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Abstract 


The pharynx of Caenorhabditis elegans is a nearly self-contained neuromuscular organ responsible for feeding. To identify genes involved in the development or function of the excitable cells of the pharynx, I screened for worms with visible defects in pharyngeal feeding behavior. Fifty-two mutations identified 35 genes, at least 22 previously unknown. The genes broke down into three broad classes: 2 pha genes, mutations in which caused defects in the shape of the pharynx, 7 phm genes, mutations in which caused defects in the contractile structures of the pharyngeal muscle, and 26 eat genes, mutants in which had abnormal pharyngeal muscle motions, but had normally shaped and normally birefringent pharynxes capable of vigorous contraction. Although the Eat phenotypes were diverse, most resembled those caused by defects in the pharyngeal nervous system. For some of the eat genes there is direct evidence from previous genetic mosaic and pharmacological studies that they do in fact affect nervous system. In eat-5 mutants the motions of the different parts of the pharynx were poorly synchronized. eat-6 and eat-12 mutants failed to relax their pharyngeal muscles properly. These pharyngeal motion defects are most easily explained as resulting from abnormal electrical excitability of the pharyngeal muscle membrane.

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Genetics. 1993 Apr; 133(4): 897–917.
PMCID: PMC1205408
PMID: 8462849

The Genetics of Feeding in Caenorhabditis Elegans

Abstract

The pharynx of Caenorhabditis elegans is a nearly self-contained neuromuscular organ responsible for feeding. To identify genes involved in the development or function of the excitable cells of the pharynx, I screened for worms with visible defects in pharyngeal feeding behavior. Fifty-two mutations identified 35 genes, at least 22 previously unknown. The genes broke down into three broad classes: 2 pha genes, mutations in which caused defects in the shape of the pharynx, 7 phm genes, mutations in which caused defects in the contractile structures of the pharyngeal muscle, and 26 eat genes, mutants in which had abnormal pharyngeal muscle motions, but had normally shaped and normally birefringent pharynxes capable of vigorous contraction. Although the Eat phenotypes were diverse, most resembled those caused by defects in the pharyngeal nervous system. For some of the eat genes there is direct evidence from previous genetic mosaic and pharmacological studies that they do in fact affect nervous system. In eat-5 mutants the motions of the different parts of the pharynx were poorly synchronized. eat-6 and eat-12 mutants failed to relax their pharyngeal muscles properly. These pharyngeal motion defects are most easily explained as resulting from abnormal electrical excitability of the pharyngeal muscle membrane.

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Selected References

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  • Albert PS, Brown SJ, Riddle DL. Sensory control of dauer larva formation in Caenorhabditis elegans. J Comp Neurol. 1981 May 20;198(3):435–451. [Abstract] [Google Scholar]
  • Albert PS, Riddle DL. Mutants of Caenorhabditis elegans that form dauer-like larvae. Dev Biol. 1988 Apr;126(2):270–293. [Abstract] [Google Scholar]
  • Avery L, Horvitz HR. A cell that dies during wild-type C. elegans development can function as a neuron in a ced-3 mutant. Cell. 1987 Dec 24;51(6):1071–1078. [Europe PMC free article] [Abstract] [Google Scholar]
  • Avery L, Horvitz HR. Pharyngeal pumping continues after laser killing of the pharyngeal nervous system of C. elegans. Neuron. 1989 Oct;3(4):473–485. [Abstract] [Google Scholar]
  • Avery L, Horvitz HR. Effects of starvation and neuroactive drugs on feeding in Caenorhabditis elegans. J Exp Zool. 1990 Mar;253(3):263–270. [Abstract] [Google Scholar]
  • Bargmann CI, Horvitz HR. Control of larval development by chemosensory neurons in Caenorhabditis elegans. Science. 1991 Mar 8;251(4998):1243–1246. [Abstract] [Google Scholar]
  • Bejsovec A, Anderson P. Functions of the myosin ATP and actin binding sites are required for C. elegans thick filament assembly. Cell. 1990 Jan 12;60(1):133–140. [Abstract] [Google Scholar]
  • Brenner S. The genetics of Caenorhabditis elegans. Genetics. 1974 May;77(1):71–94. [Europe PMC free article] [Abstract] [Google Scholar]
  • Byerly L, Masuda MO. Voltage-clamp analysis of the potassium current that produces a negative-going action potential in Ascaris muscle. J Physiol. 1979 Mar;288:263–284. [Abstract] [Google Scholar]
  • Chalfie M, Sulston J. Developmental genetics of the mechanosensory neurons of Caenorhabditis elegans. Dev Biol. 1981 Mar;82(2):358–370. [Abstract] [Google Scholar]
  • Chalfie M, Sulston JE, White JG, Southgate E, Thomson JN, Brenner S. The neural circuit for touch sensitivity in Caenorhabditis elegans. J Neurosci. 1985 Apr;5(4):956–964. [Europe PMC free article] [Abstract] [Google Scholar]
  • Culotti JG, Russell RL. Osmotic avoidance defective mutants of the nematode Caenorhabditis elegans. Genetics. 1978 Oct;90(2):243–256. [Europe PMC free article] [Abstract] [Google Scholar]
  • Davis RE, Stretton AO. Passive membrane properties of motorneurons and their role in long-distance signaling in the nematode Ascaris. J Neurosci. 1989 Feb;9(2):403–414. [Europe PMC free article] [Abstract] [Google Scholar]
  • DEBELL JT, DELCASTILLO J, SANCHEZ V. ELECTROPHYSIOLOGY OF THE SOMATIC MUSCLE CELLS OF ASCARIS LUMBRICOIDES. J Cell Physiol. 1963 Oct;62:159–177. [Abstract] [Google Scholar]
  • Driscoll M, Chalfie M. The mec-4 gene is a member of a family of Caenorhabditis elegans genes that can mutate to induce neuronal degeneration. Nature. 1991 Feb 14;349(6310):588–593. [Abstract] [Google Scholar]
  • Dusenbery DB, Sheridan RE, Russell RL. Chemotaxis-defective mutants of the nematode Caenorhabditis elegans. Genetics. 1975 Jun;80(2):297–309. [Europe PMC free article] [Abstract] [Google Scholar]
  • Files JG, Carr S, Hirsh D. Actin gene family of Caenorhabditis elegans. J Mol Biol. 1983 Mar 5;164(3):355–375. [Abstract] [Google Scholar]
  • Golden JW, Riddle DL. The Caenorhabditis elegans dauer larva: developmental effects of pheromone, food, and temperature. Dev Biol. 1984 Apr;102(2):368–378. [Abstract] [Google Scholar]
  • Greenwald IS, Horvitz HR. unc-93(e1500): A behavioral mutant of Caenorhabditis elegans that defines a gene with a wild-type null phenotype. Genetics. 1980 Sep;96(1):147–164. [Europe PMC free article] [Abstract] [Google Scholar]
  • Hall DH, Hedgecock EM. Kinesin-related gene unc-104 is required for axonal transport of synaptic vesicles in C. elegans. Cell. 1991 May 31;65(5):837–847. [Abstract] [Google Scholar]
  • Hodgkin J. Male Phenotypes and Mating Efficiency in CAENORHABDITIS ELEGANS. Genetics. 1983 Jan;103(1):43–64. [Europe PMC free article] [Abstract] [Google Scholar]
  • Hodgkin J, Barnes TM. More is not better: brood size and population growth in a self-fertilizing nematode. Proc Biol Sci. 1991 Oct 22;246(1315):19–24. [Abstract] [Google Scholar]
  • Hodgkin J, Horvitz HR, Brenner S. Nondisjunction Mutants of the Nematode CAENORHABDITIS ELEGANS. Genetics. 1979 Jan;91(1):67–94. [Europe PMC free article] [Abstract] [Google Scholar]
  • JARMAN M. Electrical activity in the muscle cells of Ascaris lumbricoides. Nature. 1959 Oct 17;184(Suppl 16):1244–1244. [Abstract] [Google Scholar]
  • Kaczmarek LK. Voltage-dependent potassium channels: minK and Shaker families. New Biol. 1991 Apr;3(4):315–323. [Abstract] [Google Scholar]
  • Kenyon C. A gene involved in the development of the posterior body region of C. elegans. Cell. 1986 Aug 1;46(3):477–487. [Abstract] [Google Scholar]
  • Lewis JA, Wu CH, Berg H, Levine JH. The genetics of levamisole resistance in the nematode Caenorhabditis elegans. Genetics. 1980 Aug;95(4):905–928. [Europe PMC free article] [Abstract] [Google Scholar]
  • Lewis JA, Elmer JS, Skimming J, McLafferty S, Fleming J, McGee T. Cholinergic receptor mutants of the nematode Caenorhabditis elegans. J Neurosci. 1987 Oct;7(10):3059–3071. [Europe PMC free article] [Abstract] [Google Scholar]
  • Papazian DM, Schwarz TL, Tempel BL, Timpe LC, Jan LY. Ion channels in Drosophila. Annu Rev Physiol. 1988;50:379–394. [Abstract] [Google Scholar]
  • Priess JR, Thomson JN. Cellular interactions in early C. elegans embryos. Cell. 1987 Jan 30;48(2):241–250. [Abstract] [Google Scholar]
  • Rand JB. Genetic analysis of the cha-1-unc-17 gene complex in Caenorhabditis. Genetics. 1989 May;122(1):73–80. [Europe PMC free article] [Abstract] [Google Scholar]
  • Rose AM, Baillie DL. Genetic organization of the region around UNC-15 (I), a gene affecting paramyosin in Caenorhabditis elegans. Genetics. 1980 Nov;96(3):639–648. [Europe PMC free article] [Abstract] [Google Scholar]
  • Thomas JH. Genetic analysis of defecation in Caenorhabditis elegans. Genetics. 1990 Apr;124(4):855–872. [Europe PMC free article] [Abstract] [Google Scholar]
  • Trent C, Tsuing N, Horvitz HR. Egg-laying defective mutants of the nematode Caenorhabditis elegans. Genetics. 1983 Aug;104(4):619–647. [Europe PMC free article] [Abstract] [Google Scholar]
  • Warmke J, Drysdale R, Ganetzky B. A distinct potassium channel polypeptide encoded by the Drosophila eag locus. Science. 1991 Jun 14;252(5012):1560–1562. [Abstract] [Google Scholar]
  • Waterston RH. The minor myosin heavy chain, mhcA, of Caenorhabditis elegans is necessary for the initiation of thick filament assembly. EMBO J. 1989 Nov;8(11):3429–3436. [Europe PMC free article] [Abstract] [Google Scholar]
  • Waterston RH, Hirsh D, Lane TR. Dominant mutations affecting muscle structure in Caenorhabditis elegans that map near the actin gene cluster. J Mol Biol. 1984 Dec 15;180(3):473–496. [Abstract] [Google Scholar]
  • Waterston RH, Thomson JN, Brenner S. Mutants with altered muscle structure of Caenorhabditis elegans. Dev Biol. 1980 Jun 15;77(2):271–302. [Abstract] [Google Scholar]
  • Yuan JY, Horvitz HR. The Caenorhabditis elegans genes ced-3 and ced-4 act cell autonomously to cause programmed cell death. Dev Biol. 1990 Mar;138(1):33–41. [Abstract] [Google Scholar]

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Funders who supported this work.

NHLBI NIH HHS (2)