of progenitor cells (like n300) suggests the affected gene acts earlier than one blocking signal reception (like let-23), as progenitor cells must exist before signaling can occur.