NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Riddle DL, Blumenthal T, Meyer BJ, et al., editors. C. elegans II. 2nd edition. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.

Cover of C. elegans II

C. elegans II. 2nd edition.

Show details

Section IIIDevelopmental Transitions

A. Heterochronic Genes

One of the genes that controls the timing of dauer larva formation is lin-14 , which also regulates other temporal transitions during development. In particular, the stage at which an animal may arrest as a dauer larva is affected by the level of lin-14 activity (Ambros, this volume). Therefore, the targets regulated by lin-14 might include genes that are required to initiate dauer development in response to environmental stimuli or to trigger differentiation into the dauer larva (Ambros and Moss 1994). Animals that have reduced lin-14 activity may form dauer larvae precociously (at the L1 molt), and those with increased lin-14 activity may form dauer larvae late (at the L3 molt). However, both types of mutants can form dauer larvae at the L2 molt, as wild-type animals might do.

If animals do not pass through the dauer stage, lin-14 controls the timing of all stages of development; in contrast, developmental timing after the dauer stage is independent of lin-14 (Liu and Ambros 1991). Those lin-14 mutant animals that have recovered from dauer larva arrest at the second molt undergo wild-type postdauer development. At the wild-type fourth molt of both continuous and postdauer development, hypodermal cells switch from a proliferating state to the terminally differentiated state (the larva-to-adult or L/A switch). In continuously developing lin-14 mutants, the L/A switch occurs at abnormally early or late molts, but during postdauer development of the same mutants, the L/A switch occurs normally. Similar differences between dauer and nondauer development are seen with other heterchronic mutants, including lin-4 and lin-28 (Liu and Ambros 1991). Thus, there appears to be a regulatory signal associated with dauer larva arrest that reprograms the temporal state of cells and allows the animal to execute cell lineages appropriate to the L3 and L4 stages (Ambros and Moss 1994). Differences in expression of the Sqt-2 phenotype may similarly reflect a reprogramming of hypodermal cells associated with dauer arrest. sqt-2 L3 larvae exhibit a roller phenotype, but L4 larvae and adults do not roll. In contrast, dauer and postdauer L4 and adult stages do roll (Cox et al. 1980).

B. Exit from the Dauer Stage

Exit from the dauer stage is affected by the same environmental factors that influence entry: pheromone, food, and temperature (Golden and Riddle 1984b). In the presence of exogenous pheromone, temperature downshifts from 25°C to 15°C induce dauer larvae to resume development, whereas temperature upshifts have no such effect. In the absence of food, removal from a pheromone-rich environment is sufficient to induce recovery in older dauer larvae but not in younger ones; dauer larvae become progressively more predisposed to recovery during the 1–2 week period after they are formed. This may result from a decrease in the dauer larva's sensitivity to pheromone.

When wild-type dauer larvae from starved cultures are put in fresh food, they become developmentally committed to recovery from the dauer state in 50–60 minutes (Golden and Riddle 1984b). One of the earliest biological markers of exit from the dauer stage is a change in surface lipophilicity; 30 minutes after exposure to food, the dauer surface starts to accept lipid probes (Proudfoot et al. 1993b). Dauer larvae begin pharyngeal pumping within 3 hours (postdauer, PD1 stage) and then molt to the L4 (PD2) stage after approximately 10 hours at 25°C. The PD1 stage retains the dauer cuticle but expands radially and grows in length prior to the PD1-PD2 molt.

Recovery from the dauer state is associated with an increase in the specific activity of enzymes of intermediary metabolism. This increase is inhibited by cycloheximide (Reape and Burnell 1991b) but not by actinomycin D (Reape and Burnell 1992). Actinomycin D treatment does prevent molting to the PD2 stage, leading Reape and Burnell (1991a) to conclude that RNA synthesis is not required for the transition from dauer to PD1, but it is required for the first postdauer molt. However, exit from the dauer stage is normally accompanied by a temporally regulated sequence of gene expression (Dalley and Golomb 1992). Steady-state levels of Hsp70 and polyubiquitin mRNA rise sharply within 75 minutes and then decline within 4 hours after exposure to food. Actin and histone mRNAs increase steadily but more slowly. In contrast, Hsp90 mRNA declines sharply within 75 minutes of exposure to fresh food. Metabolic activation is accompanied by a large decrease in intracellular pH from about 7.3 to about 6.3 within 3 hours after dauer larvae encounter food (Wadsworth and Riddle 1988). This shift occurs before feeding begins, and it coincides with, or soon follows, the commitment to resume development.

Copyright © 1997, Cold Spring Harbor Laboratory Press.
Bookshelf ID: NBK20040
PubReader format: click here to try


  • PubReader
  • Print View
  • Cite this Page

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...