- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Grell, E. H.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Grell, E. H.
GENETIC ANALYSIS OF ASPARTATE AMINOTRANSFERASE ISOZYMES FROM HYBRIDS BETWEEN DROSOPHILA MELANOGASTER AND DROSOPHILA SIMULANS AND MUTAGEN-INDUCED ISOZYME VARIANTS
E. H. Grell 1
1 Biology Division, Oak Ridge National Laboratory, Oak Ridge,
Tennessee 37830
The aspartate aminotransferases (designated GOT1 and GOT2) are two enzymes of Drosophila melanogaster for which naturally occurring electrophoretic variants were not found. There is an electrophoretic difference between D. melanogaster and D. simulans. Since the F 1 hybrid offspring of these species are sterile, a genetic analysis of the ordinary type cannot be done on differences between the two species. A method was devised to make "partial hybrids" in which one chromosome arm is homozygous for melanogaster genes in an otherwise hybrid background. By using this method, Got1 was localized to 2R and Got2 to 2L. Once a gene can be assigned to a chromosome, it may be followed in crossing schemes and mutations from mutagen treatments may be looked for. At the locus of Got1 a mutation with low activity was recovered and designated Got1lo. It was located at a genetic map position of 75 on 2R. A Got2 mutant with a greater migration to the anode was recovered and designated Got2 J. It was located at a genetic map position of 3.0, and in the salivary chromosome was between 22B1 and 22B4 inclusive.
Submitted on April 25, 1975
This article has been cited by other articles:
 |
|
 |
|
  N. Mukae, H. Yokoyama, T. Yokokura, Y. Sakoyama, and S. Nagata Activation of the innate immunity in Drosophila by endogenous chromosomal DNA that escaped apoptotic degradation Genes & Dev., October 15, 2002; 16(20): 2662 - 2671. [Abstract] [Full Text] [PDF]
|
|