Worm Breeder's Gazette 15(4): 27 (October 1, 1998)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
| 1 | Laboratory of Molecular Neurobiology, Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan |
| 2 | Laboratory of Molecular Neurobiology, Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan, PRESTO, JST |
Dauer larva formation is mainly promoted by a dauer-inducing
pheromone and prevented by food supply, but is also influenced by a
temperature. Mutations that cause constitutive dauer formation, even in
the absence of pheromone, have been isolated and nearly all of these
mutations including null mutations are temperature-sensitive:
dauer-constitutive (daf-c) mutants grow to adult stage at 15-degree,
whereas they arrest at dauer stage at 25-degree. Recently, Hobert et al.
(1997) reported that thermotaxis-defective ttx-3 mutation affects the
temperature-sensitive daf-c phenotype of daf-7 mutants, by enhancing
dauer formation at 15-degree and recovery from dauer at 25-degree (1).
The ttx-3 gene encodes a LIM homeodomain protein that is expressed
exclusively in AIY, an amphid interneuron essential for thermotaxis
(1,2). Thus, sensory signal transduction pathway used for thermotaxis
participates at least in part temperature-sensitive daf-c phenotype.
Since the daf-7 gene encodes a TGF-beta-like ligand (3,4), we
have begun to investigate whether other daf-c mutations that disrupt
TGF-beta-like signaling pathway for dauer/non-dauer developmental
decision interact with ttx-3 or ttx-1 mutation. The ttx-1 mutation
causes animals to seek cold temperatures as does ttx-3 (cryophilic
phenotype), and is likely to disrupt the function of AFD, a
thermosensory neuron required for thermotaxis (2; see Sasakura et al.,
this issue). We constructed the daf-1(m40); ttx-1(p767) double mutant
and compared it with the daf-1 single mutant in dauer formation and its
recovery. At 25-degree, all daf-1; ttx-1 mutant animals initially
entered into dauer stage, but 30% of the animals recovered from dauers
under uncrowded condition (10-20 animals/plate). By contrast, 100% of
daf-1 animals entered into and stayed at dauer stage at 25-degree under
the same uncrowded condition. At 15-degree, 35% of daf-1; ttx-1 animals
entered into dauer stage, whereas 10% of daf-1 animals became dauers.
The similar results were obtained with daf-7(e1372); ttx-3(ks5) double
mutants that we constructed in this study. About 30% of daf-7; ttx-3
animals recovered from dauers at 25-degree, although 100% of daf-7
animals stayed as dauers. At 15-degree, about 10% of daf-7; ttx-3
animals and only 1% of daf-7 animals became dauers. The ttx-1 mutant is
known to be hypersensitive to dauer-inducing pheromone (5). We thus also
investigated dauer formation/recovery of daf-1; ttx-1 mutants under
crowded condition (150-250 animals/plate). The results showed that dauer
formation is more promoted under crowded condition and is significantly
enhanced in daf-1; ttx-1 animals: 60%, 90% and 100% of double mutants
entered into dauer stage at 15-degree, 20-degree and 25-degree,
respectively, whereas 25%, 55% and 100% of daf-1 animals entered into
dauer stage at 15-degree, 20-degree and 25-degree, respectively. Taking
advantage of the interaction with daf mutations, we are in the process
of isolating new thermotaxis-defective mutations that interfere the
functions of neurons found to be essential for thermotaxis.
We thank Oliver Hobert and Kotaro Kimura for invaluable advice
on dauer assays.
(1) Hobert et al., 1997, Neuron 19, 345-357. (2) Mori and Ohshima, 1995,
Nature 376, 344-348. (3) Ren et al., 1996, Science 274, 1389-1391. (4)
Schackwitz et al., 1996, Neuron 17, 719-728. (5) Golden and Riddle,
1984, PNAS 81, 819-823.