Meiotic Drive in Natural Populations of Drosophila melanogaster. VI. A Preliminary Report on the Presence of Segregation-Distortion in a Baja California Population

ABSTRACT Functional variation among Y chromosomes in natural populations of Drosophila melanogaster was assayed by a segregation study. A total of 36 Y chromosomes was extracted and ten generations of replacement backcrossing yielded stocks with Y chromosomes in two different genetic backgrounds. Eleven of the Y chromosomes were from diverse geographic origins, and the remaining 25 were from locally captured flies. Segregation of sexes in adult offspring was scored for the four possible crosses among the two backgrounds with each Y chromosome. Although the design confounds meiotic drive and effects on viability, statistical partitioning of these effects reveals significant variation among lines in Y chromosome segregation. Results are discussed in regards to models of Y-linked segregation and viability effects, which suggest that Y-linked adaptive polymorphism is unlikely.

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Examination of a mutable system affecting the components of the segregation distorter meiotic drive system of Drosophila melanogaster.

Genetics ◽

10.1093/genetics/125.1.51 ◽

1990 ◽

Vol 125 (1) ◽

pp. 51-76

Author(s):

K G Golic

Keyword(s):

Drosophila Melanogaster ◽

Transposable Element ◽

X Chromosome ◽

Segregation Distortion ◽

Chromosomal Rearrangements ◽

Meiotic Drive ◽

Drive System ◽

Partial Loss ◽

Segregation Distorter ◽

Relationship Of

Abstract Segregation distortion in Drosophila melanogaster is the result of an interaction between the genetic elements Sd, a Rsp sensitive to Sd, and an array of modifiers, that results in the death of sperm carrying Rsp. A stock (designated M-5; cn bw) has been constructed which has the property of inducing the partial loss of sensitivity from previously sensitive cn bw chromosomes, the partial loss of distorting ability from SD chromosomes, and a concomitant acquisition of modifiers on the X chromosome and possibly also on the autosomes. By several criteria the changes exhibited under the influence of M-5; cn bw are characteristic of the transposable-element systems which produce hybrid dysgenesis. In the first place, the magnitude of these effects depends on the nature of the crosses performed. The analogy is further strengthened by the observation that the changes induced by M-5; cn bw share other stigmata of Drosophila transposable-element systems, including high sterility among the progeny of outcrosses, and the production of chromosomal rearrangements. The possible relationship of this system to the P, I and hobo transposable element systems is discussed, as well as its bearing on aspects of the Segregation Distorter phenomenon which have yet to be explained.

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ON THE COMPONENTS OF SEGREGATION DISTORTION IN DROSOPHILA MELANOGASTER. III. NATURE OF ENHANCER OF SD

Genetics ◽

10.1093/genetics/107.3.423 ◽

1984 ◽

Vol 107 (3) ◽

pp. 423-434

Author(s):

John G Brittnacher ◽

Barry Ganetzky

Keyword(s):

Drosophila Melanogaster ◽

Segregation Distortion ◽

Allelic Variation ◽

Meiotic Drive ◽

Dependent Manner ◽

X Ray ◽

Segregation Distorter ◽

In Cis ◽

General Component

ABSTRACT Analysis of X-ray-induced deletions in the Segregation Distorter (SD) chromosome, SD-5, revealed that this chromosome had a gene proximal to lt in the centric heterochromatin of 2L that strongly enhanced the meiotic drive caused by the SD chromosome. This Enhancer of Segregation Distortion [E(SD)] locus had not been characterized in earlier studies of SD chromosomes because it cannot be readily separated by recombination from the Responder (Rsp) locus in the proximal heterochromatin of 2R.—To determine whether E(SD) is a general component of all SD chromosomes and to examine further its effects on distortion, we produced deletions of E(SD) in three additional SD chromosomes. Analysis of these deletions leads to the following conclusions: (1) along with Sd and Rsp, E(SD) is common to all SD chromosomes; (2) the E(SD) allele on each SD chromosome enhances distortion by the same amount, which indicates that allelic variation at the E(SD) locus is not responsible for the different drive strengths seen among SD chromosomes; (3) E(SD) causes very little or no distortion by itself in the absence of Sd; (4) E(SD), like Sd, acts in a dosage-dependent manner; (5) E(SD) exerts its effect in cis or trans to Sd; and (6) if E(SD) + exists, its function is not related to SD.

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Segregation Distortion and Male Recombination in Natural Populations of Drosophila melanogaster

The American Naturalist ◽

10.1086/283628 ◽

1980 ◽

Vol 116 (2) ◽

pp. 297-304 ◽

Cited By ~ 3

Author(s):

R. C. Woodruff ◽

R. F. Lyman

Keyword(s):

Drosophila Melanogaster ◽

Segregation Distortion ◽

Natural Populations ◽

Male Recombination

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A Protamine Knockdown Mimics the Function of Sd in Drosophila melanogaster

G3 Genes|Genome|Genetics ◽

10.1534/g3.120.401307 ◽

2020 ◽

Vol 10 (6) ◽

pp. 2111-2115 ◽

Cited By ~ 1

Author(s):

Luke F. Gingell ◽

Janna R. McLean

Keyword(s):

Drosophila Melanogaster ◽

Nuclear Import ◽

Nuclear Transport ◽

Protein A ◽

Natural Populations ◽

Meiotic Drive ◽

Gene Complex ◽

Unique Role ◽

Spermatid Nucleus ◽

Import And Export

Segregation Distorter (SD) is an autosomal meiotic drive system found worldwide in natural populations of Drosophila melanogaster. This gene complex induces the preferential and nearly exclusive transmission of the SD chromosome in SD/SD+ males. This selfish propagation occurs through the interplay of the Sd locus, its enhancers and the Rsps locus during spermatid development. The key distorter locus, Sd, encodes a truncated but enzymatically active RanGAP (RanGTPase-activating protein), a key nuclear transport factor in the Ran signaling pathway. When encoded by Sd, RanGAP is mislocalized to the nucleus interior, which then traps Ran inside the nucleus and disrupts nuclear import. As a result of this aberrant nuclear transport, a process known as the histone-to-protamine transition that is required for proper spermatid condensation fails to occur in SD/SD+ males. In this process, sperm-specific protamine proteins enter the spermatid nucleus and replace the formerly chromatin-complexed histones. Previously, we have shown that mutations affecting nuclear import and export can enhance distortion in an SD background, thus verifying that a defect in nuclear transport is responsible for the unequal transmission of chromosomes. Herein, we show that specifically reducing protamines induces distortion in an SD background, verifying that protamines are transported via the RanGAP/GEF pathway and indicating that E(SD) plays a significant and unique role in the process of distortion.

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