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Restriction map and α-amylase activity variation among Drosophila mutation accumulation lines

Published online by Cambridge University Press:  14 April 2009

H. Tachida ,
K. Harada ,
C. H. Langley ,
C. F. Aquadro ,
T. Yamazaki ,
C. C. Cockerham  and
T. Mukai
H. Tachida*
Affiliation:
Department of Statistics, North Carolina State University, Box 8203, Raleigh, NC 27695-8203
K. Harada
Affiliation:
Department of Biology, Kyushu University33, Fukuoka 812, Japan
C. H. Langley
Affiliation:
Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC27709
C. F. Aquadro
Affiliation:
Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC27709
T. Yamazaki
Affiliation:
Department of Biology, Kyushu University33, Fukuoka 812, Japan
C. C. Cockerham
Affiliation:
Department of Statistics, North Carolina State University, Box 8203, Raleigh, NC 27695-8203
T. Mukai
Affiliation:
Department of Biology, Kyushu University33, Fukuoka 812, Japan
*
* Corresponding author: Present address: National Institute of Genetics, Mishima, Shizuoka-ken 411. Japan.

Summary

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The specific activities of α-amylase were measured for two sets of mutation accumulation lines, each set having originated from a different lethal-carrying second chromosome and SM1(Cy) chromosome and having been maintained by a balanced lethal system for about 300 generations. Significant variation was found to have accumulated among lines of both sets. Because of dysgenic crosses in the early generations of mutation accumulation, insertions or deletions of transposable elements in the Amy gene region were suspected of being the cause of this variation. In order to test this possibility, the structural changes in the 14 kb region of these chromosomes that includes the structural genes for α-amylase were investigated by restriction map analysis. We found that most part of the activity variation is due to replacements of a chromosomal region of SM1(Cy), including the structural genes for α-amylase, by the corresponding regions of the lethal chromosomes. One line also contained an insertion in this region but this line has an intermediate activity value. Thus, insertions of transposable elements into the Amy gene region were not found to be responsible for the new variation observed in α-amylase activity. If we remove those lines with structural changes from the analysis, the genetic variance of α-amylase specific activity among lines becomes non-significant in both sets of chromosomes.

Type
Research Article
Information
Genetics Research , Volume 54 , Issue 3 , December 1989 , pp. 197 - 203
Copyright
Copyright © Cambridge University Press 1989

References

Abraham, I. & Doane, W. W. (1978). Genetic regulation of tissue-specific expression of Amylase structural genes in Drosophila melanogaster. Proceedings of National Academy of Sciences, U.S.A. 75, 4446–4450.CrossRefGoogle ScholarPubMed
Bender, W., Spierer, P. & Hogness, D. S. (1983). Chromosomal walking and jumping to isolate DNA from the Ace and rosy loci and the bithorax complex in Drosophila melanogaster. Journal of Molecular Biology 168, 17–33.CrossRefGoogle ScholarPubMed
Chovnick, A., Gelbart, W. & McCarron, M. (1977). Organization of the rosy locus in Drosophila melanogaster. Cell 11, 1–10.CrossRefGoogle ScholarPubMed
Doane, W. W., Treat-Clemons, L. G., Buchberg, A. M., Gemmil, R. M., Levy, J. N., Hawley, S. A. & Paigen, K. (1983). Genetic mechanisms for tissue specific control of alpha amylase expression in Drosophila melanogaster. In Isozymes: Current Topics in Biological and Medical Research, vol. 9 (ed. Rattazi, M. C., Scandalios, J. G. and Whitt, G. S.), pp. 63–90. New York: Alan R. Liss.Google Scholar
Finnegan, D. J. & Fawcett, D. H. (1986). Transposable elements in Drosophila melanogaster. Oxford Surveys on Eukaryotic Genes 3, 1–62.Google ScholarPubMed
Gemmil, R. M., Levy, J. N. & Doane, W. W. (1985). Molecular cloning of α-amylase genes from Drosophila melanogaster. I. Clone isolation by use of a mouse probe. Genetics 110, 299–312.CrossRefGoogle Scholar
Hilliker, A. J. & Chovnick, A. (1981). Further observations on intragenic recombination in Drosophila melanogaster. Genetical Research 38, 281–296.CrossRefGoogle ScholarPubMed
Hoorn, A. J. W. & Scharloo, W. (1978). The functional significance of amylase polymorphism in Drosophila melanogaster. I. Proteins of two amylase variants. Genetica 49, 173–180.CrossRefGoogle Scholar
Lamb, B. C. (1984). The properties of meiotic gene conversion important in its effects on evolution. Heredity 53, 113–138.CrossRefGoogle ScholarPubMed
Langley, C. H., Shrimpton, A. E., Yamazaki, T., Miyashita, N., Matsuo, Y. & Aquadro, C. H. (1988). Naturally occurring variation in the restriction map of the Amy region of Drosophila melanogaster. Genetics 119, 619–629.CrossRefGoogle ScholarPubMed
Laurie-Ahlberg, C. C. (1985). Genetic variation affecting the expression of enzyme-coding genes in Drosophila: an evolutionary perspective. In Isozymes: Current Topics in Biological and Medical Research, vol. 12 (ed. Rattazi, M. C., Scandalios, J. G. and Whitt, G. S.), pp. 33–88. New York: Alan R. Liss.Google Scholar
Levy, J. N., Gemmil, R. M. & Doane, W. W. (1985). Molecular cloning of α-amylase genes from Drosophila melanogaster. II. Clone organization and verification. Genetics 110, 313–324.CrossRefGoogle ScholarPubMed
Lindsley, D. C. & Grell, E. H. (1968). Genetic Variations of Drosophila melanogaster. Publication 627. Washington, D.C.: Carnegie Institute.Google Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). Protein measurement with the Folin phenol reagent. Journal of Biological Chemistry 193, 265–275.CrossRefGoogle ScholarPubMed
Maniatis, T., Fritsch, E. F. & Sambrook, J. (1982). Molecular Cloning, A Laboratory Manual. Cold Spring Harbor Laboratory Publications, New York.Google Scholar
Maroni, G. & Laurie-Ahlberg, C. C. (1983). Genetic control of Adh expression in Drosophila melanogaster. Genetics 105, 921–933.CrossRefGoogle ScholarPubMed
Mukai, T. & Cockerham, C. C. (1977). Spontaneous mutation rates at enzyme loci in Drosophila melanogaster. Proceedings of the National Academy of Sciences, U.S.A. 74, 2514–2517.CrossRefGoogle ScholarPubMed
Mukai, T. & Voelker, R. A. (1977). The genetic structure of natural populations of Drosophila melanogaster. XIII. Further studies on linkage disequilibrium. Genetics 86, 175–185.CrossRefGoogle ScholarPubMed
Mukai, T., Harada, K. & Yoshimaru, H. (1984). Spontaneous mutations modifying the activity of Alcohol Dehydrogenase (ADH) in Drosophila melanogaster. Genetics 106, 73–84.CrossRefGoogle ScholarPubMed
Rigby, P. W. J., Dieckman, M., Rhodes, C. & Berg, P. (1977). Labelling deoxyribonucleic acid to high specific activity in vitro by nick translation with DNA polymerase I. Journal of Molecular Biology 113, 237–251.CrossRefGoogle ScholarPubMed
Scobie, N. N. & Schaffer, H. E. (1982 a). A mutator factor in a strain of Drosophila melanogaster: identified by use of mutation, reversion rates and male recombination. Genetics 101, 417–429.CrossRefGoogle Scholar
Scobie, N. N. & Schaffer, H. E. (1982 b). The location of mutator factor in a strain of Drosophila melanogaster by assaying male recombination. Genetics 101, 405–416.CrossRefGoogle Scholar
Smith, G. & Summers, M. (1980). The bidirectional transfer of DNA and RNA to nitrocellulose or diazobenzyloxy-methyl paper. Annals of Biochemistry 109, 123–129.CrossRefGoogle ScholarPubMed
Voelker, R. A., Schaffer, H. E. & Mukai, T. (1980). Spontaneous allozyme mutations in Drosophila melanogaster: rate of occurence and nature of mutants. Genetics 94, 961–968.CrossRefGoogle Scholar
Yamaguchi, O. & Mukai, T. (1974). Variation of spontaneous occurrence rates of chromosomal abberations in the second chromosome of Drosophila melanogaster. Genetics 78, 1209–1221.CrossRefGoogle Scholar
Yamazaki, T. & Matsuo, M. (1984). Genetic analysis of natural populations of Drosophila melanogaster in Japan. III. Genetic variability of inducing factors of amylase and fitness. Genetics 108, 223–235.CrossRefGoogle ScholarPubMed