TABLE 2

Locomotion rates conferred by selected gain-of-function and null mutations in the C. elegansq and Gαs signaling pathways

ProteinMutant
 genotypeReference for mutation isolationEffect of
 mutationLocomotion rate
 (body bends/min)a
N2 (wild type)+21.3 ± 1.5
EGL-30 (Gαq)egl-30(tg26)Doi and Iwasaki (2002)Gain of function50.3 ± 4.0
EGL-30 (Gαq)egl-30(ad810)Brundage et al. (1996)Putative null0.024 ± 0.003b
GSA-1 (Gαs)gsa-1(ce81)This studyGain of function47.9 ± 1.3
GSA-1 (Gαs)gsa-1(pk75)Korswagen et al. (1997)NullNDc
ACY-1acy-1(ce2)This studyGain of function48.0 ± 1.6
ACY-1acy-1(pk1279)Moorman and Plasterk (2002)Null0.75 ± 0.10b
  • a Mean ± standard error. N ≥ 10 animals.

  • b The paralysis of these mutants is not caused by general sickness, muscle, or developmental defects, because they can be acutely rescued to wild-type levels of locomotion by manipulating Gα pathway signaling (Reynolds et al. 2005, accompanying article in this issue).

  • c These mutants exhibit early larval paralysis and death caused by an apparent problem in fluid balance (Korswagen et al. 1997).

  • Note the opposite effects on locomotion rate conferred by gain-of-function and null mutations in each of these genes.