scholarly journals HOMOEOSIS IN DROSOPHILA: A NEW ENHANCER OF POLYCOMB AND RELATED HOMOEOTIC MUTATIONS

Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 357-370
Author(s):  
Takashi Sato ◽  
Michael A Russell ◽  
R E Denell

ABSTRACT A new recessive lethal mutation in Drosophila melanogaster, Enhancer of Polycomb [E(Pc)], and chromosomal deficiencies lacking this locus act as dominant enhancers of the Polycomb mutant syndrome in adults. Thus, although E(Pc)/+ flies are phenotypically normal, this locus is haplo-abnormal with respect to its effect on the Polycomb phenotype. Recombinational and deficiency mapping localize the E(Pc) locus on chromosome 2 proximally and very closely linked (∼0.1 map unit) to the engrailed gene. E(Pc) enhances the expression of all Polycomb point mutations examined including that of a deficiency, indicating that this interaction does not depend on the presence of an altered Polycomb gene product. In several respects the mutations extra sex comb, lethal(4)29, and Polycomblike resemble those at the Polycomb locus. In the presence of E(Pc), recessive alleles of extra sex comb and lethal(4)29 are rendered slightly pseudodominant, and the homoeotic effects of Polycomblike heterozygotes are also enhanced. However, E(Pc) does not affect the expression of dominant mutations within the Bithorax gene complex (Cbx) or Antennapedia gene complex (AntpNs, Antp  73b, Antpscx, AntpEfW15, ScrMsc) which give homoeotic transformations resembling those of the Polycomb syndrome. Available evidence from the study of adult phenotypes suggests that mutations at E(Pc) do not result in homoeotic changes directly but instead modify the expression of a specific set of functionally related homoeotic variants.

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.


Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 371-386
Author(s):  
Michael A Kotarski ◽  
Sally Pickert ◽  
Ross J MacIntyre

ABSTRACT The chromosomal region surrounding the structural gene for α-glycerophosphate dehydrogenase (αGpdh, 2-20.5) of Drosophila melanogaster has been studied in detail. Forty-three EMS-induced recessive lethal mutations and five previously identified visible mutations have been localized within the 25A-27D region of chromosome 2 by deficiency mapping and in some cases by a recombination analysis. The 43 lethal mutations specify 17 lethal loci. ?Gpdh has been localized to a single polytene chromosome band, 25F5, and there apparently are no lethals that map to the αGpdh locus.


1977 ◽  
Vol 32 (1-2) ◽  
pp. 125-132 ◽  
Author(s):  
Karl Georg Götz ◽  
Simon Götz

Abstract Attempts to substantiate irreversible actions of a variety of magnetic fields on the fruitfly, Drosophila melanogaster, have been successful and unsuccessful in about equal numbers. The most conspicuous mutagenic effects apparently induced by pulsed H F-fields failed to appear under continuous electromagnetic irradiation. This seems to correlate the observed damage with the VLF-components of the pulsed fields. The present investigation is motivated by the occurrence of these components both in the atmosphere and in the vicinity of electrical appliances. A strain of normally viable wild type males and subnormally viable Attached-X γ ω females was used in which the yield, and the sex ratio, of the progeny indicate, respectively, the extent of developmental damage and of sex-linked recessive lethal mutation induced by the exposure to detrimental conditions. Evaluation of 73,800 flies from subsequent generations of a control group and two test groups raised in steady, or rotating, homogeneous 9.6 kHz magnetic fields of about 2.5 G did not reveal any development of hereditare load in the test groups.


Genetics ◽  
1973 ◽  
Vol 75 (2) ◽  
pp. 279-297
Author(s):  
R E Denell

ABSTRACT A number of homoeotic mutants have been localized to the proximal right arm of chromosome 3 of Drosophila melanogaster. These include seven alleles of Antennapedia (Antp), which is associated with a transformation of antennae into legs; Nasobemia (Ns), which causes the same phenotype as Antp but was considered by Gehring (1966) not to be an allele; and three genes causing a transformation of second and third legs into first legs: Extra sex comb (Scx), Polycomb (Pc), and Multiple sex comb (Msc.). The alleles of Antp and Scx share a common recessive lethal effect, and Pc maps 0.2-0.3 units to the left of Scx.—In the present investigation, rearrangements associated with the reversion of Ns suggest that its cytological location is in or just distal to salivary chromosome doublet 84B1-2. Although Ns is viable when homozygous, four of its revertants share a common recessive lethal effect. These revertants fail to complement the recessive lethality of AntpB and Scx. Furthermore, they show a complex pattern of functional interaction with Pc and with Humeral (Hu), a dominant mutation associated with a rearrangement with one breakpoint just distal to 84B1-2. Finally, analysis of a revertant of Msc indicates that Msc is also located very close to 84B1-2. It is concluded that Ns and Scx are alleles of Antp. Pc shows many functional similarities to the Antp locus, but is probably not allelic. Evidence is presented that these dominant homoeotic genes are neomorphic in nature.


1939 ◽  
Vol 127 (847) ◽  
pp. 257-277 ◽  

In a previous communication (Grüneberg 1938), a new recessive lethal mutation has been described in the rat which produces a variety of ano­malies in various parts of the body. It was shown that all these deviations from the normal, including those disturbances which lead to the death of the lethals, are ultimately caused by an anomaly of the cartilage. All the other manifestations of the gene are therefore of a secondary nature. The histology of the abnormal cartilage will be described in the first part of this paper. For the anomaly of the cartilage, no obvious cause could be discovered by morphological means. It was pointed out, however, that this does not necessarily mean that the gene acts primarily on the cartilage. There remained the possibility that the cartilage itself was only secondarily affected by some general physiological condition of the body which pro­duced no other visible changes.


2002 ◽  
Vol 80 (1) ◽  
pp. 7-14 ◽  
Author(s):  
M. ACHARYYA ◽  
R. N. CHATTERJEE

An allele of intersex (ix5) of Drosophila melanogaster has been characterized. The genetic analysis of the allele demonstrated that like other point mutations of ix, the ix5 allele also transformed diplo-X individuals into intersexes. The ix5 mutation also affects the arrangement of sex comb bristles on the forelegs of males, although they had morphologically nearly normal male genitalia. They often fail to display a sustained pattern of courtship activity when tested. Orcein-stained squash preparations of testes from ix5 males revealed a defect in spermatogenesis. Our results, taken together with those of McRobert & Tompkins (1985), indicate that the ix+ gene also functions in male sex determination.


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