scholarly journals Hypomorphic mutations in the larval photokinesis A (lphA) gene have stage-specific effects on visual system function in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1623-1629
Author(s):  
B Gordesky-Gold ◽  
J M Warrick ◽  
A Bixler ◽  
J E Beasley ◽  
L Tompkins

Abstract Of the many genes that are expressed in the visual system of Drosophila melanogaster adults, some affect larval vision. However, with the exception of one X-linked mutation, no genes that have larval-specific effects on visual system structure or function have previously been reported. We describe the isolation and characterization of two mutant alleles that define the larval photokinesis A (lphA) gene, one allele of which is associated with a P-element insertion at cytogenetic locus 8E1-10. Larvae that express lphA mutations are, like normal animals, negatively photokinetic, but they are less responsive to white light than lphA + controls. Larvae that are heterozygous in trans for a mutant lphA allele and a deficiency that uncovers the lphA locus are blind, which indicates that the mutant allele is hypomorphic. lphA larvae respond normally to odorants and taste stimuli. Moreover, the lphA mutations do not affect adult flies' fast phototaxis or visually driven aspects of male sexual behavior, and electroretinograms recorded from the compound eyes of lphA/deficiency heterozygotes and lphA1/lphA2 females are normal. These observations suggest that the lphA gene affects a larval-specific aspect of visual system function.

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 249-258
Author(s):  
Angela M Coveny ◽  
Tammy Dray ◽  
Gregory B Gloor

Abstract We examined the influence that heterologous sequences of different sizes have on the frequency of double-strand-break repair by gene conversion in Drosophila melanogaster. We induced a double-strand break on one X chromosome in female flies by P-element excision. These flies contained heterologous insertions of various sizes located 238 bp from the break site in cis or in trans to the break, or both. We observed a significant decrease in double-strand-break repair with large heterologous insertions located either in cis or in trans to the break. Reestablishing the homology by including the same heterologous sequence in cis and in trans to the double-strand break restored the frequency of gene conversion to wild-type levels. In one instance, an allelic nonhomologous insertion completely abolished repair by homologous recombination. The results show that the repair of a double-strand break by gene conversion requires chromosome pairing in the local region of the double-strand break.


1984 ◽  
Vol 4 (7) ◽  
pp. 1343-1353 ◽  
Author(s):  
W W Mattox ◽  
N Davidson

We isolated recombinant lambda phage clones spanning 49 kilobases of DNA which contain the Beadex and heldup-a loci of Drosophila melanogaster. These cloned DNAs were used to analyze the structure of eight dominant mutant alleles of the Beadex locus which show increased gene activity. A region, only 700 base pairs in length, is altered in each of these mutants. Six of the mutations have DNA insertions within this segment. Most of these insertions resemble retrovirus-like transposable elements. In one case (Beadex2) the inserted sequences are homologous to the gypsy transposon family. The other two Beadex alleles were induced by hybrid dysgenesis and suffered deletions which included at least part of the 700-base-pair segment. These deletions appear to have resulted from imprecise excision or deletion of a nearby P element found in the wild-type parental strain. Analysis of one heldup-a allele (heldup-aD30r) indicates that a similar P element-mediated event is responsible for this lesion. In this mutant, deletion of sequences no more than 1,600 base pairs from the Beadex locus accompanies the loss of heldup-a function. The deleted sequences in heldup-aD30r include the entire 700-base-pair segment within which at least part of the Beadex locus resides, yet these flies have no Beadex phenotype. This indicates that a functional heldup-a gene is necessary for expression of the Beadex phenotype. Together, these results suggest that the Beadex functional domain is contained within a short segment of DNA near the heldup-a gene and support the hypothesis that the Beadex locus functions as a cis-acting negative regulatory element for the heldup-a gene.


1984 ◽  
Vol 4 (7) ◽  
pp. 1343-1353
Author(s):  
W W Mattox ◽  
N Davidson

We isolated recombinant lambda phage clones spanning 49 kilobases of DNA which contain the Beadex and heldup-a loci of Drosophila melanogaster. These cloned DNAs were used to analyze the structure of eight dominant mutant alleles of the Beadex locus which show increased gene activity. A region, only 700 base pairs in length, is altered in each of these mutants. Six of the mutations have DNA insertions within this segment. Most of these insertions resemble retrovirus-like transposable elements. In one case (Beadex2) the inserted sequences are homologous to the gypsy transposon family. The other two Beadex alleles were induced by hybrid dysgenesis and suffered deletions which included at least part of the 700-base-pair segment. These deletions appear to have resulted from imprecise excision or deletion of a nearby P element found in the wild-type parental strain. Analysis of one heldup-a allele (heldup-aD30r) indicates that a similar P element-mediated event is responsible for this lesion. In this mutant, deletion of sequences no more than 1,600 base pairs from the Beadex locus accompanies the loss of heldup-a function. The deleted sequences in heldup-aD30r include the entire 700-base-pair segment within which at least part of the Beadex locus resides, yet these flies have no Beadex phenotype. This indicates that a functional heldup-a gene is necessary for expression of the Beadex phenotype. Together, these results suggest that the Beadex functional domain is contained within a short segment of DNA near the heldup-a gene and support the hypothesis that the Beadex locus functions as a cis-acting negative regulatory element for the heldup-a gene.


Genetics ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 373-380
Author(s):  
D H Teng ◽  
L B Bender ◽  
C M Engele ◽  
S Tsubota ◽  
T Venkatesh

Abstract The complementary lethal interaction between the prune (pn) and Killer of prune loci of Drosophila melanogaster is an unusual and highly specific phenomenon. A lesion in pn results in a brownish-purple color of the compound eyes, while the conditional dominant Killer of prune mutation exhibits no phenotype by itself. However, a hemizygous or homozygous pn mutant carrying a copy of the Killer of prune gene dies during the late second to third instar stage of larval development. As a step toward understanding the molecular nature of this lethality and the role of pn in pigment biosynthesis, we have cloned the pn locus by using a transposon tag in the P element-induced allele, pn38. In addition, seven independent revertant lines were generated by the remobilization of transposons in pn38. The pn gene is located in a region that is transcriptionally active, and the isolated cDNAs that correspond to this area fall into three transcription units: I, II and III. Southern analysis shows that the restriction fragment length polymorphisms in five pn alleles are localized within a 1.2-kilobase genomic fragment, of which only transcription unit II is a part. The cDNA of this unit recognizes 1.65- and 1.8-kilobase messages in wild-type Drosophila adult head and body tissues that are absent or extremely reduced in pn mutants. Taken together, the results suggest that transcription unit II defines a part of the pn locus and its cDNA encodes a putative structural gene of pn.


Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1127-1135
Author(s):  
T R Heslip ◽  
R B Hodgetts

Abstract Targeted transposition is the replacement of one P element with another. We are exploiting this unique property of P elements to study the complex regulatory domain of the Dopa decarboxylase (Ddc) gene in Drosophila melanogaster. P element constructs targeted to the same site in the genome will be subjected to the same position effect. This allows the subtle effects typical of most mutations in the Ddc regulatory region to be measured in the absence of the variable influences of position effects which are associated with the current method of germline transformation. We have investigated some of the parameters affecting targeted transposition of a Ddc transposon, P[Ddc], into a P element allele at the vestigial locus. These events were detected by an increased mutant vg phenotype. The location of the donor transposon in cis or in trans to the target had little effect on the frequency of targeting. Likewise, the mobility of different donor elements, as measured by their rate of transposition to a different chromosome, varied nearly 20-fold, while the rate of targeted transposition was very similar between them. All targeted alleles were precise replacements of the target P element by P[Ddc], but in several cases the donor was inserted in the opposite orientation. The targeted alleles could be described as the result of a replicative, conversion-like event.


Genetics ◽  
1990 ◽  
Vol 124 (1) ◽  
pp. 145-156
Author(s):  
B P Brunk ◽  
P N Adler

Abstract The isolation of gain of function mutations has allowed the identification of a number of genes which are important in the normal development of the organism. We report here the isolation and characterization of Aristapedioid, a gain of function mutation which causes a partial transformation of arista towards tarsus and the loss or decrease in size of the dorso-central and scutellar bristles. Aristapedioid is the result of a P element mediated inversion which juxtaposes unrelated DNA adjacent to Suppressor 2 of zeste, causing a gain of function mutation in that gene.


1998 ◽  
Vol 72 (1) ◽  
pp. 19-24 ◽  
Author(s):  
DOROTHY B. CURRIE ◽  
TRUDY F. C. MACKAY ◽  
LINDA PARTRIDGE

A set of Drosophila melanogaster was generated, all derived from a common isogenic base stock and each with a single new P element insert on the second or third chromosome. The lines were scored for their body size, measured as thorax length. P inserts were associated with highly significant effects on body size, although the genotypes of the construct and of the control prevented deduction of the direction of mutant effects. In addition to mutant effects on the thorax length of both sexes, there were also highly significant sex-specific effects. Pleiotropic effects of inserts affecting body size on viability and bristle number, as ascertained in a separate study of these lines (Lyman et al., 1996), were weak. Insertional mutagenesis is potentially a powerful tool for investigating the genes involved in size-control in Drosophila, but the technique requires fine tuning for use on polygenic and fitness-related traits.


Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1601-1610 ◽  
Author(s):  
Y H Svoboda ◽  
M K Robson ◽  
J A Sved

Abstract Male recombination, not normally present in Drosophila melanogaster, can be produced at high rates when target P elements at homologous sites are combined in the presence of transposase protein. We have produced a set of elements by in situ deletion of a particular insertion and have found elements that have deletions stretching into either end. Elements were tested in pairs to see whether they complement each other in their ability to induce recombination. The combination of elements that are deficient for the same end produces very little recombination, but the combination of a right-end and a left-end element can generate recombination values higher than given by two complete P[CaSpeR] elements at homologous sites. This strongly suggests that "hybrid" P elements, containing ends from two different elements, can be recognized by transposase protein. We have also examined genotypes containing a normal and an end-deficient element and found that they yield reasonably high levels of recombination. We interpret the resultant gametes from such genotypes as showing that the majority of events in this genotype derive from the association of complementary ends from the same element, whereas the complementary ends from elements in trans associate in only a minority of cases.


Genetics ◽  
2001 ◽  
Vol 159 (4) ◽  
pp. 1631-1642 ◽  
Author(s):  
Stéphane Ronsseray ◽  
Antoine Boivin ◽  
Dominique Anxolabéhère

Abstract In Drosophila, clusters of P transgenes (P-lac-w) display a variegating phenotype for the w marker. In addition, X-ray-induced rearrangements of chromosomes bearing such clusters may lead to enhancement of the variegated phenotype. Since P-lacZ transgenes in subtelomeric heterochromatin have some P-element repression abilities, we tested whether P-lac-w clusters also have the capacity to repress P-element activity in the germline. One cluster (T-1), located on a rearranged chromosome (T2;3) and derived from a line bearing a variegating tandem array of seven P-lac-w elements, partially represses the dysgenic sterility (GD sterility) induced by P elements. This cluster also strongly represses in trans the expression of P-lacZ elements in the germline. This latter suppression shows a maternal effect. Finally, the combination of variegating P-lac-w clusters and a single P-lacZ reporter inserted in subtelomeric heterochromatic sequences at the X chromosome telomere (cytological site 1A) leads to strong repression of dysgenic sterility. These results show that repression of P-induced dysgenic sterility can be elicited in the absence of P elements encoding a polypeptide repressor and that a transgene cluster can repress the expression of a single homologous transgene at a nonallelic position. Implications for models of transposable element silencing are discussed.


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