Worm Breeder's Gazette 12(5): 73 (February 1, 1993)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
We have been continuing our genetic and behavioral analyses on thermotaxis-defective mutants which we and others have isolated (1-5). Here are the emerging pictures so far for genetic control of thermotaxis.
Five mutations, ttx-l( p767 )V, ttx( ks4 )111, ttx( ks5 ;putativenull) X, n2147 , ky7 ,cause animals to seek colder temperature than their cultivation temperature (cryophilic phenotype). The animals carrying these mutations, though the phenotypes vary slightly from mutation to mutation, are unable to move isothermally at around their cultivation temperature on a thermal gradient. This suggests that the underlying mechanism for the upward drive on a thermal gradient is severely disrupted. ks4 showed the cultivation temperature-dependency in thermotactic response, whereas p767 and ks5 did not. Thus, p767 and ks5 might disrupt thermosensation, and ks4 some of the steps downstream of thermosensation, such as thermal adaptation or assessment. n2147 and ky7 have defects in chemotaxis (4), and n2147 has additional defects in head foraging behavior (5).
Four mutations, tax-6 ( p675 ), ks1 , ks2 , ky8 ,cause animals to seek warmer temperature in our population assays (thermophilic phenotype). However, individual animals carrying any one of these mutations are able to move isothermally at around their cultivation temperature, which may indicate that thermosensation, thermal adaptation and assessment are only partially disrupted in those mutants. At least, three explanations for these partial phenotypes are possible: l)null mutations in genes responsible for downward drive have not been isolated yet. 2) genes causing thermophilic phenotype act downstream of genes, which are required for thermosensation, adaptation and assessment, and whose mutations could result in cryophilic phenotype. 3)thermophilic and cryophilic phenotypes may reflect different states of a gene. For example, gain-of- and loss-of-function mutations may give rise to thermophilic and cryophilic phenotypes, respectively.
Mutations in four genes, tax-2 ( p671 , p691 , p694 , ks10 , ks15 . ks31 )I, tax-3 ( p673 ), tax-4 ( p678 , ks11 , ks28 )III ky5 III, cause animals to move almost randomly on a gradient (athermotactic phenotype). All mutations in this athermotactic class have defects in chemotaxis in one way or another (2 4). In addition, ky5 has defects in head foraging behavior (5).
As first reported by Hedgecock and Russell (1), we showed here that thermotaxis-defective mutants are often defective in chemotaxis. Also, there are mutations like cryophilic n2147 and athermotactic ky5 that are abnormal in both chemotaxis and head foraging behavior. It is unlikely, though, that the abnormalities in head foraging peers are responsible for thermotaxtic defects. since dig-1 ( n1321 ),another mutation abnormal for head foraging (S), does not cause obvious defects in thermotaxis. These observations further support the hypothesis that thermo-, chemo- and even mechano- sensory transductions share molecules or neural circuits in common. As for the neural circuit of thermotaxis, we have just started a laser microsurgery to identify thermosensory neuron(s). We are killing AFD, a thermosensory candidate proposed by an EM analysis (6), of L1 animals and testing whether the operated animals mimic any of the thermotaxis-defective mutant phenotypes in adult.
To obtain a clue to elucidate the molecular mechanism of thermotaxis, we are attempting to clone ttx( ks4 ),a possible thermosensory transduction specific gene, and tax-4 ,a gene needed for both thermo- and chemotaxis. By a series of three factor crosses and deficiency mappings, ks4 so far maps to the region between lon-1 and daf-4 ,and tax-4 ( ks11 )to the region between unc-32 and unc-69 on 111. We are in process of doing mutant rescue experiments by injecting cosmids covering the candidate regions.
We thank Cori Bargmann for many valuable informations. We are also grateful to Cori Bargmann and Josh Kaplan for providing their mutants and permission to cite their unpublished data. (1) E. Hedgecock and R. Russell (1975), PNAS 72:4061, (2) D. Dusenbery et. al. (1975), Genetics 80:297, (3)I. Mori et. al. (1991), The Eighth C. elegans meeting Abst:2, (4) C. Bargmann, personal communication, (5) J. Kaplan et. al. (1992), WBG 12 No.3:105; personal communication, (6) L. Perkins et. al. (1986), Dev. Biol. 117:456
(2) D. Dusenbery et. al. (1975), Genetics 80:297.
(3)1. Mori et. al. (1991), The Eighth C. elegans meeting Abst:2.
(4) C. Bargmann, personal communication
(5) J. Kaplan et. al. (1992), WBG 12 No.3:105; personal communication
(6) L. Perkins et. al. (1986), Dev. Biol. 117:456.