Modulation of reproductive output in Drosophila by spectral properties of ambient light

1986 ◽  
Vol 64 (2) ◽  
pp. 537-542
Author(s):  
Bruce Buhr ◽  
Wayne Wiens ◽  
Marvin Dirks ◽  
Hugh Riordan

The net reproductive output was determined for two strains of Drosophila melanogaster, wild-type (+) and white-eyed (w), under conditions of varied wavelength and intensity of illumination. The reproductive output of wild-type flies raised under blue light (max. 470 nm) was significantly lower (p < 0.01) than that of organisms grown under red (max. 630 and 660 nm) or green(max. 530 nm) illumination, or under conditions of total darkness. In contrast, blue light did not depress the reproductive output of white-eyed flies. The differential reproductive response of the two strains, then, appears to be related to genetically determined properties of the eye. Changes in the radiant fluence rate over a 10-fold range were not found to significantly modify reproductive output of wild-type flies, and if flies were illuminated with red, green, or blue light at identical fluence rates, those under blue, again, had a significantly lower (p < 0.01) reproductive output than the other two. The data suggest that the emission spectrum, not the radiant light intensity, significantly affects the number of offspring produced per parent.

Genetics ◽  
1998 ◽  
Vol 149 (3) ◽  
pp. 1575-1585
Author(s):  
Edward P Bruggemann ◽  
Bernard Doan ◽  
Korie Handwerger ◽  
Gisela Storz

Abstract The Arabidopsis HY4 gene encodes the nonessential blue light photoreceptor CRY1. Loss-of-function hy4 mutants have an elongated hypocotyl phenotype after germination under blue light. We previously analyzed 20 independent hy4 alleles produced by fast neutron mutagenesis. These alleles were grouped into two classes based on their genetic behavior and corresponding deletion size: (1) null hy4 alleles that were semidominant over wild type and contained small or moderate-sized deletions at HY4 and (2) null hy4 alleles that were recessive lethal and contained large HY4 deletions. Here we describe one additional fast neutron hy4 mutant, B144, that did not fall into either of these two classes. Mutant B144 was isolated as a heterozygote with an intermediate hy4 phenotype. One allele from this mutant, hy4-B144Δ, contains a large deletion at HY4 and is recessive lethal. The other allele from this mutant, HY4-B144*, appears to be intact and functional but is unstable and spontaneously converts to a nonfunctional hy4 allele. In addition, HY4-B144* is lethal in homozygotes and suppresses local recombination. We discuss genetic and epigenetic mechanisms that may account for the unusual behavior of the HY4-B144* allele.


Genetics ◽  
1986 ◽  
Vol 113 (2) ◽  
pp. 305-319
Author(s):  
Craig H Marcus ◽  
Anne E Zitron ◽  
David A Wright ◽  
R Scott Hawley

ABSTRACT rDNA magnification in Drosophila melanogaster is defined experimentally as the ability of bb/Ybb  - males to produce exceptional progeny that are wild type with respect to rDNA associated phenotypes. Here, we show that some of these bobbed-plus progeny result not from genetic reversion at the bb locus but rather from variants at two or more autosomal loci that ameliorate the bobbed phenotype of rDNA deficient males in Drosophila. In doing so we resolve several aspects of a long-standing paradox concerning the phenomenon of rDNA magnification. This problem arose from the use of two genetic assays, which were presumed to be identical, but paradoxically, produced conflicting data on both the kinetics of reversion and the stability of magnified bb  + chromosomes. We resolve this problem by demonstrating that in one assay bobbed-plus progeny arise primarily by genetic reversion at the bobbed locus, whereas in the other assay bobbed-plus progeny arise both by reversion and by an epistatic effect of autosomal modifiers on the bobbed phenotype. We further show that such modifiers can facilitate the appearance of phenotypically bobbed-plus progeny even under conditions where genetic reversion is blocked by magnification defective mutants. Finally, we present a speculative model relating the action of these modifiers to the large increases in rDNA content observed in males undergoing magnification.


1991 ◽  
Vol 57 (3) ◽  
pp. 235-243 ◽  
Author(s):  
Claude Bazin ◽  
Françoise Lemeunier ◽  
Georges Periquet ◽  
Joël Silber

SummaryWe describe herein, a new unstable mutant of the vestigial locus, isolated from a French natural population. From this mutant vestigialalmost (vgal) wild-type flies (vgal+) and extreme vg phenotypes (vge) arose spontaneously without genomic shock. The occurrence of vgal+ or vge alleles depends mostly on the breeding temperature; vgal+ revertants arose principally at low temperature (21 °C) and vge at 28 °C. These events occur mainly in the male germ line and the phenomenon appears to be premeiotic. Our results with in situ hybridization experiments and Southern blots show that the vgal mutation is due to a 2 kb DNA insertion, which is a deleted hobo element. Genetic and molecular analyses show that two distinct events may underly the wild-type revertants. One is the excision of the resident hobo element, the other a further deletion (about 300 bp in the example characterized herein). The vge mutation is probably due to a deletion of vestigial sequences flanking the hobo insertion.


Genetics ◽  
1978 ◽  
Vol 88 (3) ◽  
pp. 469-486 ◽  
Author(s):  
A García-Bellido ◽  
P Santamaria

ABSTRACT The interpretation of the wild-type function of a gene depends on our knowledge of the phenotype caused by its absence. We have first defined the genetic extent of the achaete-scute system by studying the phenotype of different terminal and intercalary deficiencies including these genes. When these deficiencies were lethal, we have defined the phenoeffective phase of lethality and studied their phenotype in genetic mosaics (gynandromorphs and mitotic recombination clones). The achaete-scute system affects two functions, one necessary for the differentiation of the embryonic (central?) nervous system and the other necessary for the differentiation of peripheral nervous elements of the chaetes and sensillae of the adult cuticle. The possibility that these functions correspond to differential expression of a single mechanism is discussed.


Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 75-83
Author(s):  
H Roiha ◽  
G M Rubin ◽  
K O'Hare

Abstract DNA from the singed gene of Drosophila melanogaster was isolated using an inversion between a previously cloned P element at cytological location 17C and the hypermutable allele singed-weak. Five out of nine singed mutants examined have alterations in their DNA maps in this region. The singed locus is a hotspot for mutation during P-M hybrid dysgenesis, and we have analyzed 22 mutations induced by P-M hybrid dysgenesis. All 22 have a P element inserted within a 700-bp region. The precise positions of 10 P element insertions were determined and they define 4 sites within a 100-bp interval. During P-M hybrid dysgenesis, the singed-weak allele is destabilized, producing two classes of phenotypically altered derivatives at high frequency. In singed-weak, two defective P elements are present in a "head-to-head" or inverse tandem arrangement. Excision of one element results in a more extreme singed bristle phenotype while excision of the other leads to a wild-type bristle phenotype.


Genetics ◽  
1978 ◽  
Vol 90 (4) ◽  
pp. 699-712
Author(s):  
L Sandler ◽  
Paul Szauter

ABSTRACT Crossing over was measured on the normally achiasmate fourth chromosome in females homozygous for one of our different recombination-defective meiotic mutants. Under the influence of those meiotic mutants that affect the major chromosomes by altering the spatial distribution of exchanges, meiotic fourth-chromosome recombinants were recovered irrespective of whether or not the meiotic mutant decreases crossing over on the other chromosomes. No crossing over, on the other hand, was detected on chromosome 4 in either wild type or in the presence of a meiotic mutant that decreases the frequency, but that does not affect the spatial distribution, of exchange on the major chromosomes. It is concluded from these observations that (a) in wild type there are regional constraints on exchange that can be attenuated or eliminated by the defects caused by recombination-defective meiotic mutants; (b) these very constraints account for the absence of recombination on chromosome 4 in wild type; and (c) despite being normally achiasmate, chromosome 4 responds to recombination-defective meiotic mutants in the same way as do the other chromosomes.


1982 ◽  
Vol 40 (1) ◽  
pp. 19-32 ◽  
Author(s):  
K. Bruce Jacobson ◽  
E. H. Grell ◽  
John J. Yim ◽  
April L. Gardner

SUMMARYThe suppressor of sable [su(s)2] restores the function of vermilion (v), purple (pr) and speck (sp) as well as sable (s) in Drosophila melanogaster. In this report various alleles of su(s) are compared for their relative effectiveness on three target mutations, v, pr and sp. Three criteria for suppression of pr and v were employed: visible phenotype, eye pigment levels (drosopterins and xanthommatin) and enzyme levels (sepiapterin synthase and tryptophan oxygenase). For sp only the visible phenotype was examined. By all three criteria pr was found to be more easily suppressed than v; v and sp were comparable. By use of pr with various alleles of su(s) either homozygously or in heterozygous combination with su(s)+, the extent of suppression of pr can be best demonstrated by observing the levels of sepiapterin synthase; normal levels of drosopterins were found in females when sepiapterin synthase was only 20% of normal. On the other hand, the extent of suppression of v is best demonstrated by the amount of xanthommatin eye pigment, because even the suppressed vermilion fly has < 10% of wild-type activity of tryptophan oxygenase when 1-day-old flies are examined; in older flies this enzyme can be as high as 50% of wild type. From these results we also demonstrated that su(s)2, and other alleles, are not recessive but, in heterozygous combination with su(s)+, cause marked suppression of pr and slight, but reproducible, suppression of v. The purple mutation, therefore, is particularly useful for studying the mechanism of suppression as well as for obtaining new mutant alleles of su(s).


Genetics ◽  
1979 ◽  
Vol 91 (2) ◽  
pp. 255-274
Author(s):  
M Gatti ◽  
G Santini ◽  
S Pimpinelli ◽  
G Olivieri

ABSTRACT Neural ganglia of wild type third-instar larvae of Drosophila melanogasier were incubated for 13 hours at various concentrations of BUdR (1, 3, 9, 27 μg/ml) . Metaphases were collected with colchicine, stained with Hoechst 33258, and scored under a fluorescence microscope. Metaphases in which the sister chromatids were clearly differentiated were scored for the presence of sister-chromatid exchanges (SCEs) . At the lowest concentration of BUdR (1 μg/ml), no SCEs were observed in either male or female neuroblasts. The SCEs were found at the higher concentrations of BUdR (3, 9 and 27 μg/ml) and with a greater frequency in females than in males. Therefore SCEs are not a spontaneous phenomenon in D. melanogasier, but are induced by BUdR incorporated in the DNA. A striking nonrandomness was found in the distribution of SCEs along the chromosomes. More than a third of the SCEs were clustered in the junctions between euchromatin and heterochromatin. The remaining SCEs were preferentially localized within the heterochromatic regions of the X chromosome and the autosomes and primarily on the entirely heterochromatic Y chromosome.—In order to find an alternative way of measuring the frequency of SCEs in Drosophila neuroblasts, the occurrence of double dicentric rings was studied in two stocks carrying monocentric ring-X chromosomes. One ring chromosome, C(I)TR94-2, shows a rate of dicentric ring formation corresponding to the frequency of SCEs observed in the BUdR-labelled rod chromosomes. The other ring studied, R(1)2, exhibits a frequency of SCEs higher than that observed with both C(I)TR94-2 and rod chromosomes.


Genetics ◽  
1989 ◽  
Vol 122 (4) ◽  
pp. 881-890 ◽  
Author(s):  
S I Tsubota ◽  
D Rosenberg ◽  
H Szostak ◽  
D Rubin ◽  
P Schedl

Abstract We have cloned the B breakpoint in Drosophila melanogaster using DNA from a P-M-induced revertant of B, which has a P element inserted at the B breakpoint. The analysis of the B DNA reveals that there is a transposable element, B104, right at the breakpoint. This suggests that this element may have been involved in the generation of the B breakpoint and the associated tandem duplication. One possible mechanism to generate the B duplication is a recombination event between two B104 elements, one at 16A1 and the other at 16A7. DNA sequencing data of the junctions of the B104 element support this model. Four partial revertants of B are the result of insertions of transposable elements very close to the B breakpoint. This supports the hypothesis that the breakpoint is the cause of the B mutation. The clones from B were used to isolate wild-type clones from 16A1, the location of the Bar gene. Four rearrangement breakpoints associated with various Bar mutations map within a 37-kb region, suggesting that the Bar gene is very large.


Genetics ◽  
1988 ◽  
Vol 118 (3) ◽  
pp. 499-508
Author(s):  
A de-la-Concha ◽  
U Dietrich ◽  
D Weigel ◽  
J A Campos-Ortega

Abstract The neurogenic genes of Drosophila melanogaster are involved in the decision of ectodermal cells to take on a neural or an epidermal fate. We present evidence in support of the notion that six of the neurogenic genes are functionally related. We studied the phenotype of embryos lacking one of the neurogenic genes in the presence of an increased dosage of the wild-type allele of another neurogenic gene. Our analysis also included the Hairless locus, whose function is related to that of the neurogenic genes, as well as to many other genes. The effects observed were asymmetric in that triploidy for a given gene modified the phenotype of loss of the function of another gene, but triploidy of the latter gene did not modify the phenotype of loss of the function of the former gene. These asymmetries allowed us to establish a polarity of gene interactions, as well as to order the genes according to the assumed ability of some of them to modify the activity of others. In this sequence, almondex is the first link and Enhancer of split the last one. Our evidence suggests that the function of big brain is independent of the function of the other six. The consequences of this arrangement for the commitment of ectodermal cells are discussed.


Sign in / Sign up

Export Citation Format

Share Document