scholarly journals The Maternal Effect Mutation sésame Affects the Formation of the Male Pronucleus in Drosophila melanogaster

2000 ◽  
Vol 222 (2) ◽  
pp. 392-404 ◽  
Author(s):  
Benjamin Loppin ◽  
Mylène Docquier ◽  
François Bonneton ◽  
Pierre Couble
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Male Pronucleus

scholarly journals A NOTE ON THE MATERNAL EFFECT MUTANTS DAUGHTERLESS AND ABNORMAL OOCYTE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Sex Chromosome ◽  
Chromosome 2 ◽  
Dominant Marker ◽  
Enhancing Effect ◽  
X Irradiation ◽  
The Right ◽  
Chromosome Breakpoint ◽  
Special Region

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.

scholarly journals Does RNA interference influence meiotic crossing over in Drosophila melanogaster?

2008 ◽  
Vol 90 (3) ◽  
pp. 253-258 ◽  
Author(s):  
ERIC W. CROSS ◽  
MICHAEL J. SIMMONS
Keyword(s):  
Drosophila Melanogaster ◽  
Rna Interference ◽  
X Chromosome ◽  
Maternal Effect ◽  
Crossing Over ◽  
Crossover Frequency ◽  
Chromosome Iii ◽  
Chromosome Ii ◽  
Balancer Chromosomes ◽  
Balancer Chromosome

SummaryMutations in the RNA interference (RNAi) genes aubergine (aub), homeless and piwi were tested for effects on the frequency, distribution and coincidence of meiotic crossovers in the long arm of the X chromosome. Some increases in crossover frequency were seen in these tests, but they may have been due to a maternal effect of the balancer chromosomes that were used to maintain the RNAi mutations in stocks rather than to the RNAi mutations themselves. These same balancers produced strong zygotic interchromosomal effects when tested separately. Mutations in aub and piwi did not affect the frequency of crossing over in the centric heterochromatin of chromosome II; nor did a balancer chromosome III.

scholarly journals Repression of P element-mediated hybrid dysgenesis in Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 663-676 ◽  
Author(s):  
M J Simmons ◽  
J D Raymond ◽  
K E Rasmusson ◽  
L M Miller ◽  
C F McLarnon ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Gonadal Dysgenesis ◽  
De Novo ◽  
Inbred Lines ◽  
Hybrid Dysgenesis ◽  
P Element ◽  
P Elements ◽  
Hybrid Offspring ◽  
Element Movement

Abstract Inbred lines derived from a strain called Sexi were analyzed for their abilities to repress P element-mediated gonadal dysgenesis. One line had high repression ability, four had intermediate ability and two had very low ability. The four intermediate lines also exhibited considerable within-line variation for this trait; furthermore, in at least two cases, this variation could not be attributed to recurring P element movement. Repression of gonadal dysgenesis in the hybrid offspring of all seven lines was due primarily to a maternal effect; there was no evidence for repression arising de novo in the hybrids themselves. In one of the lines, repression ability was inherited maternally, indicating the involvement of cytoplasmic factors. In three other lines, repression ability appeared to be determined by partially dominant or additive chromosomal factors; however, there was also evidence for a maternal effect that reduced the expression of these factors in at least two of the lines. In another line, repression ability seemed to be due to recessive chromosomal factors. All seven lines possessed numerous copies of a particular P element, called KP, which has been hypothesized to produce a polypeptide repressor of gonadal dysgenesis. This hypothesis, however, does not explain why the inbred Sexi lines varied so much in their repression abilities. It is suggested that some of this variation may be due to differences in the chromosomal position of the KP elements, or that other nonautonomous P elements are involved in the repression of hybrid dysgenesis in these lines.

scholarly journals STUDIES ON THE SEX-SPECIFIC LETHALS OF DROSOPHILA MELANOGASTER. II. FURTHER STUDIES ON A MALE-SPECIFIC LETHAL GENE, MALELESS

Genetics ◽  
1976 ◽  
Vol 84 (2) ◽  
pp. 257-266
Author(s):  
Atsumi Tanaka ◽  
Akihiro Fukunaga ◽  
Kugao Oishi
Keyword(s):  
Drosophila Melanogaster ◽  
Larval Stage ◽  
Maternal Effect ◽  
Sex Differentiation ◽  
Pupal Stage ◽  
Imaginal Discs ◽  
Lethal Gene ◽  
Male Specific Lethal ◽  
Male Specific

ABSTRACT Effects of a second chromosome male-specific lethal gene, maleless (mle), of Drosophila melanogaster were further studied. It was shown that, although no maternal effect was seen with respect to the male-specific lethality, the lethal stage was influenced by whether parental females were homozygous or heterozygous for mle. Thus, in the former mle/mle males died mostly in the late third instar larval stage, while in the latter practically all males survived to the pupal stage. In the dying mle/mle male pupae complete differentiation of adult external head and thorax structures was often observed but that of abdominal structures was incomplete forming only a few segments in most cases. Imaginal discs from third instar mle/mle male larvae which were produced by mle/mle mothers and were destined to die as larvae were able to differentiate into adult structures upon transplantation into normal third instar larval hosts.—A somewhat elaborated version of the previously presented hypothesis (Fukunaga, Tanaka and Oishi 1975) was discussed as to the possible presence of a class of sex-specific lethals which are not related to the process of primary sex differentiation

scholarly journals Maternal repression of the P element promoter in the germline of Drosophila melanogaster: a model for the P cytotype.

Genetics ◽  
1993 ◽  
Vol 135 (1) ◽  
pp. 149-160 ◽  
Author(s):  
B Lemaitre ◽  
S Ronsseray ◽  
D Coen
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Molecular Mechanisms ◽  
Maternal Inheritance ◽  
P Element ◽  
Fusion Genes ◽  
P Elements ◽  
Somatic Tissues ◽  
By Products

Abstract The transposition of P elements in Drosophila melanogaster is regulated by products encoded by the P elements themselves. The P cytotype, which represses transposition and associated phenomena, exhibits both a maternal effect and maternal inheritance. The genetic and molecular mechanisms of this regulation are complex and not yet fully understood. In a previous study, using P-lacZ fusion genes, we have shown that P element regulatory products were able to inhibit the activity of the P promoter in somatic tissues. However, the repression observed did not exhibit the maternal effect characteristic of the P cytotype. With a similar approach, we have assayed in vivo the effect of P element regulatory products in the germline. We show that the P cytotype is able to repress the P promoter in the germline as well as in the soma. Furthermore, this repression exhibits a maternal effect restricted to the germline. On the basis of these new observations, we propose a model for the mechanism of P cytotype repression and its maternal inheritance.

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