scholarly journals ANALYSIS OF THE AUTOSOMAL MUTATION abo AND ITS INTERACTION WITH THE RIBOSOMAL DNA OF DROSOPHILA MELANOGASTER: THE ROLE OF X-CHROMOSOME HETEROCHROMATIN

Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 661-672
Author(s):  
Barry Yedvobnick ◽  
Hallie M Krider ◽  
Bryan I Levine

ABSTRACT The autosomal recessive, maternal-effect mutation abnormal oocyte (abo: 2-38) preferentially lowers the viability of XO progeny. The severity of the sex-ratio distortion is reduced by duplications of maternal or zygotic heterochromatin chromatin (SANDLER 1970, 1977; PARRY and SANDLER 1974). Utilizing X-chromosome inversions that contain modifications in the quantity and arrangement of the heterochromatic functions, Xhabo and cr  +, we have extended our investigations of nbo's influence on XO male recovery and rDNA redundancy (KRIDER,YEDVOBNICK and LEVINE 1979).——XO males bearing In(1)scs1Lsc4R or In(1)wm4Lsc4R are recovered twice as frequently as X chromosomes containing a single Xh region, implying that these inversions possess a duplication of Xhabo. abo mutant females heterozygous for In(1)scs1Lsc4R and wild-type X chromosomes generate XO progeny that do not contain elevated rDNA redundancies. XO males containing In(1)wm4 exhibit male recoveries and rDNA elevations similar to those of males bearing a wild-type X chromosome, when both derive from a common abo/abo mother. Reciprocal crosses between In(1)wm4 and Canton-S males to attached-X abo females show significant, though reduced, sex ratios in the absence of an rDNA effect. The observation that abo can elevate the rDNA redundancy of In(1)wm4, a chromosome that does not compensate, suggests that abo and cr+ functions are not directly related.

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.


Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 1063-1075
Author(s):  
M.C. Lienhard ◽  
R.F. Stocker

The development of the sensory neuron pattern in the antennal disc of Drosophila melanogaster was studied with a neuron-specific monoclonal antibody (22C10). In the wild type, the earliest neurons become visible 3 h after pupariation, much later than in other imaginal discs. They lie in the center of the disc and correspond to the neurons of the adult aristal sensillum. Their axons join the larval antennal nerve and seem to establish the first connection towards the brain. Later on, three clusters of neurons appear in the periphery of the disc. Two of them most likely give rise to the Johnston's organ in the second antennal segment. Neurons of the olfactory third antennal segment are formed only after eversion of the antennal disc (clusters t1-t3). The adult pattern of antennal neurons is established at about 27% of metamorphosis. In the mutant lozenge3 (lz3), which lacks basiconic antennal sensilla, cluster t3 fails to develop. This indicates that, in the wild type, a homogeneous group of basiconic sensilla is formed by cluster t3. The possible role of the lozenge gene in sensillar determination is discussed. The homeotic mutant spineless-aristapedia (ssa) transforms the arista into a leg-like tarsus. Unlike leg discs, neurons are missing in the larval antennal disc of ssa. However, the first neurons differentiate earlier than in normal antennal discs. Despite these changes, the pattern of afferents in the ectopic tarsus appears leg specific, whereas in the non-transformed antennal segments a normal antennal pattern is formed. This suggests that neither larval leg neurons nor early aristal neurons are essential for the outgrowth of subsequent afferents.


2005 ◽  
Vol 168 (3) ◽  
pp. 365-373 ◽  
Author(s):  
Joost Gribnau ◽  
Sandra Luikenhuis ◽  
Konrad Hochedlinger ◽  
Kim Monkhorst ◽  
Rudolf Jaenisch

In mammals, dosage compensation is achieved by X chromosome inactivation in female cells. Xist is required and sufficient for X inactivation, and Xist gene deletions result in completely skewed X inactivation. In this work, we analyzed skewing of X inactivation in mice with an Xist deletion encompassing sequence 5 KB upstream of the promoter through exon 3. We found that this mutation results in primary nonrandom X inactivation in which the wild-type X chromosome is always chosen for inactivation. To understand the molecular mechanisms that affect choice, we analyzed the role of replication timing in X inactivation choice. We found that the two Xist alleles and all regions tested on the X chromosome replicate asynchronously before the start of X inactivation. However, analysis of replication timing in cell lines with skewed X inactivation showed no preference for one of the two Xist alleles to replicate early in S-phase before the onset of X inactivation, indicating that asynchronous replication timing does not play a role in skewing of X inactivation.


The occurrence of mutants of Drosophila melanogaster distinguished by the absence or structural modification of the antennae provides a means of assessing the role of the antennae with respect to the reception of various classes of stimuli. Antennaless ( A 0 ) phenotypes of antennaless stock fail to respond to those chemical stimuli which lead the fly to its food. Their temperature reactions are normal, and their humidity responses are opposite to those of somatically wild-type flies of the same stock or of wild-type controls. Aristapedia ( ss a ), which have leg-like antennae equipped with surface pegs and cones of supposed sensory function present in the normal antenna but absent in the normal leg, respond to chemical stimuli and humidity differences. As compared with that of normal flies, the olfactory response of aristapedia ( ss a ) is somewhat less intense, the humidity reaction being somewhat stronger. These mutants do not give the characteristic responses evoked by thermal stimuli both in normal flies and antennaless phenotypes. The outstanding histological differences between the structure of the antenna of aristapedia and that of wild-type flies is the absence of the pit organ. It thus seems that the pit organ is not essential to the olfactory response and plays no essential part in the humidity response. Since antennaless ( A 0 ) responds normally to thermal stimuli, none of the putative sense organs of the antennae are essential to the recognition of temperature differences, and since aristapedia ( ss a ) responds more weakly to chemical stimuli than do normal flies, the pit organs may well be long-distance chemoreceptors. What is more certain is that either the peg-like organs or the cones on the surface of the distal joint of the antennae or both are chemoreceptors. The same remark is equally applicable to the perception of humidity differences. Experiments here recorded do not justify the identification of the function of one or other type of sensilla with one or the other type of receptivity. While it is unjustifiable to exclude the possibility that short-distance chemical stimuli play a part in the attraction of flies of opposite sex, it appears that the main role of chemoreceptivity in relation to the mating behaviour of D. melanogaster is to ensure the aggregation of flies of both sexes in situations where food is available and sexual congress can be evoked by other forms of stimulation.


Genome ◽  
2002 ◽  
Vol 45 (5) ◽  
pp. 871-880 ◽  
Author(s):  
A Gariou-Papalexiou ◽  
G Yannopoulos ◽  
A Zacharopoulou ◽  
R H Gooding

Photographic polytene chromosome maps from trichogen cells of pharate adult Glossina morsitans submorsitans were constructed. Using the standard system employed to map polytene chromosomes of Drosophila, the characteristic landmarks were described for the X chromosome and the two autosomes (L1 and L2). Sex-ratio distortion, which is expressed in male G. m. submorsitans, was found to be associated with an X chromosome (XB) that contains three inversions in each arm. Preliminary data indicate no differences in the fecundity of XAXA and XAXB females, but there are indications that G. m. submorsitans in colonies originating from Burkina Faso and Nigeria have genes on the autosomes and (or) the Y chromosome that suppress expression of sex-ratio distortion.Key words: tsetse, Glossina morsitans submorsitans, polytene chromosome maps, inversions, sex-ratio distortion.


Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 95-103
Author(s):  
R J Morrison ◽  
J D Raymond ◽  
J R Zunt ◽  
J K Lim ◽  
M J Simmons

Abstract Males carrying different X chromosomes were tested for the ability to produce daughters with attached-X chromosomes. This ability is characteristic of males carrying an X chromosome derived from 59b-z, a multiply marked X chromosome, and is especially pronounced in males carrying the unstable 59b-z chromosomes Uc and Uc-lr. Recombination experiments with one of the Uc-lr chromosomes showed that the formation of compound chromosomes depends on two widely separated segments. One of these is proximal to the forked locus and is probably proximal to the carnation locus. This segment may contain the actual site of chromosome attachment. The other essential segment lies between the crossveinless and vermilion loci and may contain multiple factors that influence the attachment process.


Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 455-470
Author(s):  
Hideh Harger ◽  
David G Holm

ABSTRACT In females of Drosophila melanogaster, compound autosomes enter the repulsion phase of meiosis uncommitted to a particular segregation pattern because their centromeres are not restricted to a bivalent pairing complex as a consequence of crossing over. Their distribution at anaphase, therefore, is determined by some meiotic property other than exchange pairing, a property that for many years has been associated with the concept of nonhomologous pairing. In the absence of heterologous rearrangements or a free Y chromosome, C(3L) and C(3R) are usually recovered in separate gametes, that is as products of meiotic segregation. Nevertheless, there is a regular, albeit infrequent, recovery of reciprocal meiotic products (the nonsegregational products) that are disomic and nullosomic for compound thirds. The frequency of these exceptions, which is normally between 0.5 and 5.0%, differs for the various strains examined, but remains constant for any given strain. Since previous studies have not uncovered a cause for this base level of nonsegregation, it has been referred to as the spontaneous frequency. In this study, crosses between males and females whose X chromosomes, as well as compound autosomes, are differentially marked reveal a highly significant positive correlation between the frequency of compound-autosome nonsegregation and the frequency of X-chromosome nondisjunction. However, an inverse correlation is found when the frequency of nondisjunction is related to the frequency of crossing over in the proximal region of the X chromosome. These findings have been examined with reference to the distributive pairing and the chromocentral models and interpreted as demonstrating (1) that nonsegregational meiotic events arise primarily as a result of nonhomologous interactions, (2) that forces responsible for the segregation of nonhomologous chromosomes are properties of the chromocentral region, and (3) that these forces come into expression after the exchange processes are complete.


2006 ◽  
Vol 2006 ◽  
pp. 1-6 ◽  
Author(s):  
Mary F. Lyon

There is longstanding evidence that X-chromosome inactivation (XCI) travels less successfully in autosomal than in X-chromosomal chromatin. The interspersed repeat elements LINE1s (L1s) have been suggested as candidates for “boosters” which promote the spread of XCI in the X-chromosome. The present paper reviews the current evidence concerning the possible role of L1s in XCI. Recent evidence, accruing from the human genome sequencing project and other sources, confirms that mammalian X-chromosomes are indeed rich in L1s, except in regions where there are many genes escaping XCI. The density of L1s is the highest in the evolutionarily oldest regions. Recent work on X; autosome translocations in human and mouse suggested failure of stabilization of XCI in autosomal material, so that genes are reactivated, but resistance of autosomal genes to the original silencing is not excluded. The accumulation of L1s on the X-chromosome may have resulted from reduced recombination or late replication. Whether L1s are part of the mechanism of XCI or a result of it remains enigmatic.


Author(s):  
Yehonatan Alcalay ◽  
Silke Fuchs ◽  
Roberto Galizi ◽  
Federica Bernardini ◽  
Roya Elaine Haghighat-Khah ◽  
...  

Sex-ratio distorters based on X-chromosome shredding are more efficient than sterile male releases for population suppression. X-shredding is a form of sex distortion that skews spermatogenesis of XY males towards the preferential transmission of Y-bearing gametes, resulting in a higher fraction of sons than daughters. Strains harboring X-shredders on autosomes were first developed in the malaria mosquito Anopheles gambiae, resulting in strong sex-ratio distortion. Since autosomal X-shredders are transmitted in a Mendelian fashion and can be selected against, their frequency in the population declines once releases are halted. However, unintended transfer of X-shredders to the Y-chromosome could produce an invasive meiotic drive element, that benefits from its biased transmission to the predominant male-biased offspring and its effective shielding from female negative selection. Indeed, linkage to the Y-chromosome of an active X-shredder instigated the development of the nuclease-based X-shredding system. Here, we analyze mechanisms whereby an autosomal X-shredder could become unintentionally Y-linked after release by evaluating the stability of an established X-shredder strain that is being considered for release, exploring its potential for remobilization in laboratory and wild-type genomes of An. gambiae and provide data regarding expression on the mosquito Y-chromosome. Our data suggest that an invasive X-shredder resulting from a post-release movement of such autosomal transgenes onto the Y-chromosome is unlikely.


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