scholarly journals THE GENETICS OF THE DORSAL-BICAUDAL-D REGION OF DROSOPHILA MELANOGASTER

Genetics ◽  
1986 ◽  
Vol 113 (3) ◽  
pp. 665-678
Author(s):  
Ruth Steward ◽  
Christiane Nüsslein-Volhard
Keyword(s):  
Maternal Effect ◽  
Complementation Group ◽  
Drosophila Embryo ◽  
Temperature Sensitive ◽  
X Ray ◽  
Dominant Phenotype ◽  
Maternal Effect Genes ◽  
D Region ◽  
Complementation Groups ◽  
Anterior Posterior

ABSTRACT The chromosomal region 36C on 2L contains two maternal-effect loci, dorsal (dl) and Bicaudal-D (Bic-D), which are involved in establishing polarity of the Drosophila embryo along the dorsal-ventral and anterior-posterior axes, respectively. To analyze the region genetically, we isolated X-ray-induced dorsal alleles, which we recognized by virtue of the haplo-insufficient temperature-sensitive dorsal-dominant phenotype in progeny of single females heterozygous for a mutagenized chromosome. From the 20,000 chromosomes tested, we isolated three deficiencies, two inversions with breakpoint in dl and one apparent dl point mutant. One of the deficiencies, Df(2L)H20 (36A6,7; 36F1,2) was used to screen for EMS-induced lethal- and maternal-effect mutants mapping in the vicinity of dl and Bic-D. We isolated 44 lethal mutations defining 11 complementation groups. We also recovered as maternal-effect mutations four dl alleles, as well as six alleles of quail and one allele of kelch, two previously identified maternal-effect genes. Through complementation tests with various viable mutants and deficiencies in the region, a total of 18 loci were identified in an interval of about 30 cytologically visible bands. The region was subdivided into seven subregions by deficiency breakpoints. One lethal complementation group as well as the two maternal loci, Bic-D and quail, are located in the same deficiency interval as is dl.

scholarly journals MATERNAL-ZYGOTIC GENE INTERACTIONS DURING FORMATION OF THE DORSOVENTRAL PATTERN IN DROSOPHILA EMBRYOS

Genetics ◽  
1983 ◽  
Vol 105 (3) ◽  
pp. 615-632 ◽  
Author(s):  
Pat Simpson
Keyword(s):  
Early Embryo ◽  
Drosophila Embryo ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Mutant Genotype ◽  
Dominant Phenotype ◽  
Zygotic Gene ◽  
Definition Of ◽  
Mutant Phenotypes ◽  
Dominant Lethality

ABSTRACT Maternal-zygotic interactions involving the three genes dorsal (dl), twist (twi) and snail (sna) are described. The results suggest that all three are involved in the process by which the dorsoventral pattern of the Drosophila embryo is established. First, the lethal embryonic mutant phenotypes are rather similar. In homozygous twi or sna embryos invagination of the ventral presumptive mesodermal cells fails to occur, and the resulting embryos are devoid of internal organs. This is very similar to the dominant phenotype described for dl; in the case of dl, however, the effect is a maternal one dependent on the mutant genotype of the female. Second, a synergistic interaction has been found whereby dominant lethality of twi  - or sna-bearing zygotes is observed in embryos derived from heterozygous dl females at high temperature. The temperature sensitivity of this interaction permitted definition of a temperature-sensitive period which is probably that of dl. This was found to extend from approximately 12 hr prior to oviposition to 2— 3 hr of embryogenesis. A zygotic action for the dl gene in addition to the maternal effect was revealed by the finding that extra doses of dl  + in the zygotes can partially rescue the dominant lethality of heterozygous twi embryos derived from heterozygous dl females. Two possible interpretations of the synergism are considered: (1) twi and sna are activated in the embryos as a result of positional signals placed in the egg as a consequence of the functioning of the dl gene during oogenesis and, thus, play a role in embryonic determination. (2) The gene products of dl  + and twi  + (or sna  +) combine to produce a functional molecule that is involved in the specification of dorsoventral pattern in the early embryo.

scholarly journals Temperature-Sensitive Lethal Pseudorevertants of ste Mutations in Saccharomyces cerevisiae

Genetics ◽  
1987 ◽  
Vol 115 (4) ◽  
pp. 627-636
Author(s):  
Margaret E Katz ◽  
Jill Ferguson ◽  
Steven I Reed
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Complementation Group ◽  
Temperature Sensitive ◽  
G1 Arrest ◽  
Pheromone Response ◽  
Cycle Arrest ◽  
Homogeneous Cell ◽  
Complementation Groups ◽  
Mutant Cells

ABSTRACT A procedure was devised to isolate mutations that could restore conjugational competence to temperature sensitive ste mutants and simultaneously confer temperature-sensitive lethal growth phenotypes. Three such mutations, falling into two complementation groups, were identified on the basis of suppression of ste5 alleles. These same mutations were later shown to be capable of suppressing ste4 and ste7 alleles. Five mutations in a single complementation group were isolated as suppressors of ste2 alleles. None of the mutations described in this study conferred a homogeneous cell cycle arrest phenotype, and all were shown to define complementation groups distinct from those previously identified in studies of cell division cycle (cdc) mutations. In no instance did pseudoreversion appear to be achieved by mutational G1 arrest of ste mutant cells. Instead, it is proposed that the mutations restore conjugation by reestablishing the normal pheromone response.

Activation of the easter zymogen is regulated by five other genes to define dorsal-ventral polarity in the Drosophila embryo

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 607-616 ◽  
Author(s):  
R. Chasan ◽  
Y. Jin ◽  
K.V. Anderson
Keyword(s):  
Maternal Effect ◽  
Serine Proteases ◽  
Drosophila Embryo ◽  
Vitelline Membrane ◽  
Mutant Form ◽  
Wild Type ◽  
Zymogen Activation ◽  
Embryonic Polarity ◽  
Dominant Mutant ◽  
Maternal Effect Genes

The product of the Drosophila easter gene, a member of the trypsin family of serine proteases, must be more active ventrally than dorsally to promote normal embryonic polarity. The majority of the easter protein in the embryo is present in the unprocessed zymogen form and appears to be evenly distributed in the extracellular space, indicating that the asymmetric activity of wild-type easter must arise post-translationally. A dominant mutant form of easter that does not require cleavage of the zymogen for activity (ea delta N) is active both dorsally and ventrally. The ea delta N mutant bypasses the requirement for five other maternal effect genes, indicating that these five genes exert their effects on dorsal-ventral patterning solely by controlling the activation of the easter zymogen. We propose that dorsal-ventral asymmetry is initiated by a ventrally-localized molecule in the vitelline membrane that nucleates an easter zymogen activation complex, leading to the production of ventrally active easter enzyme.

scholarly journals A genetic and molecular analysis of the 46C chromosomal region surrounding the FMRFamide neuropeptide gene in Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 137 (1) ◽  
pp. 121-137
Author(s):  
M A O'Brien ◽  
M S Roberts ◽  
P H Taghert
Keyword(s):  
Drosophila Melanogaster ◽  
Molecular Analysis ◽  
Chromosomal Region ◽  
Small Region ◽  
Complementation Group ◽  
P Element ◽  
X Ray ◽  
P Elements ◽  
Complementation Groups ◽  
Gene Maps

Abstract We have analyzed the FMRFamide neuropeptide gene region of Drosophila melanogaster. This gene maps to the 46C region of chromosome 2R; this interval previously was not well characterized. For this genetic and molecular analysis, we have used X-ray mutagenesis, EMS mutagenesis, and the recently reported local P element transposition method. We identified four overlapping deletions, two of which have proximal breakpoints that define a 50-60-kb region surrounding the FMRFamide gene in 46C. To this small region, we mapped three lethal complementation groups; 10 additional lethal complementation groups were mapped to more distal regions of 46CD. One of these groups corresponds to even-skipped, the other 12 are previously unidentified. Using various lines of evidence we excluded the possibility that FMRFamide corresponds to any of the three lethal complementation groups mapping to its immediate 50-60-kb vicinity. The positions of two of the three lethal complementation groups were identified with P elements using a local transposition scheme. The third lethal complementation group was excluded as being FMRFamide mutants by sequence analysis and by immunocytochemistry with proFMRFamide precursor-specific antibodies. This analysis has (1) provided a genetic map of the 46CD chromosomal region and a detailed molecular map of a portion of the 46C region and (2) provided additional evidence of the utility of local transposition for targeting nearby genes.

scholarly journals LETHALS, STERILES AND DEFICIENCIES IN A REGION OF THE X CHROMOSOME OF CAENORHABDITIS ELEGANS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 99-115 ◽  
Author(s):  
Philip M Meneely ◽  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Maternal Effect ◽  
Mutant Allele ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
X Chromosomes ◽  
X Ray ◽  
Chromosome Duplication

ABSTRACT Twenty-one X-linked recessive lethal and sterile mutations balanced by an unlinked X-chromosome duplication have been identified following EMS treatment of the small nematode, Caenorhabditis elegans. The mutations have been assigned by complementation analysis to 14 genes, four of which have more than one mutant allele. Four mutants, all alleles, are temperature-sensitive embryonic lethals. Twelve mutants, in ten genes, are early larval lethals. TWO mutants are late larval lethals, and the expression of one of these is influenced by the number of X chromosomes in the genotype. Two mutants are maternal-effect lethals; for both, oocytes made by mutant hermaphrodites are rescuable by wild-type sperm. One of the maternal-effect lethals and two larval lethals are allelic. One mutant makes defective sperm. The lethals and steriles have been mapped by recombination and by complementation testing against 19 deficiencies identified after X-ray treatment. The deficiencies divide the region, about 15% of the X-chromosome linkage map, into at least nine segments. The deficiencies have also been used to check the phenotypes of hemizygous lethal and sterile hermaphrodites.

Autonomous determination of anterior structures in the early Drosophila embryo by the bicoid morphogen

Development ◽  
1990 ◽  
Vol 109 (4) ◽  
pp. 811-820 ◽  
Author(s):  
W. Driever ◽  
V. Siegel ◽  
C. Nusslein-Volhard
Keyword(s):  
Drosophila Embryo ◽  
Beta Globin ◽  
P Transformation ◽  
Early Drosophila Embryo ◽  
Maternal Effect Genes ◽  
Translational Block ◽  
Maternal Gene ◽  
Anterior Posterior

A small number of maternal effect genes determine anterior-posterior pattern in the Drosophila embryo. Embryos from females mutant for the maternal gene bicoid lack head and thorax. bcd mRNA becomes localized to the anterior tip of the egg during oogenesis and is the source for the morphogen gradient of bcd protein. Here we show that in vitro transcribed bicoid mRNA that has its own leader sequences substituted by the Xenopus beta-globin 5′ untranslated sequences is translated more efficiently than bicoid mRNA with the natural 5′ mRNA leader when tested in vitro and in Drosophila Schneider cells. When injected into bicoid mutant embryos, only the bcd mRNA with the beta-globin leader sequence, substituted for the natural leader, is able to induce anterior development. We used P-transformation to show that sequences in the 5′ leader are neither necessary for localization of the transcript nor for the translational block of the bcd mRNA during oogenesis. For our injection experiments, we used only one of the identified splicing forms of bcd mRNA. The bcd protein species derived from this mRNA is able to induce anterior development at any position along the anterior-posterior axis. Thus bicoid protein can induce development of head and thorax independent of any other specifically localized morphogenetic factor. Our findings further support the notion that the concentration gradient of bcd protein, and not the existence of different forms of bcd protein, is responsible for specifying subregions of the embryo.

scholarly journals Mitotic mutants ofAspergillus nidulans

1975 ◽  
Vol 26 (3) ◽  
pp. 237-254 ◽  
Author(s):  
N. Ronald Morris
Keyword(s):  
Aspergillus Nidulans ◽  
Nuclear Division ◽  
Complementation Group ◽  
Gene Symbol ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Temperature Sensitive Mutants ◽  
Ofaspergillus Nidulans ◽  
Complementation Groups ◽  
Genetic Clustering

SUMMARYForty-five temperature-sensitive mutants ofAspergillus nidulanswhich are defective in nuclear division, septation or distribution of nuclei along the mycelium have been isolated, and most have been subjected to complementation analysis and mapped to chromosome. Thirty-five of the mutants were unable to complete nuclear division at the restrictive temperature. Twenty-six of these mutants exhibited a co-ordinate drop in both spindle and chromosome mitotic indices at 42 °C, indicating that they fail to enter mitosis. These mutants have been assigned to the gene symbolnim. Nine mutants exhibited a co-ordinate rise in spindle and chromosome mitotic indices at 42 °C, indicating that they are arrested in mitosis. These mutants were assigned the gene symbolbim. Five mutants failed to form septa and were given the gene symbolsep; and five mutants had an abnormal nuclear distribution and were given the gene symbolnud. All of the mutations were recessive. Most of the mutants were in different complementation groups. Mutants in the same complementation groups were phenotypically similar, but phenotypically similar mutants were not necessarily or usually in the same complementation group. There was no evidence for genetic clustering of phenotypically similar mutants. The mutants were located on all eight chromosomes.

scholarly journals Suppressors of the organ-specific differentiation gene pha-1 of Caenorhabditis elegans.

Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 69-77 ◽  
Author(s):  
H Schnabel ◽  
G Bauer ◽  
R Schnabel
Keyword(s):  
Caenorhabditis Elegans ◽  
Temperature Sensitive ◽  
Lethal Gene ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
X Ray ◽  
Organ Specific ◽  
Complementation Groups ◽  
Differentiation Gene ◽  
Two Temperature

Abstract The embryonic lethal gene pha-1 of the nematode Caenorhabditis elegans is required for late differentiation and morphogenesis of the pharynx in the developing embryo. Revertants of two temperature-sensitive alleles of pha-1 were isolated with the aim of obtaining mutations in genes that interact with pha-1. By various methods of mutagenesis, chemical, X-ray, transposon, or by spontaneous reversion, 220 recessive revertants were obtained, defining three complementation groups. The largest, sup-35 on linkage group (LG) III, maps close to but is separable from pha-1. This suppressor can exert its effect either maternally or zygotically to allow survival of pha-1(ts) embryos. The other two, sup-36 and sup-37, are required zygotically and map on LGIV and LGV, respectively. We have not noted a phenotype distinguishing any of the suppressors from wild type except for suppression of pha-1. That suppression is the null phenotype of at least sup-35 is indicated by the high frequency of mutation and by the fact that heterozygotes carrying sup-35 and a deficiency spanning the locus are also able to suppress. Five spontaneous mutations in sup-35 were found to be associated with recombination.

scholarly journals Genetics of 51D-52A, a region containing several maternal-effect genes and two maternal-specific transcripts in Drosophila.

Genetics ◽  
1990 ◽  
Vol 126 (3) ◽  
pp. 639-650
Author(s):  
E M Underwood ◽  
A S Briot ◽  
K Z Doll ◽  
R L Ludwiczak ◽  
D C Otteson ◽  
...  
Keyword(s):  
Dna Replication ◽  
Nuclear Division ◽  
Specific Pattern ◽  
Temperature Sensitive ◽  
Lethal Mutations ◽  
Chorion Genes ◽  
Important Region ◽  
Maternal Effect Genes ◽  
Complementation Groups ◽  
Sensitive Allele

Abstract Two genomic clones exhibiting a maternal-specific pattern of expression map to cytological region 52A. To elucidate the function of these clones we have undertaken a mutagenesis of the cytological region 51D-52A. This paper presents the results of this screen and the preliminary analysis of female-sterile and lethal mutations isolated. A total of twelve complementation groups have been identified, four of which are defined exclusively by female-sterile alleles. Only one visible mutation was isolated, a recessive temperature-sensitive allele of Thickened-arista (Tarts). Several of the seven lethal loci display an embryonic lethal phase. Three of the four female-sterile loci affect chorion structure with one resulting in underamplification of the chorion genes, and two (possibly three) of the four female-steriles affect nuclear division/DNA replication. Thus it appears that this is a "developmentally important" region, possibly representing a clustering of genes involved in either DNA replication or nuclear division.

Sign in / Sign up

Export Citation Format

Share Document