Desiccation tolerance in C. elegans

Hi all,
I wonder if anyone knows if there are any studies on desiccation tolerance in C. elegans? How rapid desiccation (% RH) it tolerates, how much body water it can lose, how long it can stay desiccated, etc.

Ingo -

This is probably not what you’re after, but I couldn’t resist:

Worms are incredibly tolerant – at least as a population – to desiccation. I don’t know how many times I recovered strains from dried up agar discs resuscitated with a bit of M9!


In addition to the ability to recover viable dauers from “chips” (which does indeed sometimes work, but usually not when you most badly want it to …), a quick search suggests a couple of leads for more quantitative work: a 2004 FEBS letters paper by Gal, Glazer, and Koltai uses quantitative assays of desiccation survival in C. elegans, and at a glance does not appear to cite much previous work in C. elegans; indeed, the authors state that “little is known of the mechanisms that enable C. elegans dauer juveniles (DJs) to survive exposure to dehydration, apart from their high desiccation tolerance, as recorded by Ohba and Ishibashi (1981)”.

Long before the Gal, Glazer, and Koltai paper came out, at least one dauer paper referred in its introduction to dauers being highly resistant to desiccation, but this statement seems to be unreferenced (and may similarly go back to Ohba and Ishibashi); you could try asking one or both of the authors, or indeed try asking any person who knows the dauer literature well (as I, unfortunately, do not). One statement, in a Wormbook chapter written in part by Walter Sudhaus, refers to his (Sudhaus) having unpublished quantitative data on desiccation tolerance in nematodes, including elegans.

I hope this helps.

I don’t know anything about desication tolerance of non dauer worms but desication tolerance appears to relate only to the dauer stage.
In the dauer state the mouth parts and orifices are all sealed.
It is in the dauer state that the alae is most present. Not only is it present but it is highly enlarged.
In my work I strongly postulated and geneticly showed the alae as neural receptor.
You have to imagine what the nematode is doing. It is in a super low metabolic state with Beta type cells that release the insulin to release sugar silenced. Its orifices are sealed. It’s waiting for a signal to say that not only food is present but that plenty of food is present.
This is where the alae receptors come in. The receptor numbers are so large that there ability to determine concentrations is now a statistic reality. when stimulation is high enough incoming signals trip a neural response to ultimatly reach the insulin cells.
The alae sits like a tongue waiting to tast a very specific molecule that tells it there is plenty of food for its young. The nematode also carries a negative feedback receptor that senses the pheramone of other nematodes. This may very well also be in the alae but i’m not sure of this one.
If you find information for desication tolerance at the L1 stage I’d be very interested as this is interesting in relation to parasitic worms.

this paper does a nice job talking about the genetic basis of desiccation tolerance:

Genetics. 2004 May;167(1):161-70. Links
Caenorhabditis elegans OSR-1 regulates behavioral and physiological responses to hyperosmotic environments.Solomon A, Bandhakavi S, Jabbar S, Shah R, Beitel GJ, Morimoto RI.
Department of Biochemistry, Molecular Biology and Cell Biology, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.

The molecular mechanisms that enable multicellular organisms to sense and modulate their responses to hyperosmotic environments are poorly understood. Here, we employ Caenorhabditis elegans to characterize the response of a multicellular organism to osmotic stress and establish a genetic screen to isolate mutants that are osmotic stress resistant (OSR). In this study, we describe the cloning of a novel gene, osr-1, and demonstrate that it regulates osmosensation, adaptation, and survival in hyperosmotic environments. Whereas wild-type animals exposed to hyperosmotic conditions rapidly lose body volume, motility, and viability, osr-1(rm1) mutant animals maintain normal body volume, motility, and viability even upon chronic exposures to high osmolarity environments. In addition, osr-1(rm1) animals are specifically resistant to osmotic stress and are distinct from previously characterized osmotic avoidance defective (OSM) and general stress resistance age-1(hx546) mutants. OSR-1 is expressed in the hypodermis and intestine, and expression of OSR-1 in hypodermal cells rescues the osr-1(rm1) phenotypes. Genetic epistasis analysis indicates that OSR-1 regulates survival under osmotic stress via CaMKII and a conserved p38 MAP kinase signaling cascade and regulates osmotic avoidance and resistance to acute dehydration likely by distinct mechanisms. We suggest that OSR-1 plays a central role in integrating stress detection and adaptation responses by invoking multiple signaling pathways to promote survival under hyperosmotic environments.