Table of contents

1. Introduction to Genetics51m
2. Mendel's Laws of Inheritance3h 37m
3. Extensions to Mendelian Inheritance2h 41m
4. Genetic Mapping and Linkage2h 28m
5. Genetics of Bacteria and Viruses1h 21m
6. Chromosomal Variation1h 48m
7. DNA and Chromosome Structure56m
8. DNA Replication1h 10m
9. Mitosis and Meiosis1h 34m
10. Transcription1h 0m
11. Translation58m
12. Gene Regulation in Prokaryotes1h 19m
13. Gene Regulation in Eukaryotes44m
14. Genetic Control of Development44m
15. Genomes and Genomics1h 50m
16. Transposable Elements47m
17. Mutation, Repair, and Recombination1h 6m
18. Molecular Genetic Tools19m
- Genetic Cloning
  9m
- Methods for Analyzing DNA
  9m
19. Cancer Genetics29m
- Overview of Cancer
  21m
- Cancer Mutations
  7m
20. Quantitative Genetics1h 26m
21. Population Genetics50m
- Hardy Weinberg
  19m
- Allelic Frequency Changes
  31m
22. Evolutionary Genetics29m

14. Genetic Control of Development

Early Developmental Steps

Genetics

14. Genetic Control of Development

Early Developmental Steps

Previous problemNext problem

2:57 minutes

Problem 10a

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?

Verified step by step guidance

Understand the role of the anchor cell in C. elegans development: The anchor cell is crucial for inducing vulval development by signaling to the vulval precursor cells (VPCs) through the epidermal growth factor (EGF) signaling pathway.

Recognize the role of the let-23 gene: The let-23 gene encodes the EGF receptor, which is essential for receiving the signal from the anchor cell. A loss-of-function mutation in let-23 disrupts this signaling pathway, leading to a vulva-less phenotype even in the presence of the anchor cell.

Consider the effect of anchor cell ablation in a wild-type organism: Ablating the anchor cell in a wild-type organism prevents the signaling required for vulval development, resulting in a vulva-less phenotype.

Analyze the let-23 loss-of-function mutant with anchor cell ablation: In a let-23 loss-of-function mutant, the signaling pathway is already non-functional. Ablating the anchor cell does not change the outcome because the mutant is already incapable of responding to the signal.

Conclude the expected phenotype: The phenotype of the let-23 loss-of-function mutant with anchor cell ablation will remain vulva-less, as the signaling pathway is disrupted regardless of the presence or absence of the anchor cell.

Verified video answer for a similar problem:

This video solution was recommended by our tutors as helpful for the problem above

Video duration:

Play a video:

Was this helpful?

Key Concepts

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

Anchor Cell Function

The anchor cell in C. elegans plays a crucial role in vulval development by signaling to surrounding cells to induce vulva formation. It releases signals that activate the vulval precursor cells, leading to the proper development of the vulva. Ablation of the anchor cell disrupts this signaling, resulting in a vulva-less phenotype.

let-23 Gene and Its Role

The let-23 gene encodes a receptor that is essential for the vulval induction process in C. elegans. It is part of the epidermal growth factor (EGF) signaling pathway, which mediates the response of vulval precursor cells to signals from the anchor cell. A loss-of-function mutation in let-23 impairs this signaling, preventing the normal development of the vulva.

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 a let-23 loss-of-function mutant, the expected phenotype upon anchor cell ablation would likely be a vulva-less phenotype as well, since the signaling pathway necessary for vulval development is already compromised by the mutation.

Watch next

Master Drosophilia Development with a bite sized video explanation from Kylia

Start learning

Related Videos

Related Practice

Textbook Question

Distinguish between the syncytial blastoderm stage and the cellular blastoderm stage in Drosophila embryogenesis.

555

views

Textbook Question

What is the difference between a parasegment and a segment in Drosophila development? Why do developmental biologists think of parasegments as the subdivisions that are produced during the development of flies?

1073

views

Textbook Question

Experiments have shown that any nuclei placed in the polar cytoplasm at the posterior pole of the Drosophila egg will differentiate into germ cells. If polar cytoplasm is transplanted into the anterior end of the egg just after fertilization, what will happen to nuclei that migrate into this cytoplasm at the anterior pole?

376

views

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?

298

views

Textbook Question

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.

369

views

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?

347

views

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?

338

views

Textbook Question

Early development depends on the temporal and spatial interplay between maternally supplied material and mRNA and the onset of zygotic gene expression. Maternally encoded mRNAs must be produced, positioned, and degraded [Surdej and Jacobs-Lorena (1998). Mol. Cell Biol. 18:2892–2900]. For example, transcription of the bicoid gene that determines anterior–posterior polarity in Drosophila is maternal. The mRNA is synthesized in the ovary by nurse cells and then transported to the oocyte, where it localizes to the anterior ends of oocytes. After egg deposition, bicoid mRNA is translated and unstable bicoid protein forms a decreasing concentration gradient from the anterior end of the embryo. At the start of gastrulation, bicoid mRNA has been degraded. Consider two models to explain the degradation of bicoid mRNA: (1) degradation may result from signals within the mRNA (intrinsic model), or (2) degradation may result from the mRNA's position within the egg (extrinsic model). Experimentally, how could one distinguish between these two models?

870

views

Show more practices

Download the Mobile app

Privacy

Do not sell my personal information

Accessibility

Patent notice

Sitemap

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

let-23 Gene and Its Role

Phenotypic Outcomes of Genetic Mutations

Watch next

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?