GEN3030 Chap.6 C. elegans Developmental Decisions
C. elegans Developmental Decisions
C. elegans makes developmental decisions observable through a small transparent body, reproducible lineage and powerful genetics. Heterochronic genes control developmental timing, the CED pathway governs programmed cell death, and vulval induction shows how local signalling assigns cell fate.
Lineage tracking, combined mutations, ablation and tissue-specific rescue separate timing, survival, signal production and response.
What this chapter covers
- 01
C. elegans as a model system
- 02
Invariant lineage and cellular resolution
- 03
Heterochronic genes and developmental timing
- 04
MicroRNA control of temporal transitions
- 05
Programmed cell death and CED activities
- 06
Execution separated from corpse clearance
- 07
Anchor-cell induction and vulval fate
- 08
Cell autonomy and tissue-specific rescue
Worked example · free
Test an instructive signal in a cell-fate decision
- 2Ablate the source before fate specification and verify that precursors remain alive and competent when the primary fate is lost.
- 2Express the ligand from a nearby ectopic source and ask whether the primary fate relocates or is restored near the new source.
- 2Remove the receptor in one precursor and activate the downstream pathway to test reception and functional order in that cell.
Key terms
- Heterochrony
- A change in developmental timing that causes a cell or tissue to repeat, skip or mistime a stage-specific program.
- Programmed cell death
- An active genetically regulated process that removes selected cells during normal development and tissue maintenance.
- Cell induction
- A process in which one cell or tissue provides a signal that changes developmental fate in a responding cell.
- Cell autonomy
- The property of a gene function acting within the cell whose phenotype is being assessed rather than through another tissue.
- Lineage tracing
- Following a cell and its descendants through divisions, movements and fate decisions to identify where a defect arises.
C. elegans Developmental Decisions FAQ
Why is the worm useful for developmental genetics?
Its transparent body and reproducible cell lineage allow researchers to identify whether a particular cell is born, divides, differentiates or dies after a genetic perturbation.
How is a timing defect separated from a spatial defect?
Follow the same lineage across successive stages. A heterochronic defect changes when a stage program occurs, while a spatial defect changes identity according to position.
Can more visible corpses mean more cell death?
Not necessarily. Corpse accumulation can result from failed clearance. Lineage tracking, execution markers and engulfment measurements distinguish increased killing from slower removal at matched developmental stages.
What does epistasis establish in a death pathway?
A combined phenotype can order functional activities when strong alleles and a comparable cellular outcome are used. It does not by itself prove direct protein interaction.
Why should a missing adult structure be traced through its lineage?
The same endpoint can follow failed cell birth, premature death, delayed differentiation or changed fate. Lineage observations identify the earliest divergence and therefore the most plausible developmental step. Independent fate and viability markers refine that localisation further.
Assessment move
Organise the chapter by three cellular questions: when does the lineage act, which cells live or die, and which neighbours instruct fate. For each mutation, trace the cell before interpreting the adult phenotype. Predict single and double mutants explicitly before using epistasis. Distinguish death execution from corpse clearance.
In induction questions, separate ligand source, receptor-bearing responder, downstream pathway and competence. Use timed perturbations to isolate establishment from later function. Make an invariant-lineage worksheet with a row for cell birth, division, migration, fate marker and death. When an adult structure is missing, work forward through those checkpoints instead of assuming a fate-specification defect.
A cell can fail to be born, die, adopt another fate, differentiate late or remain present without the chosen marker. Time-lapse lineage tracking and independent markers discriminate those possibilities. For heterochronic genes, compare the same lineage across successive larval stages and ask whether a stage program repeats, is skipped or occurs early. Separate changed timing from changed position.
In programmed cell death, draw protection, activation, execution and corpse clearance as distinct steps. More visible corpses can mean increased killing or slower engulfment, so count lineage losses and use execution and clearance markers. Predict each single mutant and then the combined mutant before ordering activities.
In vulval induction, label the ligand-producing anchor cell, receptor-bearing precursors, intracellular response and alternative fates. Ablation tests whether the source is required; an ectopic source tests instructive sufficiency; receptor loss in one precursor tests cell autonomy; downstream activation tests bypass. Include a competence control showing that a precursor can still adopt the fate.
When rescue is tissue-specific, ask whether expression timing overlaps the decision window. End revision with one integrated scenario in which timing, death and induction produce similar final anatomy. Identify the earliest observation that distinguishes the models. The strength of the worm system is cellular resolution, so a strong answer always traces the relevant cell rather than interpreting the adult endpoint alone.
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