Nature Publishing Group, publisher of Nature, and other science journals and reference works
Nature
my account e-alerts subscribe register
   
Tuesday 17 October 2017
Journal Home
Current Issue
AOP
Archive
Download PDF
References
Export citation
Export references
Send to a friend
More articles like this

Letters to Nature
Nature 312, 752 - 754 (20 December 1984); doi:10.1038/312752a0

Restoration of circadian behavioural rhythms by gene transfer in Drosophila

Thaddeus A. Bargiello, F. Rob Jackson & Michael W. Young

The Rockefeller University, 1230 York Avenue, New York, New York 10021, USA

The per locus of Drosophila melanogaster has a fundamental role in the construction or maintenance of a biological clock. Three classes of per mutations have been identified: per l mutants have circadian behavioural rhythms with a 29-h rather than a 24-h period, per s mutants have short-period rhythms of 19 h, and per 0 mutants have no detectable circadian rhythms1–4. Each of these mutations has a corresponding influence on the 55-s periodicity of male courtship song5. Long-and short-period circadian rhythm phenotypes can also be obtained by altering the dosage of the wild-type gene4: for example, females carrying only one dose of this X-linked gene have circadian rhythms with periodicities about 1 h longer than those carrying two doses. In a previous report6, cloned DNA was used to localize several chromosomal rearrangement breakpoints that alter per locus function. The rearrangements all affected a 7-kilobase (kb) interval that encodes a 4.5-kb poly(A)+ RNA. We report here that when a 7.1-kb fragment from a per + fly, including the sequences encoding the 4.5-kb transcript, is introduced into the genome of a per 0 (arrhythmic) fly by P element-mediated transformation, circadian rhythmicity of behaviour such as eclosion and locomotor activity is restored. The transforming DNA complements per locus deletions and is transcribed, forming a single 4.5-kb poly(A)+ RNA comparableto that produced by wild-type flies.

------------------

References

1. Konopka, R. & Benzer, S. Proc. natn. Acad. Sci. U.S.A. 68, 2112−2116 (1971). | ChemPort |
2. Young, M. W. & Judd, B. H. Genetics 88, 723−742 (1978). | ISI |
3. Smith, R. F. & Konopka, R. J. Molec. gen. Genet. 183, 243−251 (1981). | PubMed | ISI | ChemPort |
4. Smith, R. F. & Konopka, R. J. Molec. gen. Genet. 185, 30−36 (1982). | ISI |
5. Kyriacou, C. P. & Hall, J. C. Proc. natn. Acad. Sci. U.S.A. 77, 6729−6733 (1980). | ChemPort |
6. Bargiello, T. A. & Young, M. W. Proc. natn. Acad. Sci. U.S.A. 81, 2142−2146 (1984). | ChemPort |
7. Rubin, G. M. & Spradling, A. C. Nucleic Acids Res. 11, 6341−6351 (1983). | PubMed | ISI | ChemPort |
8. Spradling, A. C. & Rubin, G. M. Science 218, 341−347 (1982). | PubMed | ISI | ChemPort |
9. Spradling, A. C. & Rubin, G. M. Cell 34, 47−57 (1983). | Article | PubMed | ISI | ChemPort |
10. Goldberg, D. A., Posakony, J. W. & Maniatis, T. Cell 34, 59−73 (1983). | Article | PubMed | ISI | ChemPort |
11. Enright, J. T. in Handbook of Behavioral Neurobiology (ed. Aschoff, J.) 21−39 (Plenum, New York, 1981).
12. Jackson, F. R. J. Neurogenet. 1, 3−15 (1983). | PubMed | ChemPort |
13. Pittendrigh, C. S. Cold Spring Harb. Symp. quant. Biol. 25, 159−184 (1960). | PubMed | ISI | ChemPort |
14. Reddy, P. et al. Cell 38, 701−710 (1984). | Article | PubMed | ISI | ChemPort |



© 1984 Nature Publishing Group
Privacy Policy