Animals display periods of behavioral quiescence, when locomotion stops. In mammals, these periods of quiescence usually correspond to sleep, and are controlled by circadian and homeostatic processes. Behavioral quiescence in Drosophila is also controlled by these two processes and by some of the same neurochemicals that function in mammalian sleep(1,2), suggesting that the genetic control of behavioral quiescence is phylogenetically ancient. Locomotion of C. elegans has been observed to stop for prolonged periods during the lethargus periods, immediately prior to the molts(3). We have been measuring the quiescence associated with the L1 lethargus by videotaping single worms from the time of hatching. We digitize images at one-minute intervals and then track the path of the worm by sending the location of the developing gonad to a spreadsheet. We have found that in N2 worms grown at 22 deg, the longest consolidated quiescent period begins at 11.5+/-0.2, consistent with the reported time of onset of the L1 lethargus. When mechanically stimulated during its predicted consolidated quiescent period, the animal is able to move normally, indicating that this quiescent state is reversible. In
eat-7 , a mutant that was isolated based on small size, and decreased movement and eating when not stimulated(4), the duration of the L1 quiescent period is significantly prolonged while the time of onset of this quiescent period is unchanged. The fraction of quiescent periods in
eat-7 prior to the onset of its longest quiescent period is also slightly prolonged though this difference does not reach statistical significance. Hence,
eat-7 mutants display increased behavioral quiescence during the L1 stage. In addition to this L1 quiescent phenotype, we have found that adult
eat-7 mutants, when left unperturbed, make fewer tracks than N2 worms on a lawn of bacteria. When mechanically stimulated however,
eat-7 mutants are capable of rapid and coordinated movement, indicating that the increased behavioral quiescence cannot be explained simply by an inability to move well.
eat-7 is defined by a single dominant allele,
ad450sd , which maps between
ced-2 and
lin-1 (4), a genetic interval in which the gene
egl-4 is found. Body size, life span, and roaming behaviors are increased in
egl-4 mutants while these three phenotypes are decreased in
eat-7 mutants, suggesting that
ad450sd may be a hypermorphic
egl-4 allele. This suggestion is supported by the finding that two
egl-4 recessive alleles,
n477 and
n479 , dominantly suppress the small body phenotype of
eat-7(
ad450sd)/+ . We sequenced the EGL-4a cDNA in
eat-7 mutants and have found a Glycine to Arginine mutation. This Glycine, located in the second cGMP binding domain, is conserved in all proteins containing a cGMP or cAMP binding domain. We will report the results of experiments testing the effect of expressing the EGL-4a cDNA with the G->R mutation in wild-type worms. (1)Hendricks et al, Neuron 2000. (2) Shaw et al, Science 2000. (3)Singh and Sulston, Nematologica 1978. (4)Avery, Genetics 1993.