scholarly journals A NOTE ON THE MATERNAL EFFECT MUTANTS DAUGHTERLESS AND ABNORMAL OOCYTE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Sex Chromosome ◽  
Chromosome 2 ◽  
Dominant Marker ◽  
Enhancing Effect ◽  
X Irradiation ◽  
The Right ◽  
Chromosome Breakpoint ◽  
Special Region

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.

scholarly journals EVIDENCE FOR A SET OF CLOSELY LINKED AUTOSOMAL GENES THAT INTERACT WITH SEX-CHROMOSOME HETEROCHROMATIN IN DROSOPHILA MELANOGASTER

Genetics ◽  
1977 ◽  
Vol 86 (3) ◽  
pp. 567-582
Author(s):  
L Sandler
Keyword(s):  
Drosophila Melanogaster ◽  
Salivary Gland ◽  
Y Chromosome ◽  
Maternal Effect ◽  
Sex Chromosome ◽  
Salivary Gland Chromosome ◽  
Chromosome 2 ◽  
Chromosome Map ◽  
Heterochromatic Segment ◽  
Special Region

ABSTRACT It is proposed that there exists a special region in the euchromatin of the left arm of chromosome 2 (contained within sections 31-32 of the standard salivary gland chromosome map) that is defined by a set of genes, each one of which interacts with a specific sex-chromosome heterochromatic segment. The evidence for the existence of this region is, first, the exhibition, mapping, and analysis of five different maternal-effect, embryonic semi-lethals located in region 31-32. Secondly, in each case the consequence of the maternal effect is markedly influenced by the amount of X- or Y-chromosome heterochromatin carried by the progeny of mutant mothers. The nature of this interaction and possible reasons for the existence of the cluster of autosomal genes are discussed

scholarly journals Segregation of centric Y-autosome translocations in Drosophila melanogaster: II. Segregation determinants in females

1985 ◽  
Vol 45 (1) ◽  
pp. 81-93 ◽  
Author(s):  
Raphael Falk ◽  
Ana Rahat ◽  
Shula Baker
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Chromosome ◽  
Break Point ◽  
Chromosome Length ◽  
Segregation Pattern ◽  
Chromosome 2 ◽  
Chromosomal Segregation ◽  
Analysis Of Results ◽  
The Right

SummaryThis is a study of the chromosomal segregation patterns in females of 15 Experimental stocks of Drosophila melanogaster, each carrying one element of a T (Y; 2) with a centric break-point. In each Experimental stock the relative frequency of all eight possible meiotic configurations of four relevant chromosomal elements was followed: an attached-X chromosome, a multiply-inverted chromosome 2, a free arm of chromosome 2, and a half-translocation element. Although the 15 translocation elements were broken at different sites, there were no basic differences among the Experimental stocks in their segregation patterns. The three two-by-two configurations were the most common. Comparison of this pattern with that of the segregation pattern of stocks similar but for an inversion-free chromosome 2, showed that in the Experimental stocks exchange pairing did not play a significant role in the determination of the segregation pattern.The results of these experiments, together with the analysis of results from other published studies provide evidence against the model that had been forwarded by Grell. According to this model, chromosomes that did not participate in exchange pairing undergo another pairing cycle, in which total chromosome length is a factor in the determination of segregation.We support a modified version of Novitski's model of premetaphase chromocenter-like chromosome aggregation. Disjunction of non-exchange chromosomes is regulated by determinants located in the proximal heterochromatin of the sex chromosomes and the autosomes. However, the specificity, especially that of the autosomal determinants, is not high. Thus, if an autosome and a sex chromosome are available, their determinants may interact-to-disjoin by default. More frequently, the determinants of the left-arm autosomal element may interact-to-disjoin with those of the right-arm chromosomal element.

scholarly journals Segregation of centric Y-autosome translocations in Drosophila melanogaster: I. Segregation determinants in males

1985 ◽  
Vol 45 (1) ◽  
pp. 51-79 ◽  
Author(s):  
Raphael Falk ◽  
Shula Baker ◽  
Ana Rahat
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Chromosome ◽  
Chromosome 2 ◽  
Chromosome X ◽  
Complete Independence ◽  
Group 2 ◽  
The Right ◽  
Complete Dependence ◽  
Group 1 ◽  
Chromosome Disjunction

SummaryA special screening procedure for the detection of induced Y-autosome translocations with centric breakpoints was applied. A series of Experimental stocks was constructed, each containing a different half of one of the induced T(Y; 2)'s (T element). The three other elements that were involved in the segregation experiments in each stock were a sex chromosome (X element), an inverted chromosome 2 (A element), and a free arm of chromosome 2 (F element). It is not feasible to determine the relative frequencies of all the 16 possible gamete types by mating an Experimental stock to one tester, nor to different testers that have each at least one class of progeny of the same genotype. Each Experimental stock was mated to four different Tester stocks and the data were calibrated so that a coherent segregation pattern could be obtained.Segregation patterns in meiosis of males from 15 Experimental stocks, each with a different T element were studied. In most Experimental stocks the T element was of the left autosomal arm, while the F element was of the right autosomal arm. In four Experimental stocks the X element segregated independently of the A, F and T elements. In these Group 1 stocks, both the F and the T elements disjoined regularly from the A element. It was concluded that the T element of these stocks had no sex-chromosome disjunction determinants (‘S-determinants’) to interact with the determinants on the X element. Both the T elements and the F elements carried autosomal disjunction determinants (‘H-determinants’) that secured the segregation of the autosomal elements. The H-determinants of the left autosomal arm were qualitatively different from those of the right arm.In the remaining 11 Group-2 Experimental stocks the X and T elements disjoined regularly, indicating the presence of S-determinants on the T elements of these stocks. The segregation of the T and the A elements in these stocks varied from nearly complete dependence to complete independence. It was concluded that this gradation reflected differences in the quantity of H-determinants present on the T elements of these Experimental stocks. It was impossible to discriminate between a model of continuous H determinants activity and one of a finite discrete number of determinants. The results do not agree with the claim that there are no autosomal disjunction determinants in the proximal heterochromatin of chromosome 2.The S-determinants on the BsYy+ chromosome were located both adjacent to the centromere and distally on the long arm. The latter were probably translocated to the Y chromosome together with the Bs marker.

scholarly journals TEMPERATURE-SENSITIVE MUTATIONS IN DROSOPHILA MELANOGASTER. IX. DOMINANT COLD-SENSITIVE LETHALS ON THE AUTOSOMES

Genetics ◽  
1972 ◽  
Vol 70 (1) ◽  
pp. 75-86
Author(s):  
Raja Rosenbluth ◽  
Dean Ezell ◽  
David T Suzuki
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Ethyl Methanesulfonate ◽  
Temperature Sensitive ◽  
Chromosome 2 ◽  
Prolonged Incubation ◽  
Larval Instars ◽  
Lethal Mutations ◽  
Cold Sensitive

ABSTRACT Ethyl methanesulfonate-treated autosomes were screened for the presence of dominant cold-sensitive (DCS) lethal mutations in Drosophila melanogaster. None was found among 6,552 treated and 168 untreated third chromosomes. Twenty-three DCS-L chromosomes which caused death at 17°C but survived at 22°C and 29°C were recovered from 5,046 mutagenized chromosome 2's.—The DCS-L mutations all mapped around dp and appeared to be functionally allelic. Lethality of heterozygotes for most of the DCS-L's occurred over a prolonged interval from the embryonic through the larval instars. Prolonged incubation at 17°C did not demonstrate any maternal effect on zygotic survival.

scholarly journals Rescue from the abnormal oocyte maternal-effect lethality by ABO heterochromatin in Drosophila melanogaster.

Genetics ◽  
1991 ◽  
Vol 128 (3) ◽  
pp. 583-594 ◽  
Author(s):  
J Tomkiel ◽  
S Pimpinelli ◽  
L Sandler
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Sex Chromosome ◽  
Event Analysis ◽  
Vital Function ◽  
Early Cleavage ◽  
Maternal Genome ◽  
Loss Event ◽  
Temporal And Spatial ◽  
Fertilized Egg

Abstract The euchromatic maternal-effect mutation abnormal oocyte (abo), of Drosophila melanogaster interacts with regions of heterochromatin known as ABO, which reside on the X, Y and second chromosomes. Here, we show that survival of progeny from abo females depends in part upon the maternal dosage of ABO heterochromatin. A comparison was made of the recovery of genotypically identical progeny from abo mothers bearing sex chromosomes of various ABO contents. The results show that the recovery of daughters was decreased if mothers were ABO-/ABO-. However, no decrease was observed if mothers were ABO+/ABO-. In addition, the survival of daughters was greater when they received an ABO-X chromosome from an ABO-/ABO+ mother rather than the father. We suggest that these results reflect a complementation or interaction between the ABO-deficient X and the ABO heterochromatin in the maternal genome. This proposed interaction could occur early in oogenesis in the mother or prior to completion of meiosis I in the fertilized egg. To determine if zygotic dosage of ABO heterochromatin might also be important at very early stages of embryogenesis, we examined the timing of zygotic rescue by paternally donated ABO heterochromatin using a second mutation, paternal loss (pal). Homozygous pal males produce progeny which lose paternally derived chromosomes during the early zygotic divisions. Zygotes that have lost a paternal sex chromosome in a fraction of their nuclei will be mosaic for the amount of ABO heterochromatin. By monitoring the recovery of pal-induced mosaics from abo and abo+ females, we could determine the temporal and spatial requirements for ABO function. Results show that the survival of progeny from the abo maternal-effect lethality was increased if ABO heterochromatin was present prior to the pal-induced loss event. Analysis of mosaic patterns did not reveal a specific lethal focus. We conclude from these results that ABO heterochromatin serves its vital function prior to completion of the early cleavage divisions in progeny of abo mothers.

scholarly journals Somatic reversion of P transposable element insertion mutations in the singed locus of Drosophila melanogaster requiring specific P insertions and a trans- acting factor

1989 ◽  
Vol 54 (2) ◽  
pp. 101-112 ◽  
Author(s):  
John F. Y. Brookfield ◽  
Alan P. Lewis
Keyword(s):  
Drosophila Melanogaster ◽  
Transposable Element ◽  
Maternal Effect ◽  
P Element ◽  
Chromosome 2 ◽  
Restriction Maps ◽  
Element Insertion ◽  
Somatic Reversion ◽  
P Transposable Element ◽  
Insertion Mutations

SummaryDestabilization in somatic cells of P-element insertions in the X-linked singed gene of Drosophila melanogaster has been studied. We have shown that some but not all unstable P-element insertions in singed can form mosaics. The cause of this variation is not clear from studies of the restriction maps of the mutations tested. The transposable element movements occur early in development and require, in addition to an appropriate P-element insertion in singed, a trans-acting maternal effect component. Movements appear to occur preferentially in attached-X stocks. However, the maternal effect component maps to the central region of chromosome 2.

FURTHER CHARACTERIZATION OF GENETIC ELEMENTS ASSOCIATED WITH THE SEGREGATION DISTORTER PHENOMENON IN DROSOPHILA MELANOGASTER

Genetics ◽  
1985 ◽  
Vol 110 (4) ◽  
pp. 671-688
Author(s):  
Cecil B Sharp ◽  
Arthur J Hilliker ◽  
David G Holm
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome 2 ◽  
Major Focus ◽  
Genetic Components ◽  
Segregation Distorter ◽  
Crossover Analysis ◽  
Radiation Induced ◽  
Definition Of ◽  
The Right

ABSTRACT 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.

scholarly journals Essential Loci in Centromeric Heterochromatin of Drosophila melanogaster. I: The Right Arm of Chromosome 2

Genetics ◽  
2010 ◽  
Vol 185 (2) ◽  
pp. 479-495 ◽  
Author(s):  
Alistair B. Coulthard ◽  
Christina Alm ◽  
Iulia Cealiac ◽  
Don A. Sinclair ◽  
Barry M. Honda ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Centromeric Heterochromatin ◽  
Chromosome 2 ◽  
The Right

abnormal chromatin (abc), a maternal-effect locus in Drosophila melanogaster

1991 ◽  
Vol 98 (2) ◽  
pp. 233-243 ◽  
Author(s):  
K.B. Vessey ◽  
R.L. Ludwiczak ◽  
A.S. Briot ◽  
E.M. Underwood
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Chromosome Structure ◽  
Nuclear Division ◽  
Embryonic Cell ◽  
Female Sterility ◽  
Chromosome 2 ◽  
Maternal Effect Gene ◽  
Embryonic Cell Cycle ◽  
Effect Gene

Mutations in the maternal-effect gene abnormal chromatin (abc) in Drosophila melanogaster result in a variety of defects involving nuclear replication/division. Three recessive alleles of this gene, which maps near 51F on chromosome 2, all result in female sterility. They cause slower embryonic development that is usually abnormal from the earliest nuclear divisions and arrested by the sixth one. Nuclei tend to be large and erratically distributed, some intensely staining. Mitotic asynchrony is common. Few embryos reach the gastrula stage and none hatch. With the weakest allele, fsPL, bridges between nuclei are common; abnormal chromatin clumps that resemble yolk nuclei occur before the other nuclei reach the surface; and spindle anomalies and DNA wads with numerous centrosomes are seen. Females with the stronger alleles, fsA5 and fs27, lay fewer eggs and a smaller proportion of embryos reach blastoderm; developmental arrest occurs earlier, usually with several large nuclei distributed along the length of the embryo. Chorion defects occur in all three mutants. Mitotic asynchrony, nuclear bridging, endoreduplication and nuclear behavior aberrant from the first division suggest that the abc gene product operates in DNA replication/nuclear division. Larval (homozygous F1) neuroblast chromosome structure and mitotic indices are normal, indicating that any mitotic function is strictly maternal, i.e. abc is not a general mitotic gene. Thus abc is one of a few known genes with a maternal effect that appears to function in the embryonic cell cycle.

Genetic Analysis of Drosophila melanogaster Polytene Chromosome Region 44D–45F: Loci Required for Viability and Fertility

Genetics ◽  
2002 ◽  
Vol 160 (4) ◽  
pp. 1503-1510
Author(s):  
Stephanie E Mohr ◽  
Robert E Boswell
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome Region ◽  
Genetic Screen ◽  
P Element ◽  
Chromosome 2 ◽  
X Rays ◽  
Induced Mutations ◽  
Stage 4 ◽  
Germline Cyst ◽  
The Right

Abstract A genetic screen to identify mutations in genes in the 45A region on the right arm of chromosome 2 that are involved in oogenesis in Drosophila was undertaken. Several lethal but no female sterile mutations in the region had previously been identified in screens for P-element insertion or utilizing X rays or EMS as a mutagen. Here we report the identification of EMS-induced mutations in 21 essential loci in the 45D–45F region, including 13 previously unidentified loci. In addition, we isolated three mutant alleles of a newly identified locus required for fertility, sine prole. Mutations in sine prole disrupt spermatogenesis at or before individualization of spermatozoa and cause multiple defects in oogenesis, including inappropriate division of the germline cyst and arrest of oogenesis at stage 4.

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