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Ch. 18 - Developmental Genetics
Sanders - Genetic Analysis: An Integrated Approach 3rd Edition
Sanders3rd EditionGenetic Analysis: An Integrated ApproachISBN: 9780135564172Not the one you use?Change textbook
All textbooksSanders 3rd EditionCh. 18 - Developmental GeneticsProblem 11
Chapter 18, Problem 11

In gain-of-function let-23 and let-60 C. elegans mutants, all of the vulval precursor cells differentiate with 1° or 2° fates. Do you expect adjacent cells to differentiate with 1° fates or with 2° fates? Explain.

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Understand the context: In *C. elegans*, the vulval precursor cells (VPCs) adopt specific fates (1°, 2°, or 3°) during development. The let-23 and let-60 genes are part of the epidermal growth factor receptor (EGFR)/Ras signaling pathway, which regulates these cell fates.
Recognize the mutation type: Gain-of-function mutations in let-23 and let-60 lead to hyperactivation of the EGFR/Ras signaling pathway. This causes all VPCs to adopt either 1° or 2° fates, bypassing the default 3° fate.
Recall the normal signaling pattern: In wild-type *C. elegans*, the VPC closest to the anchor cell receives the strongest EGFR signal and adopts the 1° fate. Adjacent cells receive weaker lateral signals and adopt the 2° fate. Cells farther away adopt the default 3° fate due to lack of signaling.
Predict the outcome in mutants: In gain-of-function let-23 and let-60 mutants, the signaling pathway is constitutively active. This means that all VPCs are exposed to high levels of signaling, disrupting the normal gradient. Adjacent cells are unlikely to both adopt 1° fates because lateral inhibition (mediated by Notch signaling) prevents neighboring cells from adopting the same fate. Instead, adjacent cells will likely differentiate with alternating 1° and 2° fates.
Conclude the reasoning: The hyperactivation of the EGFR/Ras pathway ensures that all VPCs adopt induced fates (1° or 2°), but lateral inhibition ensures that adjacent cells do not both adopt 1° fates. Therefore, adjacent cells are expected to differentiate with alternating 1° and 2° fates.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Vulval Development in C. elegans

In C. elegans, vulval development is a well-studied process involving a specific pattern of cell differentiation. The vulval precursor cells (VPCs) can adopt different fates, primarily 1° (primary) and 2° (secondary) fates, which are crucial for proper vulval formation. The fate of these cells is influenced by signaling pathways, particularly those involving the let-23 and let-60 genes.
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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 let-23 and let-60 mutations in C. elegans, these mutations lead to enhanced signaling that promotes the differentiation of VPCs into 1° or 2° fates. Understanding how these mutations affect cell fate decisions is essential for predicting the behavior of adjacent cells.
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Cell Communication and Fate Specification

Cell communication plays a critical role in determining the fate of adjacent cells during development. In C. elegans, the differentiation of VPCs is influenced by both intrinsic factors (like genetic mutations) and extrinsic signals from neighboring cells. This intercellular communication can lead to a coordinated response, where adjacent cells may adopt similar fates based on the signaling environment created by the differentiated VPCs.
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Related Practice
Textbook Question

Actinomycin D is a drug that inhibits the activity of RNA polymerase II. In the presence of actinomycin D, early development in many vertebrate species, such as frogs, can proceed past the formation of a blastula, a hollow ball of cells that forms after early cleavage divisions, but development ceases before gastrulation (the stage at which cell layers are established). What does this tell you about maternal versus zygotic gene activity in early frog development?

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Textbook Question

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?

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Textbook Question

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?

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Textbook Question

In mammals, identical twins arise when an embryo derived from a single fertilized egg splits into two independent embryos, producing two genetically identical individuals.

What limits might there be, from a developmental genetic viewpoint, as to when this can occur?

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Textbook Question

In mammals, identical twins arise when an embryo derived from a single fertilized egg splits into two independent embryos, producing two genetically identical individuals.

The converse phenotype, fusion of two genetically distinct embryos into a single individual, is also known. What are the genetic implications of such an event?

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Textbook Question

The bicoid gene is a coordinate maternal-effect gene.

A female Drosophila heterozygous for a loss-of-function bicoid allele is mated to a male that is heterozygous for the same allele. What are the phenotypes of their progeny?

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