scholarly journals MATERNAL EFFECT OF MA-1+ ON XANTHINE DEHYDROGENASE OF DROSOPHILA MELANOGASTER, II. XANTHINE DEHYDROGENASE ACTIVITY DURING DEVELOPMENT

1962 ◽  
Vol 48 (10) ◽  
pp. 1712-1718 ◽  
Author(s):  
E. Glassman ◽  
J. McLean
Genetics ◽  
1984 ◽  
Vol 108 (3) ◽  
pp. 603-615
Author(s):  
C A Rushlow ◽  
W Bender ◽  
A Chovnick

ABSTRACT Experiments are described that extend the characterization of position effect variants of the rosy locus and test possible mechanisms of heterochromatic position effect.—Rosy position effect variants exhibit a variegated phenotype with respect to xanthine dehydrogenase activity in malpighian tubules.—The breakpoints of the position effect mutations are located on the DNA map of the rosy region outside of the rosy locus DNA; ryps  1136 is located in the DNA of the l(3)S12 gene immediately proximal to rosy, whereas ryps  1149 is located some 15 kb distal to rosy in the pic locus.—Southern blot experiments are described that test and reject the notion that heterochromatic position effect results from underreplication of the position-affected gene. Rather, the results of Northern blots serve to direct attention to position effect as a defect in transcription.—Histone region deletion heterozygosity and butyrate-feeding experiments failed to exhibit specific suppression of position effect at the rosy locus.


Genetics ◽  
1974 ◽  
Vol 76 (2) ◽  
pp. 289-299
Author(s):  
Margaret McCarron ◽  
William Gelbart ◽  
Arthur Chovnick

ABSTRACT A convenient method is described for the intracistronic mapping of genetic sites responsible for electrophoretic variation of a specific protein in Drosophila melanogaster. A number of wild-type isoalleles of the rosy locus have been isolated which are associated with the production of electrophoretically distinguishable xanthine dehydrogenases. Large-scale recombination experiments were carried out involving null enzyme mutants induced on electrophoretically distinct wild-type isoalleles, the genetic basis for which is followed as a nonselective marker in the cross. Additionally, a large-scale recombination experiment was carried out involving null enzyme rosy mutants induced on the same wild-type isoallele. Examination of the electrophoretic character of crossover and convertant products recovered from the latter experiment revealed that all exhibited the same parental electrophoretic character. In addition to documenting the stability of the xanthine dehydrogenase electrophoretic character, this observation argues against a special mutagenesis hypothesis to explain conversions resulting from allele recombination studies.


Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.


Genetics ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 1099-1109 ◽  
Author(s):  
A G Reaume ◽  
D A Knecht ◽  
A Chovnick

Abstract The rosy gene in Drosophila melanogaster codes for the enzyme xanthine dehydrogenase (XDH). Mutants that have no enzyme activity are characterized by a brownish eye color phenotype reflecting a deficiency in the red eye pigment. Xanthine dehydrogenase is not synthesized in the eye, but rather is transported there. The present report describes the ultrastructural localization of XDH in the Drosophila eye. Three lines of evidence are presented demonstrating that XDH is sequestered within specific vacuoles, the type II pigment granules. Histochemical and antibody staining of frozen sections, as well as thin layer chromatography studies of several adult genotypes serve to examine some of the factors and genic interactions that may be involved in transport of XDH, and in eye pigment formation. While a specific function for XDH in the synthesis of the red, pteridine eye pigments remains unknown, these studies present evidence that: (1) the incorporation of XDH into the pigment granules requires specific interaction between a normal XDH molecule and one or more transport proteins; (2) the structural integrity of the pigment granule itself is dependent upon the presence of a normal balance of eye pigments, a notion advanced earlier.


2000 ◽  
Vol 222 (2) ◽  
pp. 392-404 ◽  
Author(s):  
Benjamin Loppin ◽  
Mylène Docquier ◽  
François Bonneton ◽  
Pierre Couble

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