The meiotic behavior of some single-cistron mutants in the zeste-white region of the Drosophila melanogaster X chromosome

1981 ◽  
Vol 183 (2) ◽  
pp. 214-219 ◽  
Author(s):  
Leonard G. Robbins
Genetics ◽  
1980 ◽  
Vol 94 (2) ◽  
pp. 361-381
Author(s):  
Leonard G Robbins

ABSTRACT Heterozygosity for a deficiency for the entire zeste-white region of the X chromosome of Drosophila melanogaster females causes both reduced recombination and increased nondisjunction. The location of the dosage-sensitive sites responsible for these two meiotic defects has been studied by use of a set of deficiencies that subdivide the region. Recombination is reduced when the zw7-zwll region is present in one dose, while nondisjunction is increased only if the doses of both the zw8-zwl0 and zwb-zwll segments are reduced. Examination of truns heterozygotes of two deficiencies explicitly demonstrates the compound nature of the meiotic dose effect and further delimits the location of the proximal disjunctional site to the zwl2-zwll interval. In inversion/deficiency heterozygotes, reduced dose ofthe zw8-zwl0 region alone, without reduced dose of the proximal site, yields increased nondisjunction, suggesting that the proximal element that affects disjunction is the same as that which affects recombination. Thus, the zeste-white region contains at least two dosagesensitive loci that affect meiosis: reduced dosage of one locus, in the zw7-zwfl interval, causes reduced recombination; reduced dose of another, in the zw8-zw10 region, increases the probability that nonexchange chromosomes will nondisjoin. Aslight effect on the regional distribution of exchange may also be a property of the zw8-zwlO region locus, but could be an effect of yet another locus or of structural heterozygosity. The implications of these results for understanding meiotic control and the prospects for further analysis of the structure of the zeste-white interval are considered.


Genetics ◽  
1972 ◽  
Vol 72 (4) ◽  
pp. 615-638 ◽  
Author(s):  
M P Shannon ◽  
T C Kaufman ◽  
M W Shen ◽  
B H Judd

ABSTRACT Aspects of the developmental genetics of lethal and semi-lethal mutants representing 13 complementation groups (cistrons) in the 3A-3C region of the X chromosome of Drosophila melanogaster are given. Each of these cistrons is associated with a particular chromomere in the salivary gland chromosome. Mutants within each cistron have similar lethality patterns and morphological attributes, and the characteristics of a given cistron are distinct with respect to other cistrons. These results provide additional evidence that only one function is associated with each chromomere.—The results of the lethality pattern analysis are also compared with previous studies of lethal mutants of Drosophila.


Genetics ◽  
1977 ◽  
Vol 87 (4) ◽  
pp. 655-684
Author(s):  
Leonard G Robbins

ABSTRACT The meiotic effects of heterozygosity for a deficiency of the zeste-white region of the X chromosome include reduced recombination and increased non-disjunction of the entire chromosome complement. Reduced dosage of a gene or genes in the zeste-white interval, rather than structural heterozygosity, is responsible for the meiotic effect. A model for the recombination effects of reduced enzyme concentration has been developed, and its consequences are comparable with the results obtained for deficiency heterozygosity. Thus, all of the observations can be accounted for by imagining a dosage-sensitive locus in the zeste-white region that codes for an enzyme involved in the recombination process. The interaction of the interchromosomal effect of heterozygous inversions with the deficiency has been examined, and the possibility of using the model for the analysis of other meiotic phenomena is considered.


Genetics ◽  
1975 ◽  
Vol 79 (4) ◽  
pp. 601-611
Author(s):  
C P Liu ◽  
J K Lim

ABSTRACT Recessive lethal mutations in the 3A1 to 3C2 region of the X chromosome of Drosophila melanogaster were detected in 113 of 33,544 sperm treated by feeding 5 mM methyl methanesulfonate in 1% sucrose for 22 hours. Seven of the 113 lethals were sterile, leaving 106 for analysis by complementation tests. With only one exception, these mutants were found to have lesions restricted to single loci. One of these single-site mutations was in gt, 2 in tko, 18 in zw-1, 12 in zw-8, 6 in zw-4, 3 in zw-10, 3 in zw-13, 21 in zw-2, 7 in zw-3, 5 in zw-6, 6 in zw-12, 1 in zw-7, 12 in zw-5, 5 in zw-11, and 3 in zw-9, One of the lethals, m69, was non-complementary to two adjacent loci, zw-2 and zw-3, possibly indicating a deletion encompassing two loci. The results confirm that there are at least 15 recessive lethal loci in the region and are consistent with the hypothesis of Lim and Snyder (1968 and 1974) that inability of monofunctional alkylating chemicals to induce deletion-associated mutations is a characteristic of the compounds.


Genetics ◽  
1980 ◽  
Vol 96 (1) ◽  
pp. 187-200 ◽  
Author(s):  
Leonard G Robbins

ABSTRACT The possibility that essential loci in the zeste-white region of the Drosophila melanogaster X chromosome are expressed both maternally and zygotically has been tested. Maternal gene activity was varied by altering gene dose, and zygotic gene activity was manipulated by use of position-effect variegation of a duplication. Viability is affected when both maternal and zygotic gene activity are reduced, but not when either maternal or zygotic gene activity is normal. Tests of a set of overlapping deficiencies demonstrate that at least three sections of the zeste-white region yield maternal zygotic lethal interactions. Single-cistron mutations at two loci in one of these segments have been tested, and maternal heterozygosity for mutations at both loci give lethal responses of mutant-duplication zygotes. Thus, at least four of the 13 essential functions coded in the zeste-white region are active both maternally and zygotically, suggesting that a substantial fraction of the genome may function at both stages. The normal survival of zygotes when either maternal gene expression or zygotic gene expression is normal, and their inviability when both are depressed, suggests that a developmental stage exists when maternally determined functions and zygotically coded functions are both in use.


Genetics ◽  
1979 ◽  
Vol 91 (3) ◽  
pp. 537-551
Author(s):  
L Sandler ◽  
Joseph O'Tousa

ABSTRACT Previous studies of reversed acrocentric compound-X chromosomes suggested peculiar influences of heterochromatin on both the synthesis and meiotic behavior of such compounds. It seemed, with respect to synthesis, that the long arm of the Y chromosome on an X.YL chromosome was necessary in order for the heterochromatic exchange giving rise to reversed acrocentrics to occur, even though YL itself did not participate in the compound-generating event. With respect to behavior, the resulting compounds appeared, presumably as a consequence of their singular generation, to contain an interstitial heterochromatic region that caused the distribution of exchanges between the elements of the compound to be abnormal (many zero and two-exchange tetrads with few, if any, single-exchange tetrads). Removing the interstitial heterochromatin (or, curiously, appending YL as a second arm of the compound) eliminated the recombinational anomalies and resulted in typical tetrad distributions.—We provide evidence that these peculiarities, while presumably real, were likely the consequence of a special X.YL chromosome that was used to synthesize the reversed acrocentrics examined in the early studies and are not general properties of either reversed acrocentric compounds or of interstitial heterochromatin. However, we show that specific heterochromatic regions do, in fact, profoundly influence the behavior of (apparently all) reversed acrocentric compound-X chromosomes. In particular, we demonstrate that specific portions of the Y chromosome and of the basal X-chromosome heterochromatin, when present as homologs for reversed acrocentric compounds, markedly and coordinately increase bath the frequency of exchange between the elements of the compound and the fertility (egg production) of compound-bearing females. It is, we suppose, some aspect of this heterochromatic effect, produced by the% special X.YL chromosome, that caused the earlier-analyzed compounds to exhibit the observed anomalies.


Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1303-1316
Author(s):  
Michael W Nachman

Introns of four X-linked genes (Hprt, Plp, Glra2, and Amg) were sequenced to provide an estimate of nucleotide diversity at nuclear genes within the house mouse and to test the neutral prediction that the ratio of intraspecific polymorphism to interspecific divergence is the same for different loci. Hprt and Plp lie in a region of the X chromosome that experiences relatively low recombination rates, while Glra2 and Amg lie near the telomere of the X chromosome, a region that experiences higher recombination rates. A total of 6022 bases were sequenced in each of 10 Mus domesticus and one M. caroli. Average nucleotide diversity (π) for introns within M. domesticus was quite low (π = 0.078%). However, there was substantial variation in the level of heterozygosity among loci. The two telomeric loci, Glra2 and Amg, had higher ratios of polymorphism to divergence than the two loci experiencing lower recombination rates. These results are consistent with the hypothesis that heterozygosity is reduced in regions with lower rates of recombination, although sampling of additional genes is needed to establish whether there is a general correlation between heterozygosity and recombination rate as in Drosophila melanogaster.


Genetics ◽  
1982 ◽  
Vol 101 (3-4) ◽  
pp. 461-476
Author(s):  
Todd R Laverty ◽  
J K Lim

ABSTRACT In this study, we show that at least one lethal mutation at the 3F-4A region of the X chromosome can generate an array of chromosome rearrangements, all with one chromosome break in the 3F-4A region. The mutation at 3F-4A (secondary mutation) was detected in an X chromosome carrying a reverse mutation of an unstable lethal mutation, which was mapped in the 6F1-2 doublet (primary mutation). The primary lethal mutation at 6F1-2 had occurred in an unstable chromosome (Uc) described previously (Lim 1979). Prior to reversion, the 6F1-2 mutation had generated an array of chromosome rearrangements, all having one break in the 6F1-2 doublet (Lim 1979, 1980). In the X chromosomes carrying the 3F-4A secondary lethal mutation the 6F1-2 doublet was normal and stable, as was the 3F-4A region in the X chromosome carrying the primary lethal mutation. The disappearance of the instability having a set of genetic properties at one region (6F1-2) accompanied by its appearance elsewhere in the chromosome (3F-4A) implies that a transposition of the destabilizing element took place. The mutant at 3F-4A and other secondary mutants exhibited all but one (reinversion of an inversion to the normal sequence) of the eight properties of the primary lethal mutations. These observations support the view that a transposable destabilizing element is responsible for the hypermutability observed in the unstable chromosome and its derivaties.


Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 627-636
Author(s):  
C Q Lai ◽  
T F Mackay

Abstract To determine the ability of the P-M hybrid dysgenesis system of Drosophila melanogaster to generate mutations affecting quantitative traits, X chromosome lines were constructed in which replicates of isogenic M and P strain X chromosomes were exposed to a dysgenic cross, a nondysgenic cross, or a control cross, and recovered in common autosomal backgrounds. Mutational heritabilities of abdominal and sternopleural bristle score were in general exceptionally high-of the same magnitude as heritabilities of these traits in natural populations. P strain chromosomes were eight times more mutable than M strain chromosomes, and dysgenic crosses three times more effective than nondysgenic crosses in inducing polygenic variation. However, mutational heritabilities of the bristle traits were appreciable for P strain chromosomes passed through one nondysgenic cross, and for M strain chromosomes backcrossed for seven generations to inbred P strain females, a result consistent with previous observations on mutations affecting quantitative traits arising from nondysgenic crosses. The new variation resulting from one generation of mutagenesis was caused by a few lines with large effects on bristle score, and all mutations reduced bristle number.


Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Leonard G Robbins

Abstract Rex is a multicopy genetic element that maps within an X-linked ribosomal RNA gene (rDNA) array of D. melanogaster. Acting maternally, Rex causes recombination between rDNA arrays in a few percent of early embryos. With target chromosomes that contain two rDNA arrays, the exchanges either delete all of the material between the two arrays or invert the entire intervening chromosomal segment. About a third of the embryos produced by Rex homozygotes have cytologically visible chromosome damage, nearly always involving a single chromosome. Most of these embryos die during early development, displaying a characteristic apoptosis-like phenotype. An experiment that tests whether the cytologically visible damage is rDNA-specific is reported here. In this experiment, females heterozygous for Rex and an rDNA-deficient X chromosome were crossed to males of two genotypes. Some of the progeny from the experimental cross entirely lacked rDNA, while all of the progeny from the control cross had at least one rDNA array. A significantly lower frequency of early-lethal embryos in the experimental cross, proportionate to the fraction of rDNA-deficient embryos, demonstrates that Rex preferentially damages rDNA.


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