scholarly journals GENETICS OF PARTHENOGENESIS IN DROSOPHILA MELANOGASTER. I. THE MODES OF DIPLOIDIZATION IN THE GYNOGENESIS INDUCED BY A MALE-STERILE MUTANT, ms(3)K81

Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 237-248
Author(s):  
Yoshiaki Fuyama

ABSTRACT Sperm that are produced by males homozygous for ms(3)K81, a male sterile mutant of Drosophila melanogaster, are defective in syngamy but are capable of activating eggs to develop gynogenetically. The activated eggs usually produce haploid embryos, but a small fraction (10-4-10-5) of them give rise to diploid impaternate adults. To know the cytological mechanisms by which these impaternates restore diploidy, the genotypes of impaternate progeny obtained from females doubly heterozygous for visible markers were examined. The results show that, as generally found among parthenogenetic Drosophila, diploidy is restored after completing meiosis either by pronuclear fusion or by gamete duplication (doubling of a haploid cleavage nucleus). The fusion of two nonsister nuclei following meiosis II (central fusion) was indicated to be a predominant mode of diploidization in this species. Two meiotic mutants, mei-9 and mei-S332, which are known to greatly increase meiotic nondisjunction, did not cause an increased incidence of impaternates. This seems to exclude the possibility that some impaternates might have been derived from diploid egg nuclei produced through nondisjunction.

Genetics ◽  
1986 ◽  
Vol 114 (2) ◽  
pp. 495-509
Author(s):  
Yoshiaki Fuyama

ABSTRACT A strain of Drosophila melanogaster, named gyn-F9, can reproduce by gynogenesis. On mating with a male sterile mutant, ms(3)K81, gyn-F9 females produced impaternate progeny at a rate of about 15 flies per female, which was almost 2000 times as frequent as that of the control. When the females were mated with normally fertile males, the number of offspring varied extremely from parent to parent, with average fertility being much lower than that of normal females. Nearly one-third of these bisexual progeny were either triploid females or intersexes. Among the rest of the progeny, some were diploid impaternates having developed without syngamy. The gynogenetic property of gyn-F9 is primarily governed by a few genes, most likely two recessive genes, one each located on the second and third chromosomes. The impaternates were found to restore their diploidy by the fusion of two nonsister nuclei out of the four egg pronuclei which result from the second meiotic division (central fusion). Although nondisjunction occurs frequently in the meiosis of gyn-F9, this is unlikely to bring about an appreciable number of diploid gametes developing into impaternates. Possible mechanisms of the evolutionary origin of parthenogenesis are discussed in relation to these findings.


2009 ◽  
Vol 35 (6) ◽  
pp. 1151-1155
Author(s):  
Ming-Guang CHU ◽  
Shuang-Cheng LI ◽  
Shi-Quan WANG ◽  
Qi-Ming DENG ◽  
Jing ZHANG ◽  
...  

1993 ◽  
Vol 13 (3) ◽  
pp. 1708-1718 ◽  
Author(s):  
M Schäfer ◽  
D Börsch ◽  
A Hülster ◽  
U Schäfer

We have analyzed a locus of Drosophila melanogaster located at 98C on chromosome 3, which contains two tandemly arranged genes, named Mst98Ca and Mst98Cb. They are two additional members of the Mst(3)CGP gene family by three criteria. (i) Both genes are exclusively transcribed in the male germ line. (ii) Both transcripts encode a protein with a high proportion of the repetitive motif Cys-Gly-Pro. (iii) Their expression is translationally controlled; while transcripts can be detected in diploid stages of spermatogenesis, association with polysomes can be shown only in haploid stages of sperm development. The genes differ markedly from the other members of the gene family in structure; they do not contain introns, they are of much larger size, and they have the Cys-Gly-Pro motifs clustered at the carboxy-terminal end of the encoded proteins. An antibody generated against the Mst98Ca protein recognizes both Mst98C proteins in D. melanogaster. In a male-sterile mutation in which spermiogenesis is blocked before individualization of sperm, both of these proteins are no longer synthesized. This finding provides proof of late translation for the Mst98C proteins and thereby independent proof of translational control of expression. Northern (RNA) and Western immunoblot analyses indicate the presence of homologous gene families in many other Drosophila species. The Mst98C proteins share sequence homology with proteins of the outer dense fibers in mammalian spermatozoa and can be localized to the sperm tail by immunofluorescence with an anti-Mst98Ca antibody.


Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 749-760 ◽  
Author(s):  
Armin Schmidt ◽  
Gioacchino Palumbo ◽  
Maria P Bozzetti ◽  
Patrizia Tritto ◽  
Sergio Pimpinelli ◽  
...  

Abstract The sting mutation, caused by a P element inserted into polytene region 32D, was isolated by a screen for male sterile insertions in Drosophila melanogaster. This sterility is correlated with the presence of crystals in spermatocytes and spermatids that are structurally indistinguishable from those produced in males carrying a deficiency of the Y-linked crystal (cry) locus. In addition, their morphology is needle-like in Ste+ flies and star-shaped in Ste flies, once again as observed in cry– males. The sti mutation leads to meiotic drive of the sex chromosomes, and the strength of the phenomenon is correlated with the copy number of the repetitive Ste locus. The same correlation is also true for the penetrance of the male sterile mutation. A presumptive sti null allele results in male sterility and lethal maternal effect. The gene was cloned and shown to code for a putative protein that is 866 amino acids long. A C-terminal domain of 82 amino acids is identified that is well conserved in proteins from different organisms. The gene is expressed only in the germline of both sexes. The interaction of sting with the Ste locus can also be demonstrated at the molecular level. While an unprocessed 8-kb Ste primary transcript is expressed in wild-type males, in X/Y homozygous sti males, as in X/Y cry– males, a 0.7-kb mRNA is produced.


Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 219-229 ◽  
Author(s):  
G K Yasuda ◽  
G Schubiger ◽  
B T Wakimoto

Abstract The vast majority of known male sterile mutants of Drosophila melanogaster fail to produce mature sperm or mate properly. The ms(3) K81(1) mutation is one of a rare class of male sterile mutations in which sterility is caused by developmental arrest after sperm entry into the egg. Previous studies showed that males homozygous for the K81(1) mutation produce progeny that arrest at either of two developmental stages. Most embryos arrest during early nuclear cycles, whereas the remainder are haploid embryos that arrest at a later stage. This description of the mutant phenotype was based on the analysis of a single allele isolated from a natural population. It was therefore unclear whether this unique paternal effect phenotype reflected the normal function of the gene. The genetic analysis and initial molecular characterization of five new K81 mutations are described here. Hemizygous conditions and heteroallelic combinations of the alleles were associated with male sterility caused by defects in embryogenesis. No other mutant phenotypes were observed. Thus, the K81 gene acted as a strict paternal effect gene. Moreover, the biphasic pattern of developmental arrest was common to all the alleles. These findings strongly suggested that the unusual embryonic phenotype caused by all five new alleles was due to loss of function of the K81+ gene. The K81 gene is therefore the first clear example of a strict paternal effect gene in Drosophila. Based on the embryonic lethal phenotypes, we suggest that the K81+ gene encodes a sperm-specific product that is essential for the male pronucleus to participate in the first few embryonic nuclear divisions.


1993 ◽  
Vol 13 (3) ◽  
pp. 1708-1718
Author(s):  
M Schäfer ◽  
D Börsch ◽  
A Hülster ◽  
U Schäfer

We have analyzed a locus of Drosophila melanogaster located at 98C on chromosome 3, which contains two tandemly arranged genes, named Mst98Ca and Mst98Cb. They are two additional members of the Mst(3)CGP gene family by three criteria. (i) Both genes are exclusively transcribed in the male germ line. (ii) Both transcripts encode a protein with a high proportion of the repetitive motif Cys-Gly-Pro. (iii) Their expression is translationally controlled; while transcripts can be detected in diploid stages of spermatogenesis, association with polysomes can be shown only in haploid stages of sperm development. The genes differ markedly from the other members of the gene family in structure; they do not contain introns, they are of much larger size, and they have the Cys-Gly-Pro motifs clustered at the carboxy-terminal end of the encoded proteins. An antibody generated against the Mst98Ca protein recognizes both Mst98C proteins in D. melanogaster. In a male-sterile mutation in which spermiogenesis is blocked before individualization of sperm, both of these proteins are no longer synthesized. This finding provides proof of late translation for the Mst98C proteins and thereby independent proof of translational control of expression. Northern (RNA) and Western immunoblot analyses indicate the presence of homologous gene families in many other Drosophila species. The Mst98C proteins share sequence homology with proteins of the outer dense fibers in mammalian spermatozoa and can be localized to the sperm tail by immunofluorescence with an anti-Mst98Ca antibody.


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