DNA Distribution in Spermatid Nuclei of Normal and Segregation Distorter Males of DROSOPHILA MELANOGASTER

Using the DNA-specific dye BAO [2,5-bis-(4'-aminophenyl-(1')]-1,3,4-oxadiazol), we have examined spermiogenesis in wild-type males of Drosophila melanogaster and in males carrying various combinations of the Sd and Rsp mutations involved in segregation distortion. Wild-type strains, even those newly collected from nature, are heterogeneous with respect to the incidence of spermiogenic abnormalities, principally in having a variable number of spermatid nuclei per cyst that fail to undergo complete elongation. Among segregation distorter males, Rsp/Rsp homozygotes have the greatest incidence of nuclear nonelongation or incomplete elongation, Rsp/Rsp ⁺ heterozygotes are intermediate, while Rsp⁺/ Rsp⁺ homozygotes have the least amount of abnormality. Indeed, Sd Rsp⁺/Sd⁺Rsp⁺ males have significantly fewer spermiogenic aberrations than do wild-type strains.     

Population Dynamics of the Segregation Distorter Polymorphism of DROSOPHILA MELANOGASTER

Two two-locus models of the population dynamics of the segregation distortion (SD) polymorphism of Drosophila melanogaster are described. One model is appropriate for understanding the population genetics of SD in nature, whereas the other is a special case appropriate for understanding an artificial population that has been extensively analysed. The models incorporate the general features of the Sd and Rsp loci which form the core of the SD system. It is shown that the SD polymorphism can be established only when there is sufficiently tight linkage between Sd and Rsp. An approximate treatment, valid for tight linkage, is given of all the equilibria of the system and their stabilities. It is shown that the observed composition of natural and artificial populations with respect to the Sd and Rsp loci is predicted well by the model, provided that restrictions are imposed on the fertilities of certain genotypes. Highly oscillatory paths towards equilibrium are usually to be expected on the basis of this model. The selection pressures on inversions introduced into this system are also investigated.     

Defective Histone Transition during Spermiogenesis in Heterozygous SEGREGATION DISTORTER Males of DROSOPHILA MELANOGASTER

Males of Drosophila melanogaster that are heterozygous for the segregation distorter (SD) chromosome produce a gross excess of SD-bearing offspring because most of the non-SD-bearing sperm are dysfunctional. These dysfunctional sperm exhibit abnormalities in chromatin condensation and compaction during spermiogenesis. Use of the fluorescent dye sulfoflavine, which is specific for basic proteins, has now revealed that the dysfunctional sperm are also defective in the normal transition from somatic to spermatid-specific histones.     

Further Characterization of Genetic Elements Associated with the Segregation Distorter Phenomenon in DROSOPHILA MELANOGASTER

Segregation Distorter, SD, associated with the second chromosome of Drosophila melanogaster, is known to cause sperm bearing the non-SD homologue to dysfunction in heterozygous males. In earlier studies, using different, independently derived, SD chromosomes, three major loci were identified as contributing to the distortion of segregation ratios in males. In this study the genetic components of the SD-5 chromosome have been the subjects of further investigation, and our findings offer the following information. Crossover analysis confirms the mapping of the Sd locus to a position distal to but closely linked with the genetic marker pr. Spontaneous and radiation-induced recombinational analyses and deficiency studies provide firm support to the notion that the Rsp (Responder) locus lies within the proximal heterochromatin of chromosome 2, between the genetic markers lt and rl and most likely in the heterochromatin of the right arm. The major focus of this study, however, has been on providing a better definition of the genetic properties of the Enhancer of SD [E(SD)]. Our findings place this locus within the region of the two most proximal essential genes in the heterochromatin of the left arm of chromosome 2. Moreover, our analysis reveals a probable association of the E(SD) locus with a meiotic drive independent of that caused by Sd.     

Suppressor Systems of Segregation Distorter (SD) Chromosomes in Natural Populations of DROSOPHILA MELANOGASTER

Several natural populations of D. melanogaster were investigated for the presence (or absence) of the Segregation Distorter ( SD) chromosomes and their suppressor systems. The SD chromosomes were found, at frequencies of a few percent, in two independent samples taken in different years from a Raleigh, North Carolina, population, whereas no SD chromosomes were found in samples collected from several populations in Texas. The populations in these localities were found to contain suppressor X chromosomes in high frequencies (75% or higher). They also contained relatively low frequencies of partial suppressor or insensitive second chromosomes of varying degrees, but completely insensitive second chromosomes were practically absent in all populations examined. The frequencies of suppressor X chromosomes, as well as those of the partially insensitive or suppressor second chromosomes, were the same among the populations investigated. This suggests the possibility that the development of a suppressor system of SD in a population could be independent of the presence of an SD chromosome. Segregation distortion appeared to be occurring in natural genetic backgrounds, but the degree of distortion varied among males of different genotypes. There were many instances in which the SD chromosomes showed transmission frequencies from their heterozygous male parents that were smaller than 0.6 and, in several cases, even smaller than 0.5. The presence of a recessive suppressor, or suppressors, of SD in natural populations was suggested.     

Sex Chromosome Meiotic Drive in DROSOPHILA MELANOGASTER Males

In Drosophila melanogaster males, deficiency for X heterochromatin causes high X-Y nondisjunction and skewed sex chromosome segregation ratios (meiotic drive). Y and XY classes are recovered poorly because of sperm dysfunction. In this study it was found that X heterochromatic deficiencies disrupt recovery not only of the Y chromosome but also of the X and autosomes, that both heterochromatic and euchromatic regions of chromosomes are affected and that the "sensitivity" of a chromosome to meiotic drive is a function of its length. Two models to explain these results are considered. One is a competitive model that proposes that all chromosomes must compete for a scarce chromosome-binding material in Xh(-) males. The failure to observe competitive interactions among chromosome recovery probabilities rules out this model. The second is a pairing model which holds that normal spermiogenesis requires X-Y pairing at special heterochromatic pairing sites. Unsaturated pairing sites become gametic lethals. This model fails to account for autosomal sensitivity to meiotic drive. It is also contradicted by evidence that saturation of Y-pairing sites fails to suppress meiotic drive in Xh(- ) males and that extra X-pairing sites in an otherwise normal male do not induce drive. It is argued that meiotic drive results from separation of X euchromatin from X heterochromatin.     

On the Components of Segregation Distortion in DROSOPHILA MELANOGASTER

The segregation distorter (SD) complex is a naturally occurring meiotic drive system with the property that males heterozygous for an SD-bearing chromosome 2 and an SD⁺-bearing homolog transmit the SD-bearing chromosome almost exclusively. This distorted segregation is the consequence of an induced dysfunction of those sperm that receive the SD⁺ homolog. From previous studies, two loci have been implicated in this phenomenon: the Sd locus which is required to produce distortion, and the Responder (Rsp) locus that is the site at which Sd acts. There are two allelic alternatives of Rsp—sensitive (Rsp^sens) and insensitive (Rsp^ins); a chromosome carrying Rsp^ins is not distorted by SD. In the present study, the function and location of each of these elements was examined by a genetic and cytological characterization of X-ray-induced mutations at each locus. The results indicate the following: (1) the Rsp locus is located in the proximal heterochromatin of 2R; (2) a deletion for the Rsp locus renders a chromosome insensitive to distortion; (3) the Sd locus is located to the left of pr (2-54.5), in the region from 37D2-D7 to 38A6-B2 of the salivary chromosome map; (4) an SD chromosome deleted for Sd loses its ability to distort; (5) there is another important component of the SD system, E(SD), in or near the proximal heterochromatin of 2L, that behaves as a strong enhancer of distortion. The results of these studies allow a reinterpretation of results from earlier analyses of the SD system and serve to limit the possible mechanisms to account for segregation distortion.     

On the Models of Segregation Distortion in DROSOPHILA MELANOGASTER

The Segregation Distorter system of Drosophila melanogaster consists of two major elements, Sd and Rsp. There are two allelic alternatives of Rsp-sensitive (Rsp(s)) and insensitive (Rsp(i)); a chromosome carrying Rsp(i) is not distorted. According to the model proposed by Hartl (1973), these two elements interact to cause segregation distortion. For a sperm to complete the maturation process, it is assumed that the Rsp locus has to be complexed with the product of the Sd locus. This product is assumed to be a multimetric regulatory protein. Three kinds of regulatory multimers may be distinguished: Sd(+)/Sd(+), which is assumed to complex with both Rsp(s) and Rsp(i); Sd(+)/Sd heteromultimers, which complex preferentially with Rsp(i); and Sd/Sd homomultimers, which complex with neither Rsp(s) nor Rsp(i). Most of the regulatory protein in the Sd(+)/Sd heterozygous male is assumed to be the Sd(+)/Sd heteromultimer.--Some modifications of Hartl's model were made by Ganetzky (1977). Rather than the binding of a product of Sd at the Rsp locus being a necessary condition for normal spermigenesis, this binding causes sperm dysfunction. It is assumed that the product of Sd complexes more readily with Rsp(s) than with Rsp(i) and that the amount of Sd product is limited with respect to the number of binding sites available. No function is ascribed to the Sd(+) locus. In order to explain reduced male fertility of some genotypes, Ganetzky further assumes that the Sd product, when not competed for by an Rsp(s) locus, can bind to an Rsp(i) locus.--Two consequences of these models were critically examined: according to these models (1) an Sd Rsp(s)/Sd(+)Rsp(s) male should not show any segregation distortion, and (2) an Sd Rsp(s)/Sd Rsp(s) male should show much reduced fertility, if not complete sterility.--The results of the present study bear on these two points. (1) Rsp(s) locus seems to consist of multiple alleles, each having a different degree of ability to interact with the product of the Sd locus. An Sd Rsp(s)/Sd(+)Rsp(s) male shows a certain degree of segregation distortion when the two Rsp(s) alleles are different, but it shows a normal Mendelian segregation ratio when the Rsp(s) alleles are homozygous. The first prediction of the models is supported by actual observation when the two Rsp(s) alleles are the same. (2) There is a suggestion of slight reduction in fertility, but generally Sd Rsp(s)/Sd Rsp(s) males are quite fertile. Thus, the second prediction is not supported by actual observation. The mechanism of segregation distortion is still open for future studies.     

The Brood Pattern of Mitomycin-C-Induced Translocations in DROSOPHILA MELANOGASTER Males: The Effect of Time

Translocations between the two large autosomes were scored in the progeny of males that had been fed mitomycin-C. The frequencies were the same in spermatogonia sampled after 12 and 25 days and in spermatozoa stored for the same periods in untreated females.     

黑腹果蝇的分离变相因子

众所周知,一对基因在杂合状态中保持相对的独立性,而在配子形成时,又按原样以相同比例分离到不同的配子中去,这是生物中最基本的遗传规律———孟德尔分离定律。但实际上并不是所有基因的分离都严格遵循孟德尔分离定律,存在于黑腹果蝇中的分离变相因子（ＳｅｇｒｅｇａｔｉｏｎＤｉｓｔｏｒｔｅｒ,以下简称ＳＤ）就是一种具有减数分裂驱动（ｍｅｉｏｔｉｃｄｒｉｖｅ）性质的、违反孟德尔分离定律的特殊遗传因子,从六十年代发现至今引起了人们的广泛关注,本文从其遗传背景,结构特征及进化规律等方面分别介绍一些近期的研究结果。１…     

The Mechanism of a Brooding Effect Associated with Segregation Distortion in DROSOPHILA MELANOGASTER

The fecundities of 55 genotypes of the form SD(i)/SD(j) generated by 11 different SD chromosomes have been examined. Five of the genotypes are lethal The fecundities of the rest fall into a pattern of fertility and sterility that is highly suggestive of intracistronic complementation. The complementation leading to male fertility is only partial complementation: the fecundity of most fertile genotypes is less than half that of controls. The three components of the SD system, the Sd locus, the Ac locus, and the modifiers in 2R, were examined separately, and it appears that the complementation is a phenomenon associated with the Sd locus. A hypothesis of the molecular events involved in segregation distortion is formulated in the light of these observations. The model is based on the assumption that the Sd locus produces a multimeric molecule that regulates the activity of the Ac(=Rsp) locus during spermatogenesis.