scholarly journals GENETIC CHARACTERIZATION OF THE REGION BETWEEN 86F1,2 AND 87B15 ON CHROMOSOME 3 OF DROSOPHILA MELANOGASTER

Genetics ◽  
1981 ◽  
Vol 98 (4) ◽  
pp. 775-789
Author(s):  
J Gausz ◽  
H Gyurkovics ◽  
G Bencze ◽  
A A M Awad ◽  
J J Holden ◽  
...  

ABSTRACT The region between 86F1,2 and 87B15 on chromosome 3 of Drosophila melanogaster, which contains about 27 polytene chromosome bands including the 87A7 heat-shock locus, has been screened for EMS-induced visible and lethal mutations. We have recovered 268 lethal mutations that fall into 25 complementation groups. Cytogenetic localization of the complementation groups by deficiency mapping is consistent with the notion that each band encodes a single genetic function. We have also screened for mutations at the 87A7 heat shock locus, using a chromosome that has only one copy of the gene encoding the 70,000 dalton heat-shock protein (hsp70). No lethal or visible mutations at 87A7 were identified from 10,719 mutagenized chromosomes, and no female-sterile mutations at 87A7 were recovered from the 1,520 chromosomes whose progeny were tested for female fertility. We found no evidence that a functional hsp70 gene is required for development under laboratory conditions.

Genetics ◽  
1984 ◽  
Vol 106 (2) ◽  
pp. 249-265
Author(s):  
Jym Mohler ◽  
Mary Lou Pardue

ABSTRACT The region containing subdivisions 93C, 93D and 93E on chromosome 3 of Drosophila melanogaster has been screened for visible and lethal mutations. Treatment with three mutagens, γ irradiation, ethyl methanesulfonate and diepoxybutane, has produced mutations that fall into 20 complementation groups, including the previously identified ebony locus. No point mutations affecting the heat shock locus in 93D were detected; however, a pair of deficiencies that overlap in the region of this locus was isolated. Flies heterozygous in trans for this pair of deficiencies are capable of producing all of the major heat shock puffs (except 93D) and the major heat shock proteins. In addition, these flies show recovery of normal protein synthesis following a heat shock.


Genetics ◽  
1986 ◽  
Vol 112 (4) ◽  
pp. 785-802
Author(s):  
Madeline A Crosby ◽  
Elliot M Meyerowitz

ABSTRACT We have conducted a genetic analysis of the region flanking the 68C glue gene cluster in Drosophila melanogaster by isolating lethal and semilethal mutations uncovered by deficiencies which span this region. Three different mutagens were used: ethyl methanesulfonate (EMS), ethyl nitrosourea (ENU) and diepoxybutane (DEB). In the region from 68A3 to 68C11, 64 lethal, semilethal, and visible mutations were recovered. These include alleles of 13 new lethal complementation groups, as well as new alleles of rotated, low xanthine dehydrogenase, lethal(3)517 and lethal(3)B76. Six new visible mutations from within this region were recovered on the basis of their reduced viability; all proved to be semiviable alleles of lethal complementation groups. No significant differences were observed in the distributions of lethals recovered using the three different mutagens. Each lethal was mapped on the basis of complementation with overlapping deficiencies; mutations that mapped within the same interval were tested for complementation, and the relative order of the lethal groups within each interval was determined by recombination. The cytological distribution of genes within the 68A3-68C11 region is not uniform: the region from 68A2,3 to 68B1,3 (seven to ten polytene chromosome bands) contains at least 13 lethal complementation groups and the mutation low xanthine dehydrogenase; the adjoining region from 68B1,3 to 68C5,6 (six to nine bands) includes the 68C glue gene cluster, but no known lethal or visible complementation groups; and the interval from 68C5,6 to 68C10,11 (three to five bands) contains at least three lethal complementation groups and the visible mutation rotated. The developmental stage at which lethality is observed was determined for a representative allele from each lethal complementation group.


Genetics ◽  
1981 ◽  
Vol 98 (3) ◽  
pp. 505-527
Author(s):  
Jacqueline G Siegel

ABSTRACT This report describes a genetic study of salivary map region 39DE of the Drosophila genome, which is known to include the histone gene sequences (Pardue 1975; Lifton et al. 1977). Small deficiences extending proximally into 39DE were constructed by the segmental aneuploid method of Lindsley et al. (1972). The translocational deficiencies obtained in this manner were γ-irradiated to remove the Y translocational arms. One of these newly reconstituted deficiencies was then used to screen 10,000 γ-irradiated second chromosomes for lethal mutations. The 32 lethals recovered from the screen were tested against several deficiencies and markers, crossed inter se and categorized according to their genetic properties. From these data, a preliminary complementation map was constructed of salivary region 39A-39F. The salivary map positions of certain of the complementation groups suggest that the mutants in these groups may affect histone gene functions.


Genetics ◽  
1983 ◽  
Vol 105 (3) ◽  
pp. 581-600
Author(s):  
T Hazelrigg ◽  
T C Kaufman

ABSTRACT Using X-ray mutagenesis we have induced and recovered phenotypic revertants of four dominant mutations thought to be associated with the Antennapedia complex of Drosophila melanogaster. These include seven revertants of Antennapedia-73b (Antp73b), six of Extra Sex Combs of Wakimoto (Scxw), three of Deformed (Dfd) and one of Humeral (Hu). Fifteen of the 17 revertants are associated with chromosomal aberrations and localize Antp73b, Scxw and Hu to polytene chromosome bands 84B1,2. The Dfd lesion is apparently located in or adjacent to bands 84A4,5. Since all of the dominants are reverted by events that delete their respective chromosomal loci, we conclude that all four are the result of a gain-of-function lesions. Complementation analysis of the various revertant chromosomes has shown that Scxw and Hu are dominant allelic variants of the Antp locus. The Dfd lesion represents a dominant mutation at a locus just proximal to Antp and previously only occupied by recessive lethal mutations. Characterization of the revertants of Scxw and a comparison with the properties of the original mutation has revealed that the original lesion has effects on both the Antp and Sex Combs Reduced (Scr) loci and that these defects are in some cases separable by the reverting event.


Genetics ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 569-583
Author(s):  
D F Eberl ◽  
L A Perkins ◽  
M Engelstein ◽  
A J Hilliker ◽  
N Perrimon

Abstract Polytene section 17 of the X chromosome of Drosophila melanogaster, previously known to contain six putative lethal complementation groups important in oogenesis and embryogenesis, has here been further characterized genetically and developmentally. We constructed fcl+Y, a duplication of this region, which allowed us to conduct mutagenesis screens specific for the region and to perform complementation analyses (previously not possible). We recovered 67 new lethal mutations which defined 15 complementation groups within Df(1)N19 which deletes most of polytene section 17. The zygotic lethal phenotypes of these and preexisting mutations within polytene section 17 were examined, and their maternal requirements were analysed in homozygous germline clones using the dominant female sterile technique. We present evidence that an additional gene, which produces two developmentally regulated transcripts, is located in this region and is involved in embryogenesis, although no mutations in this gene were identified. In this interval of 37 to 43 polytene chromosome bands we have defined 17 genes, 12 (71%) of which are of significance to oogenesis or embryogenesis.


Genetics ◽  
1979 ◽  
Vol 93 (4) ◽  
pp. 917-934 ◽  
Author(s):  
Janos Gausz ◽  
Gabor Bencze ◽  
Henrik Gyurkovics ◽  
Michael Ashburner ◽  
David Ish-Horowicz ◽  
...  

ABSTRACT Ethyl methanesulphonate (EMS) was used to induce 39 lethal and 13 karmoisin mutations within Df(3R)kar3J, a nine-band deficiency extending from 87C1 to 87C9 (inclusive). Five complementation groups (four lethal and one visible) were identified and cytologically mapped between 8764-5 and 87C9, one complementation group per band, with the exception of complementation group A, which is localized to 87C4-5. These positions were determined using a set of overlapping deficiencies, each having at least one break-point in the 87C1-9 region. Mutations within a single complementation group have similar lethal phases or subvital phenotypes, consistent with the notion that each complementation group represents a single functional locus. No mutations localized to 87CI-C3. The inability to induce mutations in the 87C1 heat-shock puff locus is consistent with the current interpretation of a duplication of coding sequences at the 87A7 and 87C1 heat-shock puffs.


Genetics ◽  
1988 ◽  
Vol 120 (2) ◽  
pp. 503-517
Author(s):  
G E Marchant ◽  
D G Holm

Abstract The heterochromatin of the third chromosome is the largest uncharacterized region of the Drosophila melanogaster genome, and the last major block of D. melanogaster heterochromatin to be thoroughly analyzed. In the present study, this region was genetically dissected by generating and analyzing a series of attached, detached and reattached third chromosomes. Separate detachment experiments were conducted for all 12 possible combinations of four newly synthesized sister-strand compound-3L and three newly synthesized sister-strand compound-3R chromosomes. A total of 443 recessive lethal detachment products carrying putative heterochromatic deficiencies were tested for complementation in a several-stage complementation analysis. The results revealed the presence of seven separable vital regions in the heterochromatin of chromosome 3. Attempts to reattach deficiency-carrying detachment products established that six of these vital regions are on the left arm, but only one is on the right arm. An analysis of the types and frequencies of detachment-product deficiencies generated in each detachment experiment permitted the genetic characterization of the progenitor compounds. It was also possible to determine the proximal-distal orientation of the genes on each arm, and to identify possible breakpoints for each lethal detachment product produced. The results of this study suggest that vital genes in the heterochromatin of the third chromosome are not randomly distributed between, nor within, the heterochromatic blocks of the left and right arms.


Genetics ◽  
1988 ◽  
Vol 119 (3) ◽  
pp. 579-593
Author(s):  
B G Leicht ◽  
J J Bonner

Abstract In an effort to (1) characterize the 67 interval of chromosome 3 of Drosophila melanogaster genetically and (2) isolate mutations of the 67B1 small heat shock protein (hsp) gene cluster specifically, we undertook a mutational analysis of the 67A-D subinterval. Using a deficiency of the 67A2 to 67D11-13 region, Df(3L)AC1, we screened 8700 diepoxybutane-treated chromosomes and 7800 ethyl methanesulfonate-treated chromosomes for visible and lethal mutations throughout this interval and recovered 74 independent recessive lethal mutations, but no visible mutations. One of the lethal mutations, d29A6, was identified as an overlapping deficiency extending from 66F3 to 67B1. An additional 6000 diepoxybutane-treated chromosomes were screened for lethality over d29A6, yielding another four lethal mutations within the 67A2-B1 subinterval. These 78 lethal mutations, along with two others isolated in other laboratories, define 23 essential loci--6 within the 67A2-B1 subinterval and 17 within the 67A2 to D11-13 subinterval. Many of these loci appear to be required for imaginal development only, exhibiting late larval to pharate adult lethal phases. Examination of the 67A2-B1 lethal complementation groups for (1) earlier onset of lethality following a heat shock, (2) missing or altered small hsps on two-dimensional protein gels, and (3) restoration of viability by transformed wild-type copies of the small hsp genes indicates that none of these mutations affect the small hsps. On the basis of this analysis and the known homology of the genes, we conclude that the small hsps are functionally equivalent.


Genetics ◽  
1989 ◽  
Vol 121 (2) ◽  
pp. 273-280
Author(s):  
J O'Donnell ◽  
R Boswell ◽  
T Reynolds ◽  
W Mackay

Abstract Eleven chromosomal deficiencies and several rearrangements in the Pu-tud region of chromosome 2R have been generated and examined cytologically. The Pu locus has been localized to chromosome bands 57C5-6 and tud to 57C7-8. Mutagenesis within the region defined by the deletion intervals has resulted in the isolation of 92 new lethal mutations. Seventy-six of these mutations have been separated into 16 complementation groups that have been ordered and placed cytologically by deletion mapping. All new alleles fully complement tud for both lethal and grandchildless phenotypes. The largest number of new mutations, a total of 25, are Pu alleles.


Genetics ◽  
1988 ◽  
Vol 118 (1) ◽  
pp. 109-120
Author(s):  
D F Eberl ◽  
A J Hilliker

Abstract This study attempted to assay the zygotic contribution of X chromosome genes to the genetic control of embryonic morphogenesis in Drosophila melanogaster. A systematic screen for X-linked genes which affect the morphology of the embryo was undertaken, employing the phenotype of whole mount embryos as the major screening criterion. Of 800 EMS-induced lethal mutations analyzed, only 14% were embryonic lethal, and of these only a minority affected embryonic morphogenesis. By recombination and complementation analyses, the mutations that affected embryonic morphogenesis were sequestered into 26 complementation groups. Fourteen of the loci correspond to genes previously identified in a large-scale screen in which fixed cuticles were examined, and 12 new loci have been identified. Most of the mutations which disrupt embryonic morphology had specific and uniform mutant phenotypes. Mutations were recovered which disrupt major morphogenetic events such as gastrulation, germ band retraction and head involution. No mutations were found which arrest the embryos prior to blastoderm formation. However, a novel class was found, one comprised of mutations which interfere with the development of internal structures but not cuticular structures. Nevertheless, saturation of the X chromosome for genes important for embryonic morphogenesis is probably incomplete.


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