scholarly journals Genetic Analysis of Delta, a Neurogenic Gene of Drosophila melanogaster

Genetics ◽  
1987 ◽  
Vol 116 (3) ◽  
pp. 433-445
Author(s):  
Harald Vässin ◽  
Jose A Campos-Ortega
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Phenotypic Expression ◽  
Wild Type Allele ◽  
Wild Type ◽  
Type Allele ◽  
Embryonic Lethal ◽  
Complementation Groups ◽  
Interallelic Complementation ◽  
Hypomorphic Alleles

ABSTRACT We report here the results of a genetic analysis of the gene Delta (Dl) of Drosophila melanogaster. Dl has been mapped to the band 92A2, on the basis of two pieces of evidence: (1) this band is the common breakpoint of several chromosomal aberrations associated with Dl mutations and (2) recombination mapping of alleles of five different lethal complementation groups that are uncovered by Df(3R)DlFX3 (breakpoints at 91F11; 92A3). Dl was found to map most distally of all five complementation groups. The analysis of a large number of Dl alleles demonstrates the considerable genetic and functional complexity of Dl. Three types of Dl alleles are distinguishable. Most alleles behave as amorphic or hypomorphic recessive embryonic lethal alleles, which in addition cause various defects in heterozygosity over the wild-type allele. The defects are due to haplo-insufficient expression of the locus and can be suppressed by a duplication of the wild-type allele. The second class is comprised of three alleles with antimorphic expression. The phenotype of these alleles can only be reduced, rather than suppressed, by a duplication of the wild-type allele. The third group is comprised of three visible, predominantly hypomorphic alleles with an antimorphic component of phenotypic expression. The pattern of interallelic complementation is complex. On the one hand, there is a group of hypomorphic, fully penetrant embryonic lethal alleles which complement each other. On the other hand, most alleles, including all amorphic alleles, are viable over the visible ones; alleles of antimorphic expression, however, are lethal over visible alleles. These results are compatible with a rather complex genetic organization of the Dl locus.

Genetic Analysis of theHybrid male rescueLocus of Drosophila

Genetics ◽  
2000 ◽  
Vol 155 (1) ◽  
pp. 225-231 ◽  
Author(s):  
H Allen Orr ◽  
Shannon Irving
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Wild Type Allele ◽  
Wild Type ◽  
Hybrid Male ◽  
Gain Of Function ◽  
Hybrid Inviability ◽  
Type Allele ◽  
Proximate Causes

AbstractSeveral hybrid rescue mutations—alleles that restore the viability of normally lethal hybrids—have been discovered in Drosophila melanogaster and its relatives. Here we analyze one of these genes, Hybrid male rescue (Hmr), asking two questions about its role in hybrid inviability. (1) Does the wild-type allele from D. melanogaster (Hmrmel) cause hybrid embryonic inviability? (2) Does Hmrmel cause hybrid larval inviability? Our results show that the wild-type product of Hmr is neither necessary nor sufficient for hybrid embryonic inviability. Hmrmel does, however, appear to lower the viability of hybrid larvae. The data further suggest (though do not prove) that Hmrmel acts as a gain-of-function poison in hybrids. These findings support previous claims that hybrid embryonic and larval lethalities are genetically distinct and suggest that Hmrmel is at least one of the proximate causes of hybrid larval inviability.

THE DEVELOPMENTAL GENETICS OF THE TEMPERATURE-SENSITIVE LETHAL ALLELE OF THE SUPPRESSOR OF FORKED, l(1)su(f)ts67g, IN DROSOPHILA MELANOGASTER

Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 487-510
Author(s):  
Marianne E Dudick ◽  
Theodore R F Wright ◽  
Lynda Lee Brothers
Keyword(s):  
Drosophila Melanogaster ◽  
Ribosomal Protein ◽  
Sensitive Period ◽  
Developmental Genetics ◽  
Temperature Sensitive ◽  
Wild Type Allele ◽  
Wild Type ◽  
Type Allele ◽  
Lethal Allele

ABSTRACT A temperature-sensitive lethal allele of suppressor of forked, l(1)su(f)ts67g (ts67), has been discovered and characterized as follows: Flies which are hemizygous for ts67 live at 18° and 25° but die at 30° primarily as larvae. The temperature-sensitive period for ts67 homozygotes or hemizygotes begins in second instar and ends at pupation. ts67 is lethal at 30° when heterozygous with suppressor of forked (su(f)), a deficiency for suppressor of forked (su(f)  -), and a non-conditional lethal allele of suppressor of forked (3DES). It is viable at 30° when heterozygous with the wild-type allele of suppressor of forked. At 25° but not at 18° forked bristles are suppressed in flies of the following genotypes: fsts67/Y, fsts67/fsts67, fsts67/fssu(f), futs67/fs3DES, futs67/fssu(f)  -, futs67/fssu(f). There is some suppression of forked bristles at 25° in the heterozygote, fsts67/fs+su(f). The forked bristle phenotype is not suppressed at either temperature in flies of the genotypes futs67/Y, futs67/futs67/ (fs and fu indicating suppressible and unsuppressible alleles of forked). The temperature-sensitive period for suppression of forked bristles begins at pupation and extends through the period of bristle synthesis. The deficiency phenotype (bristles reduced in size or absent, wing wrinkled or blistered, eyes rough) typical of flies of the genotype fssu(f)/fssu(f)  - at 18° and 25°, is exhibited by flies of the genotypes fsts67/fssu(f)  - at 25° and futs67/fssu(f) at 29°. An allele of lozenge (lz1) which can be suppressed by su(f) is suppressed at 25° but not at 18° in lz1ts67/Y males. ts67 homozygous females are fertile at 25° but sterile at 30°. The hypothesis is discussed that the su(f) locus codes for a ribosomal protein and that suppression and enhancement are affected by mutations at the locus by mutant ribosome-induced misreading. The possibility is presented that ts67 may be used to determine the translation time in development of any gene.

scholarly journals THE REGULATION OF WHITE LOCUS EXPRESSION: A DOMINANT MUTANT ALLELE AT THE WHITE LOCUS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1980 ◽  
Vol 95 (2) ◽  
pp. 341-353
Author(s):  
Paul M Bingham
Keyword(s):  
Drosophila Melanogaster ◽  
Mutant Allele ◽  
Chromosomal Rearrangements ◽  
Wild Type Allele ◽  
Wild Type ◽  
Type Allele ◽  
Dominant Mutant ◽  
White Locus ◽  
Somatic Pairing

ABSTRACT A new mutant allele (wDZL)at the white locus of Drosophila melanogaster is dominant to the wild-type allele, but apparently only when the two alleles are synapsed. When chromosomal rearrangements prevent somatic pairing between the two white alleles, wDZL is rendered recessive to wild type. This observation suggests that the dominance of wDZL is sensitive to a synapsis (transvection) effect. On the basis of this and other properties, it is proposed that wDZL causes the repression of transcription of a synapsed w+ allele, but not of a w+ allele elsewhere in the same nucleus. One model to account for this supposes that wDzL produces a repressor of white-locus transcription. This repressor is presumed to be so unstable that other white genes, removed from wDZL but in the same nucleus, are not detectably repressed. These properties may be simply understood if it is assumed that the repressor produced by the wDZL allele is an RNA molecule.

scholarly journals HYPOMORPHIC LETHAL MUTATIONS AND THEIR IMPLICATIONS FOR THE INTERPRETATION OF LETHAL COMPLEMENTATION STUDIES IN DROSOPHILA

Genetics ◽  
1983 ◽  
Vol 105 (4) ◽  
pp. 957-968
Author(s):  
David Nash ◽  
Frank C Janca
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Small Region ◽  
Essential Genes ◽  
Activity Levels ◽  
Lethal Mutations ◽  
Homozygous Mutant ◽  
Complementation Groups ◽  
Interallelic Complementation ◽  
Hypomorphic Alleles

ABSTRACT In a small region of the X chromosome of Drosophila melanogaster, we have found that a third of the mutations that appear to act as lethals in segmental haploids are viable in homozygous mutant individuals. These viable mutations fall into four complementation groups. The most reasonable explanation of these mutations is that they are a subset of functionally hypomorphic alleles of essential genes: hypomorphic mutations with activity levels above a threshold required for survival, but below twice that level, should behave in this manner. We refer to these mutations as "haplo-specific lethal mutations." In studies of autosomal lethals, haplo-specific lethal mutations can be included in lethal complementation tests without being identified as such. Accidental inclusion of disguised haplo-specific lethals in autosomal complementation tests will generate spurious examples of interallelic complementation.

scholarly journals Genetic analysis of the brahma gene of Drosophila melanogaster and polytene chromosome subdivisions 72AB.

Genetics ◽  
1994 ◽  
Vol 137 (3) ◽  
pp. 803-813 ◽  
Author(s):  
B J Brizuela ◽  
L Elfring ◽  
J Ballard ◽  
J W Tamkun ◽  
J A Kennison
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Polytene Chromosome ◽  
Single Gene ◽  
Homeotic Genes ◽  
Catalytic Subunits ◽  
Gtp Binding ◽  
Dependent Protein ◽  
Complementation Groups ◽  
Interallelic Complementation

Abstract The brahma gene is required for activation of the homeotic genes of the Antennapedia and bithorax complexes in Drosophila. We have isolated and characterized 21 mutations in brahma. We show that both maternal and zygotic functions of brahma are required during embryogenesis. In addition, the severe abnormalities caused by loss of maternal brahma expression show that the homeotic genes are not the only targets for brahma activation. The complex pattern of interallelic complementation for the 21 brahma alleles suggests that brahama may act as a multimer. In addition to mutations in brahma, we have isolated mutations in four other essential genes within polytene chromosome subdivisions 72AB. Based on a compilation of similar studies that include about 24% of the genome, we estimate that about 3600 genes in Drosophila can mutate to cause recessive lethality, with fewer than 900 additional genes essential only for gametogenesis. We have identified three times more transcripts than lethal complementation groups in 72AB. One transcript in 72AB is the product of the essential arf-like gene and encodes a member of the ARF subfamily of small GTP-binding proteins. Two other transcripts are probably the products of a single gene whose protein products are similar to the catalytic subunits of cAMP-dependent protein kinases.

scholarly journals Functional interactions of neurogenic genes of Drosophila melanogaster.

Genetics ◽  
1988 ◽  
Vol 118 (3) ◽  
pp. 499-508
Author(s):  
A de-la-Concha ◽  
U Dietrich ◽  
D Weigel ◽  
J A Campos-Ortega
Keyword(s):  
Drosophila Melanogaster ◽  
The Other ◽  
Gene Interactions ◽  
Wild Type Allele ◽  
Wild Type ◽  
Present Evidence ◽  
Type Allele ◽  
Functional Interactions ◽  
Neurogenic Genes ◽  
Enhancer Of Split

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.

scholarly journals Genetic Analysis of the Heterochromatin of Chromosome 3 in Drosophila Melanogaster. II. Vital Loci Identified through Ems Mutagenesis.

Genetics ◽  
1988 ◽  
Vol 120 (2) ◽  
pp. 519-532
Author(s):  
G E Marchant ◽  
D G Holm
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Single Copy ◽  
Chromosome 3 ◽  
Temperature Sensitive ◽  
Chromosome 2 ◽  
Complementation Groups ◽  
Sensitive Allele ◽  
Interallelic Complementation ◽  
The Right

Abstract Chromosome 3 of Drosophila melanogaster contains the last major blocks of heterochromatin in this species to be genetically analyzed. Deficiencies of heterochromatin generated through the detachment of compound-3 chromosomes revealed the presence of vital loci in the heterochromatin of chromosome 3, but an extensive complementation analysis with various combinations of lethal and nonlethal detachment products gave no evidence of tandemly repeated vital genes in this region. These findings indicate that the heterochromatin of chromosome 3 is genetically similar to that of chromosome 2. A more thorough genetic analysis of the heterochromatic regions has been carried out using the chemical mutagen ethyl methanesulfonate (EMS). Seventy-five EMS-induced lethals allelic to loci uncovered by detachment-product deficiencies were recovered and tested for complementation. In total, 12 complementation groups were identified, ten in the heterochromatin to the left of the centromere and two to the right. All but two complementation groups in the left heterochromatic block could be identified as separate loci through deficiency mapping. The interallelic complementation observed between some EMS-induced lethals, as well as the recovery of a temperature-sensitive allele for each of the two loci, provided further evidence that single-copy, transcribed vital genes reside in the heterochromatin of chromosome 3. Cytological analysis of three detachment-product deficiencies provided evidence that at least some of the genes uncovered in this study are located in the most distal segments of the heterochromatin in both arms. This study provides a detailed genetic analysis of chromosome 3 heterochromatin and offers further information on the genetic nature and heterogeneity of Drosophila heterochromatin.

scholarly journals CYP2C19 Polymorphisms in Indonesia: Comparison among Ethnicities and the Association with Clinical Outcomes

Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 300
Author(s):  
Muhammad Miftahussurur ◽  
Dalla Doohan ◽  
Ari Fahrial Syam ◽  
Iswan Abbas Nusi ◽  
Phawinee Subsomwong ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Clinical Outcomes ◽  
Proton Pump ◽  
Poor Metabolizers ◽  
Wild Type Allele ◽  
Wild Type ◽  
Type Allele ◽  
Sydney System ◽  
Intermediate Metabolizers ◽  
Cyp2c19 Polymorphisms

CYP2C19 polymorphisms are important factors for proton pump inhibitor-based therapy. We examined the CYP2C19 genotypes and analyzed the distribution among ethnicities and clinical outcomes in Indonesia. We employed the polymerase chain reaction-restriction fragment length polymorphism method to determine the CYP2C19 genotypes and evaluated inflammation severity with the updated Sydney system. For CYP2C19*2, 46.4% were the homozygous wild-type allele, 14.5% were the homozygous mutated allele, and 39.2% were the heterozygous allele. For CYP2C19*3, 88.6% were the homozygous wild-type allele, 2.4% were the homozygous mutated allele, and 9.0% were the heterozygous allele. Overall, the prevalence of rapid, intermediate, and poor metabolizers in Indonesia was 38.5, 41.6, and 19.9%, respectively. In the poor metabolizer group, the frequency of allele *2 (78.8%) was higher than the frequency of allele *3 (21.2%). The Papuan had a significantly higher likelihood of possessing poor metabolizers than the Balinese (OR 11.0; P = 0.002). The prevalence of poor metabolizers was lower compared with the rapid and intermediate metabolizers among patients with gastritis and gastroesophageal reflux disease. Intermediate metabolizers had the highest prevalence, followed by rapid metabolizers and poor metabolizers. Dosage adjustment should therefore be considered when administering proton pump inhibitor-based therapy in Indonesia.

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