scholarly journals Inseparability of X-Heterochromatic Functions Responsible for X:Y Pairing, Meiotic Drive, and Male Fertility in Drosophila melanogaster

Genetics ◽  
1987 ◽  
Vol 116 (3) ◽  
pp. 399-407
Author(s):  
Bruce McKee ◽  
Dan L Lindsley
Keyword(s):  
Drosophila Melanogaster ◽  
Male Fertility ◽  
Meiotic Drive ◽  
Male Meiosis ◽  
Recovery Ratio ◽  
Strongly Correlated ◽  
Wild Type ◽  
Autosome Translocation ◽  
Ratio Distortion ◽  
Sperm Recovery

ABSTRACT Deficiencies encompassing part or all of the X heterochromatin of Drosophila melanogaster have been linked to three abnormalities in male meiosis and spermatogenesis: X-Y nondisjunction, skewed sperm recovery ratios favoring sperm with reduced chromatin content, and sterility in males carrying either a Y-autosome translocation or mal  +  Y. In this study, 18 X heterochromatic deficiencies of varying sizes were tested in XY males for their spermatogenic phenotypes. All 18 proved to be either mutant for all three phenotypes or wild type for all three. Although variable among mutant deficiencies, expression levels of all three phenotypes were strongly correlated. Deficiencies that cause high levels of nondisjunction also cause severe recovery ratio distortion and are completely sterile in conjunction with mal  +  Y. Low nondisjunction deficiencies cause comparable mild effects for the other phenotypes. The same deficiencies were also tested in males carrying a large heterochromatic free X duplication Dp(1;f)3. For all deficiencies which induce nondisjunction in XY males, the Y and free duplication pair regularly and the X fails to pair in XYDp males. Drive levels are constant across deficiencies in these males. Thus elimination of variability in the pairing phenotype also eliminates variability in sperm recovery ratios.

scholarly journals A quantitative genetic analysis of fitness and its components in Drosophila melanogaster

1986 ◽  
Vol 47 (1) ◽  
pp. 59-70 ◽  
Author(s):  
Trudy F. C. Mackay
Keyword(s):  
Drosophila Melanogaster ◽  
Natural Populations ◽  
Strongly Correlated ◽  
Wild Type ◽  
Relative Contribution ◽  
Quantitative Characters ◽  
Quantitative Genetic ◽  
Bristle Number ◽  
Metric Traits ◽  
Average Fitness

SummaryForty-one third chromosomes extracted from a natural population of Drosophila melanogaster were assessed for net fitness and for the quantitative characters viability, net fertility, female productivity, male weight, abdominal bristle number, and sternopleural bristle number. Net homozygous and heterozygous fitness of the third chromosomes was estimated by competition against a marked balancer third chromosome. Average fitness of the homozygous lines relative to wild-type heterozygotes was 0·13, indicating substantial inbreeding depression for net fitness. All significant correlations of quantitative characters with fitness and with each other were high and positive. Homozygous fitness is strongly correlated with net fertility, viability, and female productivity, moderately associated with male weight, and not significantly associated with bristle traits. The combination of metric traits which best predicts homozygous fitness is the simple multiple of viability and female productivity. Heterozygous fitness is not correlated with homozygous fitness; furthermore, the relative contribution of metric traits to fitness in a heterozygous population is likely to be different from that deduced from homozygous lines. These observations are consistent with a model of genetic variation for fitness in natural populations caused by segregation of rare deleterious recessive alleles.

scholarly journals Distorter genes of the mouse t-complex impair male fertility when heterozygous

1987 ◽  
Vol 49 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Fertility ◽  
Genetic Background ◽  
Inbred Strains ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Male Mice ◽  
Wild Type ◽  
T Complex ◽  
Ratio Distortion ◽  
Harmful Effects

SummaryMale mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.

scholarly journals Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR

1998 ◽  
Vol 71 (2) ◽  
pp. 119-125 ◽  
Author(s):  
DIETER WEICHENHAN ◽  
BÄRBEL KUNZE ◽  
WALTHER TRAUT ◽  
HEINZ WINKING
Keyword(s):  
Transmission Ratio Distortion ◽  
Chromosome 1 ◽  
Transmission Ratio ◽  
Recovery Ratio ◽  
Wild Type ◽  
Variable Cluster ◽  
Ratio Distortion ◽  
Normal Transmission ◽  
Mendelian Transmission ◽  
Mouse Chromosome 1

The house mouse, Mus musculus, harbours a variable cluster of long-range repeats in chromosome 1. As shown in previous studies, some high-copy clusters such as the MUT cluster are cytogenetically apparent as a homogeneously staining region (HSR) and are associated with a distortion of the Mendelian recovery ratio when transmitted by heterozygous females. The effect is caused by a decreased viability of +/+ embryos. It is compensated by maternal or paternal MUT. In this study, a deletion derivative of MUT, MUTdel, shows normal transmission ratios and no compensating capability. In this respect, MUTdel behaves like a wild-type cluster. Hence, both properties – transmission ratio distortion and compensating capability – map to the deleted region. The deletion comprises three-quarters of the MUT HSR and does not extend to the nearest markers adjacent to the HSR.

scholarly journals ANALYSIS OF THE AUTOSOMAL MUTATION abo AND ITS INTERACTION WITH THE RIBOSOMAL DNA OF DROSOPHILA MELANOGASTER: THE ROLE OF X-CHROMOSOME HETEROCHROMATIN

Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 661-672
Author(s):  
Barry Yedvobnick ◽  
Hallie M Krider ◽  
Bryan I Levine
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Autosomal Recessive ◽  
Wild Type ◽  
X Chromosomes ◽  
Cr Functions ◽  
Chromosome Inversions ◽  
Ratio Distortion ◽  
Sex Ratio Distortion

ABSTRACT The autosomal recessive, maternal-effect mutation abnormal oocyte (abo: 2-38) preferentially lowers the viability of XO progeny. The severity of the sex-ratio distortion is reduced by duplications of maternal or zygotic heterochromatin chromatin (SANDLER 1970, 1977; PARRY and SANDLER 1974). Utilizing X-chromosome inversions that contain modifications in the quantity and arrangement of the heterochromatic functions, Xhabo and cr  +, we have extended our investigations of nbo's influence on XO male recovery and rDNA redundancy (KRIDER,YEDVOBNICK and LEVINE 1979).——XO males bearing In(1)scs1Lsc4R or In(1)wm4Lsc4R are recovered twice as frequently as X chromosomes containing a single Xh region, implying that these inversions possess a duplication of Xhabo. abo mutant females heterozygous for In(1)scs1Lsc4R and wild-type X chromosomes generate XO progeny that do not contain elevated rDNA redundancies. XO males containing In(1)wm4 exhibit male recoveries and rDNA elevations similar to those of males bearing a wild-type X chromosome, when both derive from a common abo/abo mother. Reciprocal crosses between In(1)wm4 and Canton-S males to attached-X abo females show significant, though reduced, sex ratios in the absence of an rDNA effect. The observation that abo can elevate the rDNA redundancy of In(1)wm4, a chromosome that does not compensate, suggests that abo and cr+ functions are not directly related.

Observations on chromosomal male sterility in Drosophila melanogaster

1984 ◽  
Vol 26 (1) ◽  
pp. 67-77
Author(s):  
James. C. Stone
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Functional Unit ◽  
Primary Spermatocyte ◽  
Male Meiosis ◽  
Centromeric Heterochromatin ◽  
Control Element ◽  
Male Sterile ◽  
Cis Acting ◽  
Autosome Translocation

Observations on a variety of metazoans have shown that the X chromosome becomes functionally inactive earlier in male meiosis than the remainder of the genome. Genetic analyses of male-sterile chromosome rearrangements in Drosophila suggest that the X chromosome in this species behaves as a distinct functional unit, and have further suggested that X-chromosome expression is regulated in the primary spermatocyte by a cis-acting control element located in the centromeric heterochromatin. Attempts to test the X-inactivation hypothesis of chromosomal sterility in Drosophila and attempts to map the hypothetical control element are described here. Cytological observations on a male-sterile X-autosome translocation are also discussed.

scholarly journals A Chlamydomonas Homologue of the Putative Murine t Complex Distorter Tctex-2 Is an Outer Arm Dynein Light Chain

1997 ◽  
Vol 137 (5) ◽  
pp. 1081-1090 ◽  
Author(s):  
Ramila S. Patel-King ◽  
Sharon E. Benashski ◽  
Alistair Harrison ◽  
Stephen M. King
Keyword(s):  
Molecular Analysis ◽  
Light Chain ◽  
Meiotic Drive ◽  
Cytoplasmic Dynein ◽  
Transmission Ratio Distortion ◽  
Dynein Light Chain ◽  
Wild Type ◽  
Biochemical Model ◽  
T Complex ◽  
Ratio Distortion

Molecular analysis of a 19,000-Mr protein from the Chlamydomonas flagellum reveals that it is homologous to the t complex–encoded protein Tctex-2, which is a candidate for one of the distorter products that cause the extreme transmission ratio distortion (meiotic drive) of the murine t complex. The 19,000-Mr protein is extracted from the axoneme with 0.6 M NaCl and comigrates with the outer dynein arm in sucrose density gradients. This protein also is specifically missing in axonemes prepared from a mutant that does not assemble the outer arm. These data raise the possibility that Tctex-2 is a sperm flagellar dynein component. Combined with the recent identification of Tctex-1 (another distorter candidate) as a light chain of cytoplasmic dynein, these results lead to a biochemical model for how differential defects in spermiogenesis that result in the phenomenon of meiotic drive might be generated in wild-type vs t-bearing sperm.

Functional identification of the Segregation distorter locus of Drosophila melanogaster by germline transformation.

Genetics ◽  
1994 ◽  
Vol 137 (1) ◽  
pp. 201-209 ◽  
Author(s):  
J R McLean ◽  
C J Merrill ◽  
P A Powers ◽  
B Ganetzky
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome Segregation ◽  
Genomic Dna ◽  
Tandem Duplication ◽  
Meiotic Drive ◽  
Wild Type ◽  
Functional Identification ◽  
Germline Transformation ◽  
Segregation Distorter ◽  
Distorter Locus

Abstract Segregation Distorter (SD) is a meiotic drive system in D. melanogaster that results in the failure of SD/SD+ males to transmit SD+ homologs owing to the induced dysfunction of spermatids carrying the normal chromosome. Segregation distorter (Sd), the gene primarily responsible for this distorted transmission, is associated with a novel 12-kb restriction fragment containing a tandem duplication of a 5-kb wild-type segment of genomic DNA. When introduced into appropriate genetic backgrounds by germline transformation, this 12-kb fragment causes full levels of distortion and directs the expression of an SD-specific 4-kb transcript. Transformants that have lost part of this segment are unable to cause distortion and do not express the 4-kb transcript. These results identify the tandem duplication as Sd.

Mutations affecting the indirect flight muscles of Drosophila melanogaster

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 61-81
Author(s):  
Ilan I. Deak ◽  
Paul R. Bellamy ◽  
Marianne Bienz ◽  
Yvonne Dubuis ◽  
Elke Fenner ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Polyacrylamide Gel Electrophoresis ◽  
Strongly Correlated ◽  
Wild Type ◽  
Protein Patterns ◽  
Thin Filaments ◽  
Thoracic Muscle ◽  
Muscle Region ◽  
Flight Muscles ◽  
Chromosomal Mutations

The development of the indirect flight muscles of Drosophila melanogaster was studied by analysing mutations that cause flightlessness. Twenty-five mutations on the X-chromosome and two on the third chromosome were examined. The X-chromosomal mutations form ten complementation units. The ten loci were assigned preliminary map positions by meiotic recombination and deficiencies and duplications. The two autosomal mutationsrepresent two genes. Gynandromorph analyses suggest that many of these mutations have their primary effect inthe presumptive thoracic muscle region of the embryo. The mutations cause a variety of characteristic defects, such as absence of the bulk of the thoracic muscle mass, or absence of only one of the two fibrillar musclegroups. Electronmicroscopic studies of sixteen mutants representing all twelve loci reveal abnormal myofibrillar organization in some of these mutants, e.g. aberrant or missing Z-bands, or absence of the thin filaments. Mutant protein patterns, obtained by SDS-polyacrylamide gel electrophoresis, show the following differences from wild type: ten mutants are characterized by absence or reduction of the 54 K protein, and most mutants exhibit a reduction and modification of the 80 and 90 K proteins. The absence or reduction of the 54 K proteinwas strongly correlated with aberrant Z-bands.

scholarly journals Genetic analysis of Stellate elements of Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1181-1197 ◽  
Author(s):  
G Palumbo ◽  
S Bonaccorsi ◽  
L G Robbins ◽  
S Pimpinelli
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Copy Number ◽  
Meiotic Drive ◽  
Genetic System ◽  
Male Meiosis ◽  
Meiotic Abnormalities ◽  
Y Chromosomes ◽  
Sperm Development ◽  
Dependent Failure

Abstract Repeated elements are remarkably important for male meiosis and spermiogenesis in Drosophila melanogaster. Pairing of the X and Y chromosomes is mediated by the ribosomal RNA genes of the Y chromosome and X chromosome heterochromatin, spermiogenesis depends on the fertility factors of the Y chromosome. Intriguingly, a peculiar genetic system of interaction between the Y-linked crystal locus and the X-linked Stellate elements seem to be also involved in male meiosis and spermiogenesis. Deletion of the crystal element of the Y, via an interaction with the Stellate elements of the X, causes meiotic abnormalities, gamete-genotype dependent failure of sperm development (meiotic drive), and deposition of protein crystals in spermatocytes. The current hypothesis is that the meiotic abnormalities observed in cry- males is due to an induced overexpression of the normally repressed Ste elements. An implication of this hypothesis is that the strength of the abnormalities would depend on the amount of the Ste copies. To test this point we have genetically and cytologically examined the relationship of Ste copy number and organization to meiotic behavior in cry- males. We found that heterochromatic as well as euchromatic Ste repeats are functional and that the abnormality in chromosome condensation and the frequency of nondisjunction are related to Ste copy number. Moreover, we found that meiosis is disrupted after synapsis and that cry-induced meiotic drive is probably not mediated by Ste.

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