Non-mendelian female sterility in Drosophila melanogaster: Hereditary transmission of reactivity levels

Bucheton, Alain; Picard, Georges

doi:10.1038/hdy.1978.22

Cited by 65 publications

(25 citation statements)

References 12 publications

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“…This sterility is the result of an interaction between a chromosomal factor I and a cytoplasmic factor R (P~lisson & Picard, 1979). The R-factor is maternally inherited but in the absence of chromosomes from the reactive strain it gradually disappears (Bucheton, 1978;Bucheton & Picard, 1978;b andb). The I-factor in Drosophila melanogaster exhibits a phenomenon called 'chromosomal contamination': crossing experiments with semi-sterile females, which have received from their father a single Icarrying chromosome, show that most or all their chromosomes, formerly devoid of I-factors, have irreversibly acquired one or more I-factors (P~lisson, 1978(P~lisson, and Picard 1978(P~lisson, c and 1979.…”

Section: Discussionmentioning

confidence: 99%

Nucleo-cytoplasmic interactions causing partial female sterility in the spider mite Tetranychus urticae Koch (Acari: Tetranychidae)

Boer

1982

Genetica

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Section: Discussionmentioning

confidence: 99%

Nucleo-cytoplasmic interactions causing partial female sterility in the spider mite Tetranychus urticae Koch (Acari: Tetranychidae)

Boer

1982

Genetica

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“…Early in the analysis of the R-reactivity Bucheton et al (BUCHETON and PICARD 1978;BUCHETON 1979) showed that there were differences between lines and that the strength of the R-reactivity could be influenced both by the maternal age and by the external temperature. They concluded that the Rreactivity appeared to be under complex control involving both extra-chromosomal and classical nuclear inheritance.…”

Section: Xiushan Wu Department Of Genetics Stockholm University S-mentioning

confidence: 99%

Variation in the strength of R-reactivity and I-inductivity in inbred lines of Drosophila melanogaster

2008

Hereditas

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Wu, X. 1990. Variation in the strength of R-reactivity and I-inductivity in inbred lines of Drosophilu melanogaster. -Hereditas 1 / 3 : 169-177. Lund, Sweden. ISSN 0018-0661. Received June 19, 1990. Accepted August 21, 1990 Two sets of two sister lines of Drosophila melanogaster, with common genome and cytoplasms of different origin, originally showed intermediate R-effects. All four lines had been kept at constant protocol for about 150 generations. From each of the four lines three sublines were established from single females and the strength of R-reactivity was tested by chromosomal loss technique. In two of the four sets, there was heterogeneity between the sublines. One subline in both cases was similar to the three sublines from the sister lines. The remaining two sets remained unchanged. Specific reactions were found in particular combinations of R-and I-lines. Six sets of independently arising I-lines with K-genome showed different response in the strength of their I-inductivity. The evolutionary relation in the strength of R-reactivity of R-type lines and the implication of the specific reactions are discussed. Xiushan Wu, Department of Genetics, Stockholm University, S-106 91 Stockholm, SwedenEarly in the analysis of the R-reactivity Bucheton et al. (BUCHETON and PICARD 1978;BUCHETON 1979) showed that there were differences between lines and that the strength of the R-reactivity could be influenced both by the maternal age and by the external temperature. They concluded that the Rreactivity appeared to be under complex control involving both extra-chromosomal and classical nuclear inheritance.By introducing genome from an inbred R-type line into cytoplasms from various sources LUNING and LAKE (1985a) showed that the cytoplasms contain extra-chromosomal elements with different effects on the strength of the R-reactivity. In subsequent tests LUNING (1988a) showed that some of these lines maintained in mass culture for 100 generations at unchanged protocol did not exhibit any detectable alterations in the strength of the Rreactivity. On the other hand, he found that homozygosity for the marker-gene yellow sooner or later resulted in shifts towards weak R-type. Those tests also gave some indications of some oscillation in the strength of the R-elements balanced by selective forces.These observations raised the question whether there occurred heterogeneities in the mass-mated lines and if the separation of sister lines for over 150 generations had resulted in diversification. From the cytoplasms into which a common R-type genome had been introduced by LUNING and LAKE (1 985a) three out of seven cytoplasms had weaker R-type than the rest. These three were tested for changes in R-reactivity, as there were possibilities for changes towards both stronger and weaker Rreactions. In one of these three sets, one of the two sister lines later changed from R-type to I-type (YITERBORN 1985). Of the other two pairs, one cytoplasm was derived from an old inbred lab-stock, Canton S, and the other came from a female wil...

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“…We prefer the model in which extrachromosomal P element DNA regulates the activity of chromosomalP elements. Moreover, this simple model has potential application in an independent system of hybrid dysgenesis called the I-R system, which has many formal similarities to the P-M system (25)(26)(27)(28)(29)(30).…”

Section: Methodsmentioning

confidence: 99%

Transposase titration in Drosophila melanogaster: a model of cytotype in the P-M system of hybrid dysgenesis.

Simmons¹,

Bucholz²

1985

Proc. Natl. Acad. Sci. U.S.A.

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In the P-M system of hybrid dysgenesis of Drosophila melanogaster, some M strains possess chromosomal P elements. The chromosomes from one of these pseudo-M strains reduced the instability ofa P element-insertion mutation of the singed bristle locus. We suggest that this reduction is an indication of competition for a transposase that binds to the P elements on the chromosomes from the pseudo-M strain as well as to the P elements at the singed locus; the pseudo-M strain's P elements might therefore be said to titrate the transposase, reducing its availability to interact with the P elements at the singed locus. We hypothesize that a similar mechanism regulates the movement of P elements in the P strains of D. melanogaster, although in this case we propose that the titrating elements are extrachromosomal and that they are generated by the action of the transposase itself.In the P-M system of hybrid dysgenesis in Drosophila melanogaster, transposable P elements are activated in a cellular condition called the M cytotype (1-4). Their activity leads to a syndrome of germ-line traits that includes frequent mutation, chromosome breakage, and sterility (5). These dysgenic traits are seen in the hybrid progeny of crosses between females with the M cytotype and males with transposable P elements. The latter usually come from strains with a cellular condition that represses P element activity. This condition, called the P cytotype, is characteristic of many strains derived recently from natural populations, especially those from Africa and North and South America (6, 7). Strains with the P cytotype are referred to as P strains, although some with only a weak ability to induce hybrid dysgenesis are designated as Q strains.The structural and functional analysis ofP elements cloned from one strong P strain has revealed that these constitute a heterogeneous family (8). Some elements have a conserved structure and are able to transpose themselves and other P elements when they are put into the Mcytotype (9, 10). Other elements are missing a segment of the conserved sequence and, although they may be transposed, are unable to cause their own transposition. These defective elements are apparently derived from the large conserved elements by different internal deletions. Their mobility in the presence of a large conserved element indicates that the latter encodes a transacting transposition function, or transposase (9-11). All of the P elements studied so far possess 31-base-pair inverted repeats at their ends. Because a deletion in one repeat abolishes the ability of the affected element to be transposed (12), these repeats are thought to serve as the recognition sites for the action of the P transposase.The virtual inactivity of P elements in a germ line with the P cytotype raises the issue of transpositional control. To explain this, O'Hare and Rubin (8) have postulated that P elements encode a regulator that suppresses transposition. In their model, a structurally complete P element encodes two functions: one, the reg...

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Non-mendelian female sterility in Drosophila melanogaster: Hereditary transmission of reactivity levels

Cited by 65 publications

References 12 publications

Nucleo-cytoplasmic interactions causing partial female sterility in the spider mite Tetranychus urticae Koch (Acari: Tetranychidae)

Nucleo-cytoplasmic interactions causing partial female sterility in the spider mite Tetranychus urticae Koch (Acari: Tetranychidae)

Variation in the strength of R-reactivity and I-inductivity in inbred lines of Drosophila melanogaster

Transposase titration in Drosophila melanogaster: a model of cytotype in the P-M system of hybrid dysgenesis.

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