The analog inhibitor, α-methyl dopa, as a screening agent for mutants elevating levels of dopa decarboxylase activity in Drosophila melanogaster

1974 ◽  
Vol 133 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Allen F. Sherald ◽  
Theodore R. F. Wright
Genetics ◽  
1976 ◽  
Vol 84 (2) ◽  
pp. 287-310
Author(s):  
Theodore R F Wright ◽  
Glenn C Bewley ◽  
Allen F Sherald

ABSTRACT Of 84 lethals isolated over the dopa decarboxylase (DDC) deficiency Df(2L)50, 8 have been identified as DDC-deficient alleles on the basis of their effect on DDC activity when heterozygous over the CyO balancer chromosome with activities ranging from 28% to 53% of controls. Some of the Ddc-deficient alleles exhibit intracistronic complementation. Most of the complementing pairs of alleles are much reduced in viability, e.g. < 5% of expected, and express a common syndrome of mutant phenes which can reasonably be inferred to derive from inadequately sclerotinized cuticle. Individuals heterozygous for the noncomplementing allele, Ddcn7, over the 12-band DDC deficiency, Df(2L)130, die at the end of embryogenesis as unhatched larvae with unpigmented mouth parts. The Ddc alleles and the l(2)amd α-methyl dopa (αMD) hypersensitive alleles are both located within the 11 band region 37B10-C7. The l(2)amd locus is immediately to the right of hk(2-53.9).Ddc has been mapped within 0.004 Map Units to the right of l(2)amd with a maximum estimated recombination frequency of 0.01%. None of the Ddc/CyO strains are sensitive to the dietary administration of α-methyl dopa (αMD), and complementation occurs between the Ddc deficient alleles and the l(2)amd alleles both on the basis of viability and DDC activity. No effect on DDC by the amd alleles has been found to date. Even in the complementing heterozygote, amdH1/amdH89, the level of activity, thermostability, and in vitro αMD inhibition of DDC remains unaffected. Although no biochemical phene has yet been established for the αMD hypersensitive amd alleles, it seems likely that the two groups of mutants are functionally related.


Genetics ◽  
1976 ◽  
Vol 84 (2) ◽  
pp. 267-285
Author(s):  
Theodore R F Wright ◽  
Ross B Hodgetts ◽  
Allen F Sherald

ABSTRACT A detailed cytogenetic investigation of 16 overlapping deficiencies in the 36C-40A region on the left arm of the second chromosome (2L) in Drosophila melanogaster is reported. These deficiencies permit a localization of both the dopa-decarboxylase-dosage-sensitive region and the α-methyl-dopa-hypersensitive locus, l(2)amd, to the same region, 37B10-37C7.


Genetics ◽  
1992 ◽  
Vol 132 (2) ◽  
pp. 443-452 ◽  
Author(s):  
C F Aquadro ◽  
R M Jennings ◽  
M M Bland ◽  
C C Laurie ◽  
C H Langley

Abstract Forty-six second-chromosome lines of Drosophila melanogaster isolated from five natural populations were surveyed for restriction map variation in a 65-kb region surrounding the gene (Ddc) encoding dopa decarboxylase (DDC). Sixty-nine restriction sites were scored, 13 of which were polymorphic. Average heterozygosity per nucleotide was estimated to be 0.005. Eight large (0.7-5.0 kb) inserts, two small inserts (100 and 200 bp) and three small deletions (100-300 bp) were also observed across the 65-kb region. We see no evidence for a reduction in either nucleotide heterozygosity or insertion/deletion variation in the central 26-kb segment containing Ddc and a dense cluster of lethal complementation groups and transcripts (greater than or equal to 9 genes) compared to that seen in the adjacent regions (totaling 39 kb) in which only a single gene and transcript has been detected, or to that observed for other gene regions in D. melanogaster. The distribution of restriction site variation shows no significant departure from that expected under an equilibrium neutral model. However insertions and deletions show a significant departure from neutrality in that they are too rare in frequency, consistent with them being deleterious on average. Significant linkage disequilibrium among variants exists across much of the 65-kb region. Lower regional rates of recombination combined with the influence of polymorphic chromosomal inversions, rather than epistatic selection among genes in the dense cluster, probably are sufficient explanations for the creation and/or maintenance of the linkage disequilibrium observed in the Ddc region. We have also assayed adult DDC enzyme activity in these same lines. Twofold variation in activity among lines is observed within our sample. Significant associations are observed between level of DDC enzyme activity and restriction map variants. Surprisingly, one line with a 5.0-kb insert within an intron and one line with a 1.5-kb insert near the 5' end of Ddc each show normal adult DDC activities.


1990 ◽  
Vol 52 ◽  
pp. 231
Author(s):  
Naova HAMAUE ◽  
Toru ENDO ◽  
Akiyoshi YANAI ◽  
Yasuteru SHIROSHITA ◽  
Yoshio MONMA ◽  
...  

1991 ◽  
Vol 88 (7) ◽  
pp. 2721-2725 ◽  
Author(s):  
A. Gjedde ◽  
J. Reith ◽  
S. Dyve ◽  
G. Leger ◽  
M. Guttman ◽  
...  

1981 ◽  
Vol 1 (6) ◽  
pp. 475-485
Author(s):  
J Hirsh ◽  
N Davidson

We have isolated chromosomal deoxyribonucleic acid clones containing the Drosophila dopa decarboxylase gene. We describe an isolation procedure which can be applied to other nonabundantly expressed Drosophila genes. The dopa decarboxylase gene lies within or very near polytene chromosome band 37C1-2. The gene is interrupted by at least one intron, and the primary mode of regulation is pretranslational. At least two additional sequences hybridized by in vivo ribonucleic acid-derived probes are found within a 35-kilobase region surrounding the gene. The developmental profile of ribonucleic acid transcribed from one of these regions differs from that of the dopa decarboxylase transcript.


1989 ◽  
Vol 49 ◽  
pp. 186
Author(s):  
Naoya Hamaue ◽  
Hiroyuki Sato ◽  
Haruko Kameda ◽  
Yoshio Monma ◽  
Masaru Minami ◽  
...  

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