scholarly journals THE GENETIC AND CYTOLOGICAL ORGANIZATION OF THE Y CHROMOSOME OF DROSOPHILA MELANOGASTER

Genetics ◽  
1981 ◽  
Vol 98 (3) ◽  
pp. 529-548
Author(s):  
James A Kennison

ABSTRACT Cytological and genetic analyses of 121 translocations between the Y chromosome and the centric heterochromatin of the X chromosome have been used to define and localize six regions on the Y chromosome of Drosophila melanogaster necessary for male fertility. These regions are associated with nonfluorescent blocks of the Y chromosome, as revealed using Hoechst 33258 or quinacrine staining. Each region appears to contain but one functional unit, as defined by failure of complementation among translocations with breakpoints within the same block. The distribution of translocation breakpoints examined appears to be nonrandom, in that breaks occur preferentially in the nonfluorescent blocks and not in the large fluorescent blocks.

1993 ◽  
Vol 90 (23) ◽  
pp. 11132-11136 ◽  
Author(s):  
J Gepner ◽  
T S Hays

A clone encoding a portion of the highly conserved ATP-binding domain of a dynein heavy-chain polypeptide was mapped to a region of the Drosophila melanogaster Y chromosome. Dyneins are large multisubunit enzymes that utilize the hydrolysis of ATP to move along microtubules. They were first identified as the motors that provide the force for flagellar and ciliary bending. Seven different dynein heavy-chain genes have been identified in D. melanogaster by PCR. In the present study, we demonstrate that one of the dynein genes, Dhc-Yh3, is located in Y chromosome region h3, which is contained within kl-5, a locus required for male fertility. The PCR clone derived from Dhc-Yh3 is 85% identical to the corresponding region of the beta heavy chain of sea urchin flagellar dynein but only 53% identical to a cytoplasmic dynein heavy chain from Drosophila. In situ hybridization to Drosophila testes shows Dhc-Yh3 is expressed in wild-type males but not in males missing the kl-5 region. These results are consistent with the hypothesis that the Y chromosome is needed for male fertility because it contains conventional genes that function during spermiogenesis.


Genetics ◽  
1981 ◽  
Vol 99 (1) ◽  
pp. 49-64
Author(s):  
Rezaur Rahman ◽  
Dan L Lindsley

ABSTRACT The genetic limits of sixty-four deficiencies in the vicinity of the euchromatic-heterochromatic junction of the X chromosome were mapped with respect to a number of proximal recessive lethal mutations. They were also tested for male fertility in combination with three Y chromosomes carrying different amounts of proximal X-chromosome-derived material (BSYy+, y+Ymal126 and y  +  Ymal  +). All deficiencies that did not include the locus of bb and a few that did were male-fertile in all male-viable Df(1)/Dp(1;Y) combinations. Nineteen bb deficiencies fell into six different classes by virtue of their male-fertility phenotypes when combined with the duplicated Y chromosomes. The six categories of deficiencies are consistent with a formalism that invokes three factors or regions at the base of the X, one distal and two proximal to bb, which bind a substance critical for precocious inactivation of the X chromosome in the primary spermatocyte. Free duplications carrying these regions or factors compete for the substance in such a way that, in the presence of such duplications, proximally deficient X chromosomes are unable to command sufficient substance for proper control of X-chromosome gene activity preparatory to spermatogenesis. We conclude that there is no single factor at the base of the X that is required for the fertility of males whose genotype is otherwise normal.


Genetics ◽  
1994 ◽  
Vol 136 (2) ◽  
pp. 559-571 ◽  
Author(s):  
P B Talbert ◽  
C D LeCiel ◽  
S Henikoff

Abstract The variegating mutation brownDominant (bwD) of Drosophila melanogaster is associated with an insertion of heterochromatin into chromosome arm 2R at 59E, the site of the bw gene. Mutagenesis produced 150 dominant suppressors of bwD variegation. These fall into two classes: unlinked suppressors, which also suppress other variegating mutations; and linked chromosome rearrangements, which suppress only bwD. Some rearrangements are broken at 59E, and so might directly interfere with variegation caused by the heterochromatic insertion at that site. However, most rearrangements are translocations broken proximal to bw within the 52D-57D region of 2R. Translocation breakpoints on the X chromosome are scattered throughout the X euchromatin, while those on chromosome 3 are confined to the tips. This suggests that a special property of the X chromosome suppresses bwD variegation, as does a distal autosomal location. Conversely, two enhancers of bwD are caused by translocations from the same part of 2R to proximal heterochromatin, bringing the bwD heterochromatic insertion close to the chromocenter with which it strongly associates. These results support the notion that heterochromatin formation at a genetic locus depends on its location within the nucleus.


Genetics ◽  
2002 ◽  
Vol 161 (4) ◽  
pp. 1551-1559 ◽  
Author(s):  
Massimo Belloni ◽  
Patrizia Tritto ◽  
Maria Pia Bozzetti ◽  
Gioacchino Palumbo ◽  
Leonard G Robbins

AbstractDrosophila melanogaster males deficient for the crystal (cry) locus of the Y chromosome that carry between 15 and 60 copies of the X-linked Stellate (Ste) gene are semisterile, have elevated levels of nondisjunction, produce distorted sperm genotype ratios (meiotic drive), and evince hyperactive transcription of Ste in the testes. Ste seems to be the active element in this system, and it has been proposed that the ancestral Ste gene was “selfish” and increased in frequency because it caused meiotic drive. This hypothetical evolutionary history is based on the idea that Ste overexpression, and not the lack of cry, causes the meiotic drive of cry– males. To test whether this is true, we have constructed a Ste-deleted X chromosome and examined the phenotype of Ste–/cry– males. If hyperactivity of Ste were necessary for the transmission defects seen in cry– males, cry– males completely deficient for Ste would be normal. Although it is impossible to construct a completely Ste– genotype, we find that Ste–/cry– males have exactly the same phenotype as Ste+/cry– males. The deletion of all X chromosome Ste copies not only does not eliminate meiotic drive and nondisjunction, but it also does not even reduce them below the levels produced when the X carries 15 copies of Ste.


1979 ◽  
Vol 21 (1) ◽  
pp. 21-24 ◽  
Author(s):  
John H. Williamson ◽  
Eva Meidinger

Drosophila melanogaster males with two supernumerary Y chromosomes, i.e. triplo-Y males, are completely sterile. Their mating behavior is normal, and spermatogenesis and spermiogenesis appear normal, but no sperm are transferred. Most, if not all, of the detrimental effects of a third Y chromosome on male fertility are attributable to the long arm of the Y chromosome.


Genetics ◽  
1984 ◽  
Vol 106 (3) ◽  
pp. 423-434
Author(s):  
Terrence W Lyttle

ABSTRACT Many translocations between the Y chromosome and a major autosome have no effect on the fertility of Drosophila melanogaster males. However, when such translocation-bearing males also carry an X chromosome deficient for a large portion of the centric heterochromatin, they are generally sterile. This has been interpreted to be the result of an interaction between the deficiency and the subterminally capped autosome. Using this observation as a starting point, we have developed a selection scheme for radiation-induced translocation resealings that depends on the prediction that fertility in the presence of such a deficient X is restored whenever the displaced autosomal tip is brought back in association with an autosomal centromere. The observation and the prediction form the basis for what is referred to as the autosomal continuity model for male fertility.—Such a mutagenesis scheme offers several advantages. (1) It is efficient, producing upward of 1% resealings in some cases. (2) It is simple; since fertility is the basis for the selective screen, many males can be tested in a single vial. (3) It can be used to simultaneously generate both duplications and deficiencies specific for chromosomal material adjacent to the original translocation breakpoints. (4) The target for mutagenesis can be mature sperm.—Analysis of the pattern of male-fertile rearrangements obtained from several translocation lines using this protocol indicates that continuity of the autosomal tips and their centromeres is neither a necessary nor sufficient condition for male fertility in the presence of a bobbed-deficient X. Thus, the simple autosomal continuity model is not adequate to explain this complicated mechanism of chromosomal control of fertility and will have to be revised accordingly. Potential future lines of inquiry toward this goal are discussed.


1984 ◽  
Vol 26 (1) ◽  
pp. 67-77
Author(s):  
James. C. Stone

Observations on a variety of metazoans have shown that the X chromosome becomes functionally inactive earlier in male meiosis than the remainder of the genome. Genetic analyses of male-sterile chromosome rearrangements in Drosophila suggest that the X chromosome in this species behaves as a distinct functional unit, and have further suggested that X-chromosome expression is regulated in the primary spermatocyte by a cis-acting control element located in the centromeric heterochromatin. Attempts to test the X-inactivation hypothesis of chromosomal sterility in Drosophila and attempts to map the hypothetical control element are described here. Cytological observations on a male-sterile X-autosome translocation are also discussed.


Genetics ◽  
1983 ◽  
Vol 103 (2) ◽  
pp. 219-234
Author(s):  
James A Kennison

ABSTRACT The frequencies of newly induced male-sterilizing lesions on both the X and Y chromosomes of Drosophila melanogaster were determined after either 4000 r of γ-irradiation or adult feeding of ethyl methanesulfonate. The Y chromosome is approximately twice as sensitive as the X chromosome to newly induced male-sterilizing lesions after γ-irradiation, but slightly less sensitive after ethyl methanesulfonate treatment. A large proportion of the radiation-induced lesions are associated with Y-autosome or X-autosome translocations, with the Y chromosome recovered in translocations far in excess of the frequency expected from metaphase lengths. Although translocations between the X and Y chromosomes or between autosomes do not appear to sterilize heterozygous males, interchanges between sex chromosomes and autosomes often sterilize males carrying them in a dominant manner, suggesting that the organization of the genome is critical for normal spermatogenesis. Complementation tests between recessive Y-linked male-sterilizing mutants do not reveal the existence of any additional fertility loci beyond the six previously defined.


Genetics ◽  
1976 ◽  
Vol 82 (1) ◽  
pp. 25-34
Author(s):  
W Kunz

ABSTRACT The number of rRNA cistrons is measured by filter saturation hybridization in different stocks of D. hydei, where the wild-type X chromosome has one nucleolus organizer (NO) and the wild-type Y has two separated NO's. (see PDF) females having no X chromosomal NO show an rDNA content exceeding that of a Y chromosome. An even greater increase in the rRNA cistron number is measured in two translocation stocks where the (see PDF) is combined with one half of a Y and, therefore, each stock contains only one of the two Y chromosomal NO's. But when the same Y fragments are brought together with a wild-type X chromosome they lose about one-half of their rRNA cistrons within one generation. Males with two complementary Y fragments but having no X chromosomal NO show a considerably higher rDNA content than the (see PDF) females, although both are equal in respect of their NO number. Consideration is given to related phenomena in Drosophila melanogaster.


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