EGG-LAYING DEFECTIVE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Carol Trent ¹, Nancy Tsung ¹, and H. Robert Horvitz ¹

¹ Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

We have isolated 145 fertile mutants of C. elegans that are defective in egg laying and have characterized 59 of them genetically, behaviorally and pharmacologically. These 59 mutants define 40 new genes called egl, for egg-laying abnormal. Most of the other mutants are defective in previously identified genes. The egl mutants differ with respect to the severity of their egg-laying defects and the presence of behavioral or morphological pleiotropies. We have defined four distinct categories of mutants based on their responses to the pharmacological agents serotonin and imipramine, which stimulate egg laying by wild-type hermaphrodites. These drugs test the functioning of the vulva, the vulval and uterine muscles and the hermaphrodite-specific neurons (HSNs), which innervate the vulval muscles. Mutants representing 14 egl genes fail to respond to serotonin and to imipramine and are likely to be defective in the functioning of the vulva or the vulval and uterine muscles. Four mutants (representing four different genes) lay eggs in response to serotonin but not to imipramine and appear to be egg-laying defective because of defects in the HSNs; three of these four were selected specifically for these drug responses. Mutants representing seven egl genes lay eggs in response to serotonin and to imipramine. One egl mutant responds to imipramine but not to serotonin. The remaining egl mutants show variable or intermediate responses to the drugs. Two of the HSN-defective mutants, egl-1 and her-1(n695), lack HSN cell bodies and are likely to be expressing the normally male-specific program of HSN cell death. Whereas egl-1 animals appear to be defective specifically in HSN development, her-1(n695) animals exhibit multiple morphological pleiotropies, displaying partial transformation of the sexual phenotype of many cells and tissues. At least two of the egl mutants appear to be defective in the processing of environmental signals that modulate egg laying and may define new components of the neural circuitry that control egg laying.

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				F Solari, A Bateman, and J Ahringer The Caenorhabditis elegans genes egl-27 and egr-1 are similar to MTA1, a member of a chromatin regulatory complex, and are redundantly required for embryonic patterning Development, January 6, 1999; 126(11): 2483 - 2494. [Abstract] [PDF]

				C. Malone, W. Fixsen, H. Horvitz, and M Han UNC-84 localizes to the nuclear envelope and is required for nuclear migration and anchoring during C. elegans development Development, January 6, 1999; 126(14): 3171 - 3181. [Abstract] [PDF]

				M. Herman, Q Ch'ng, S. Hettenbach, T. Ratliff, C Kenyon, and R. Herman EGL-27 is similar to a metastasis-associated factor and controls cell polarity and cell migration in C. elegans Development, January 2, 1999; 126(5): 1055 - 1064. [Abstract] [PDF]

				J. S. Duerr, D. L. Frisby, J. Gaskin, A. Duke, K. Asermely, D. Huddleston, L. E. Eiden, and J. B. Rand The cat-1 Gene of Caenorhabditis elegans Encodes a Vesicular Monoamine Transporter Required for Specific Monoamine-Dependent Behaviors J. Neurosci., January 1, 1999; 19(1): 72 - 84. [Abstract] [Full Text] [PDF]

				R. Y. N. Lee, E. R. Sawin, M. Chalfie, H. R. Horvitz, and L. Avery EAT-4, a Homolog of a Mammalian Sodium-Dependent Inorganic Phosphate Cotransporter, Is Necessary for Glutamatergic Neurotransmission in Caenorhabditis elegans J. Neurosci., January 1, 1999; 19(1): 159 - 167. [Abstract] [Full Text] [PDF]

				J. Maloof, J Whangbo, J. Harris, G. Jongeward, and C Kenyon A Wnt signaling pathway controls hox gene expression and neuroblast migration in C. elegans Development, January 1, 1999; 126(1): 37 - 49. [Abstract] [PDF]

				D. Gems, A. J. Sutton, M. L. Sundermeyer, P. S. Albert, K. V. King, M. L. Edgley, P. L. Larsen, and D. L. Riddle Two Pleiotropic Classes of daf-2 Mutation Affect Larval Arrest, Adult Behavior, Reproduction and Longevity in Caenorhabditis elegans Genetics, September 1, 1998; 150(1): 129 - 155. [Abstract] [Full Text]

				A Duggan, C Ma, and M Chalfie Regulation of touch receptor differentiation by the Caenorhabditis elegans mec-3 and unc-86 genes Development, January 10, 1998; 125(20): 4107 - 4119. [Abstract] [PDF]

				J. Zhu, R. J. Hill, P. J. Heid, M. Fukuyama, A. Sugimoto, J. R. Priess, and J. H. Rothman end-1 encodes an apparent GATA factor that specifies the endoderm precursor in Caenorhabditis elegans embryos Genes & Dev., November 1, 1997; 11(21): 2883 - 2896. [Abstract] [Full Text] [PDF]

				G. I. Patterson, A. Koweek, A. Wong, Y. Liu, and G. Ruvkun The DAF-3 Smad protein antagonizes TGF-beta -related receptor signaling in the Caenorhabditis elegans dauer pathway Genes & Dev., October 15, 1997; 11(20): 2679 - 2690. [Abstract] [Full Text] [PDF]

				H C Korswagen, J H Park, Y Ohshima, and R H Plasterk An activating mutation in a Caenorhabditis elegans Gs protein induces neural degeneration. Genes & Dev., June 15, 1997; 11(12): 1493 - 1503. [Abstract] [PDF]

				S Takagi, C Benard, J Pak, D Livingstone, and S Hekimi Cellular and axonal migrations are misguided along both body axes in the maternal-effect mau-2 mutants of Caenorhabditis elegans Development, January 12, 1997; 124(24): 5115 - 5126. [Abstract] [PDF]

				H. Chamberlin, R. Palmer, A. Newman, P. Sternberg, D. Baillie, and J. Thomas The PAX gene egl-38 mediates developmental patterning in Caenorhabditis elegans Development, January 10, 1997; 124(20): 3919 - 3928. [Abstract] [PDF]