The genetic analysis of achiasmate segregation in Drosophila melanogaster. III. The wild-type product of the Axs gene is required for the meiotic segregation of achiasmate homologs.

Abstract The regular segregation of achiasmate chromosomes in Drosophila melanogaster females is ensured by two distinct segregational systems. The segregation of achiasmate homologs is assured by the maintenance of heterochromatic pairing; while the segregation of heterologous chromosomes is ensured by a separate mechanism that may not require physical association. AxsD (Aberrant X segregation) is a dominant mutation that specifically impairs the segregation of achiasmate homologs; heterologous achiasmate segregations are not affected. As a result, achiasmate homologs frequently participate in heterologous segregations at meiosis I. We report the isolation of two intragenic revertants of the AxsD mutation (Axsr2 and Axsr3) that exhibit a recessive meiotic phenotype identical to that observed in AxsD/AxsD females. A third revertant (Axsr1) exhibits no meiotic phenotype as a homozygote, but a meiotic defect is observed in Axsr1/Axsr2 females. Therefore mutations at the AxsD locus define a gene necessary and specific for homologous achiasmate segregation during meiosis. We also characterize the interactions of mutations at the Axs locus with two other meiotic mutations (ald and ncd). Finally, we propose a model in which Axs+ is required for the normal separation of paired achiasmate homologs. In the absence of Axs+ function, the homologs are often unable to separate from each other and behave as a single segregational unit that is free to segregate from heterologous chromosomes.

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SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster

The Journal of Cell Biology ◽

10.1083/jcb.200904040 ◽

2010 ◽

Vol 188 (3) ◽

pp. 335-349 ◽

Cited By ~ 24

Author(s):

Rihui Yan ◽

Sharon E. Thomas ◽

Jui-He Tsai ◽

Yukihiro Yamada ◽

Bruce D. McKee

Keyword(s):

Drosophila Melanogaster ◽

Sister Chromatid ◽

Sister Chromatid Cohesion ◽

Early Prophase ◽

Wild Type ◽

Sister Chromatids ◽

Chromatid Cohesion ◽

Mutant Phenotypes ◽

Meiosis I ◽

Novel Protein

Sister chromatid cohesion is essential to maintain stable connections between homologues and sister chromatids during meiosis and to establish correct centromere orientation patterns on the meiosis I and II spindles. However, the meiotic cohesion apparatus in Drosophila melanogaster remains largely uncharacterized. We describe a novel protein, sisters on the loose (SOLO), which is essential for meiotic cohesion in Drosophila. In solo mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientation and causing nondisjunction of both homologous and sister chromatids. Centromeric foci of the cohesin protein SMC1 are absent in solo mutants at all meiotic stages. SOLO and SMC1 colocalize to meiotic centromeres from early prophase I until anaphase II in wild-type males, but both proteins disappear prematurely at anaphase I in mutants for mei-S332, which encodes the Drosophila homologue of the cohesin protector protein shugoshin. The solo mutant phenotypes and the localization patterns of SOLO and SMC1 indicate that they function together to maintain sister chromatid cohesion in Drosophila meiosis.

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Identification of the Telomere elongation mutation in Drosophila

10.7287/peerj.preprints.26708 ◽

2018 ◽

Author(s):

Hemakumar M. Reddy ◽

Thomas A. Randall ◽

Radmila Capkova Frydrychova ◽

James M. Mason

Keyword(s):

Drosophila Melanogaster ◽

Next Generation Sequencing ◽

Ltr Retrotransposons ◽

Wild Type ◽

Dominant Mutation ◽

Site Specific ◽

Site Specific Recombination ◽

Telomere Elongation ◽

Drosophila Genetic Reference Panel ◽

Generation Sequencing

Background. Telomeres in Drosophila melanogaster are similar to those of other eukaryotes in terms of their function, although they are formed by non-LTR retrotransposons instead of telomerase-based short repeats. The length of the telomeres in Drosophila depends on the number of copies of these transposable elements. A dominant mutation, Tel1, causes a several-fold elongation of telomeres. Methods. In this study we identified the Tel1 mutation by a combination of transposon-induced, site-specific recombination and next generation sequencing. Results. Recombination located Tel1 to a 15 kb region in 92A. Comparison of the DNA sequence in this region with the Drosophila Genetic Reference Panel of wild type genomic sequences delimited Tel1 to a 3 bp deletion inside intron 8 of Ino80. Discussion. The mapped Tel1 mutation (3-bp deletion found in Ino80) did not appear to affect the quantity or length of the Ino80 transcript. Tel1 causes a significant reduction in transcripts of CG18493, a gene nested in an intron 8 of Ino80, which is expressed in ovaries and expected to encode a serine-type peptidase.

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Persistent one-way walking in a circular arena in Drosophila melanogaster Canton-S strain

10.1101/145888 ◽

2017 ◽

Author(s):

Chengfeng Xiao ◽

Shuang Qiu ◽

R Meldrum Robertson

Keyword(s):

Drosophila Melanogaster ◽

Genetic Analysis ◽

Y Chromosome ◽

Genetic Background ◽

Chromosome 2 ◽

Wild Type ◽

Promoting Effect ◽

Directional Change ◽

Pleiotropic Function

AbstractWe describe persistent one-way walking of Drosophila melanogaster in a circular arena. Wild-type Canton-S adult flies walked in one direction, counter-clockwise or clockwise, for minutes, whereas white-eyed mutant w1118 changed directions frequently. Locomotion in the circular arena could be classified into four components: counter-clockwise walking, clockwise walking, nondirectional walking and pausing. Genetic analysis revealed that while wild-type genetic background was associated with reduced directional change and reduced numbers of one-way (including counterclockwise and clockwise) and nondirectional walks, the white (w+) locus promoted persistent oneway walking by increasing the maximal duration of one-way episodes. The promoting effect of w+ was further supported by the observations that (1) w+ duplicated to the Y chromosome, (2) four genomic copies of mini-white inserted on the autosomes, and (3) pan-neuronal overexpression of the White protein increased the maximal duration of one-way episodes, and that RNAi knockdown of w+ in the neurons decreased the maximal duration of one-way episodes. These results suggested a pleiotropic function of w+ in promoting persistent one-way walking in the circular arena.

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Genetic Analysis of theHybrid male rescueLocus of Drosophila

Genetics ◽

10.1093/genetics/155.1.225 ◽

2000 ◽

Vol 155 (1) ◽

pp. 225-231 ◽

Cited By ~ 4

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.

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Analysis of gene expression during development in the homeotic mutant Contrabithorax of Drosophila melanogaster

Development ◽

10.1242/dev.34.1.19 ◽

1975 ◽

Vol 34 (1) ◽

pp. 19-31

Author(s):

Gines Morata

Keyword(s):

Gene Expression ◽

Drosophila Melanogaster ◽

Genetic Analysis ◽

Normal Level ◽

X Rays ◽

Wild Type ◽

Homeotic Transformation ◽

Homeotic Mutant ◽

A Cell ◽

Final Expression

Contrabithorax, a mutant of the bithorax system in Drosophila melanogaster produces a partial homeotic transformation of mesothorax (wing) into metathorax (haltere). The wing of a fly homozygous or heterozygous for the mutant is a mosaic of wing and haltere structures. A genetic analysis of the mutant suggests that its phenotype is due to some form of derepression in the wing of two other genes of the bithorax system (bithorax and postbithorax) which are not normally active there. This repression is not complete. The activity of the two genes is below the normal level resulting in only a partial transformation of wing into haltere. Clones of marked cells were generated by X-rays and were found to include both transformed (haltere) and untransformed (wing) territory; this was true even for those generated late in development. Thus the final expression of a cell depends not on its immediate ancestry but perhaps on the level of the products of the wild-type alleles of bithorax and postbithorax.

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Identification of the Telomere elongation mutation in Drosophila

10.7287/peerj.preprints.26708v1 ◽

2018 ◽

Cited By ~ 1

Author(s):

Hemakumar M. Reddy ◽

Thomas A. Randall ◽

Radmila Capkova Frydrychova ◽

James M. Mason

Keyword(s):

Drosophila Melanogaster ◽

Next Generation Sequencing ◽

Ltr Retrotransposons ◽

Wild Type ◽

Dominant Mutation ◽

Site Specific ◽

Site Specific Recombination ◽

Telomere Elongation ◽

Drosophila Genetic Reference Panel ◽

Generation Sequencing

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Genetic Analysis of Delta, a Neurogenic Gene of Drosophila melanogaster

Genetics ◽

10.1093/genetics/116.3.433 ◽

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.

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The molecular analyses of an antimorphic mutation of Drosophila melanogaster, Scutoid.

Genetics ◽

10.1093/genetics/119.3.647 ◽

1988 ◽

Vol 119 (3) ◽

pp. 647-661

Author(s):

S McGill ◽

W Chia ◽

R Karp ◽

M Ashburner

Keyword(s):

Drosophila Melanogaster ◽

Molecular Analysis ◽

Molecular Level ◽

Wild Type ◽

Dominant Mutation ◽

Molecular Analyses ◽

Chromosome Arm

Abstract A dominant mutation of Drosophila melanogaster, Scutoid (Sco), acts as an antimorphic allele of the no-ocelli (noc) gene. In Sco the noc region has been transposed from 35B to 35D on chromosome arm 2L and the noc gene is now adjacent to snail (sna). Induced revertants of Sco are frequently mutant for sna or are aberrations broken very close to sna. A molecular analysis of the Sco chromosome has confirmed that noc is transposed and fused to the sna region. However, only part of the noc region is included within the transposition. The breakpoints of 19 chromosomally aberrant Sco revertants have been mapped at the molecular level. Fourteen of these breakpoints map to the noc region, spread over about 80 kb of DNA. The breakpoints of the remaining five are not within the DNA of the noc region and appear to map within sequences from the sna region. This has been shown directly for three of these, those associated with T(2;3)ScoR+13, In(2L)ScoR+24 and In(2L)ScoR+26. Thus mutation of either noc or sna, genes which are apparently unrelated in their wild-type functions, can revert the antimorphic phenotype of Sco.

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GENETIC ANALYSIS OF THE ACHAETE-SCUTE SYSTEM OF DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/91.3.491 ◽

1979 ◽

Vol 91 (3) ◽

pp. 491-520

Author(s):

A García-Bellido

Keyword(s):

Drosophila Melanogaster ◽

Genetic Analysis ◽

Gene Product ◽

Point Mutations ◽

Type Condition ◽

Wild Type ◽

Complex Organization

ABSTRACT Several mutations in the achaete-scute region of Drosophila have been analyzed phenotypically and cytologically. One group of them corresponds to point mutations, another t o rearrangements with one breakpoint in this region. Trans heterozygotes of the different point mutations or of the different rearrangements show poor complementation or fail to complement; therefore, they could be interpreted as mutations affecting the same gene product. However, left-right inversion recombinants and duplication-deficiency combinations between rearrangements with different cytological breakpoints uncover a complex organization of the achaete-scute region. This region seems to contain several independent achaete and scute functions, as well as a lethal function, arranged as a tandem reverse repeat at both sides of a lethal locus. Since all of the mutants show the same phenotype qualitatively, though different quantitatively, we suggest that these functions are of a reiterative nature. The achaete-scute wild-type condition may well be dependent on a multimeric gene product made of several evolutionary related monomers.

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Functional expression of a yeast mitochondrial intron-encoded protein requires RNA processing at a conserved dodecamer sequence at the 3' end of the gene.

Molecular and Cellular Biology ◽

10.1128/mcb.9.4.1507 ◽

1989 ◽

Vol 9 (4) ◽

pp. 1507-1512 ◽

Cited By ~ 22

Author(s):

H Zhu ◽

H Conrad-Webb ◽

X S Liao ◽

P S Perlman ◽

R A Butow

Keyword(s):

Genetic Analysis ◽

Rna Processing ◽

Fold Increase ◽

Functional Expression ◽

Rrna Gene ◽

Yeast Mitochondria ◽

Wild Type ◽

Site Specific ◽

Var1 Gene ◽

A Site

All mRNAs of yeast mitochondria are processed at their 3' ends within a conserved dodecamer sequence, 5'-AAUAAUAUUCUU-3'. A dominant nuclear suppressor, SUV3-I, was previously isolated because it suppresses a dodecamer deletion at the 3' end of the var1 gene. We have tested the effects of SUV3-1 on a mutant containing two adjacent transversions within a dodecamer at the 3' end of fit1, a gene located within the 1,143-base-pair intron of the 21S rRNA gene, whose product is a site-specific endonuclease required in crosses for the quantitative transmission of that intron to 21S alleles that lack it. The fit1 dodecamer mutations blocked both intron transmission and dodecamer cleavage, neither of which was suppressed by SUV3-1 when present in heterozygous or homozygous configurations. Unexpectedly, we found that SUV3-1 completely blocked cleavage of the wild-type fit1 dodecamer and, in SUV3-1 homozygous crosses, intron conversion. In addition, SUV3-1 resulted in at least a 40-fold increase in the amount of excised intron accumulated. Genetic analysis showed that these phenotypes resulted from the same mutation. We conclude that cleavage of a wild-type dodecamer sequence at the 3' end of the fit1 gene is essential for fit1 expression.

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