scholarly journals Genetic analysis of the enhancer of zeste locus and its role in gene regulation in Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 126 (1) ◽  
pp. 185-199 ◽  
Author(s):  
R S Jones ◽  
W M Gelbart
Keyword(s):  
Gene Regulation ◽  
Drosophila Melanogaster ◽  
Ectopic Expression ◽  
Polycomb Group ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Eye Color ◽  
Polycomb Group Genes ◽  
Enhancer Of Zeste ◽  
Gene Complexes

Abstract The Enhancer of zeste [E(z)] locus of Drosophila melanogaster is implicated in multiple examples of gene regulation during development. First identified as dominant gain-of-function modifiers of the zeste1-white (z-w) interaction, mutant E(z) alleles also produce homeotic transformations. Reduction of E(z)+ activity leads to both suppression of the z-w interaction and ectopic expression of segment identity genes of the Antennapedia and bithorax gene complexes. This latter effect defines E(z) as a member of the Polycomb-group of genes. Analysis of E(z)S2, a temperature-sensitive E(z) allele, reveals that both maternally and zygotically produced E(z)+ activity is required to correctly regulate the segment identity genes during embryonic and imaginal development. As has been shown for other Polycomb-group genes, E(z)+ is required not to initiate the pattern of these genes, but rather to maintain their repressed state. We propose that the E(z) loss-of-function eye color and homeotic phenotypes may both be due to gene derepression, and that the E(z)+ product may be a general repressing factor required for both examples of negative gene regulation.

scholarly journals Needs and Targets for the multi sex combs Gene Product in Drosophila melanogaster

Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 1823-1838 ◽  
Author(s):  
Olivier Saget ◽  
Françoise Forquignon ◽  
Pedro Santamaria ◽  
Neel B Randsholt
Keyword(s):  
Drosophila Melanogaster ◽  
Ectopic Expression ◽  
Polycomb Group ◽  
Homeotic Genes ◽  
Maternal Control ◽  
Gap Gene ◽  
Sex Combs ◽  
Normal Expression ◽  
Selector Genes ◽  
Mutant Phenotypes

Abstract We have analyzed the requirements for the multi sex combs (mxc) gene during development to gain further insight into the mechanisms and developmental processes that depend on the important trans-regulators forming the Polycomb group (PcG) in Drosophila melanogaster. mxc is allelic with the tumor suppressor locus lethal (1) malignant blood neoplasm (l(1)mbn). We show that the mxc product is dramatically needed in most tissues because its loss leads to cell death after a few divisions. mxc has also a strong maternal effect. We find that hypomorphic mxc mutations enhance other PcG gene mutant phenotypes and cause ectopic expression of homeotic genes, confirming that PcG products are cooperatively involved in repression of selector genes outside their normal expression domains. We also demonstrate that the mxc product is needed for imaginal head specification, through regulation of the ANT-C gene Deformed. Our analysis reveals that mxc is involved in the maternal control of early zygotic gap gene expression previously reported for some PcG genes and suggests that the mechanism of this early PcG function could be different from the PcG-mediated regulation of homeotic selector genes later in development. We discuss these data in view of the numerous functions of PcG genes during development.

E(z): a polycomb group gene or a trithorax group gene?

Development ◽  
1996 ◽  
Vol 122 (7) ◽  
pp. 2189-2197 ◽  
Author(s):  
D. LaJeunesse ◽  
A. Shearn
Keyword(s):  
Polycomb Group ◽  
Bithorax Complex ◽  
Trithorax Group ◽  
Polycomb Group Genes ◽  
Enhancer Of Zeste ◽  
Selector Genes ◽  
Homeotic Selector Genes ◽  
Polycomb Group Gene ◽  
Anterior Posterior ◽  
Homeotic Selector

The products of the Polycomb group of genes are cooperatively involved in repressing expression of homeotic selector genes outside of their appropriate anterior/posterior boundaries. Loss of maternal and/or zygotic function of Polycomb group genes results in the ectopic expression of both Antennapedia Complex and Bithorax Complex genes. The products of the trithorax group of genes are cooperatively involved in maintaining active expression of homeotic selector genes within their appropriate anterior/posterior boundaries. Loss of maternal and/or zygotic function of trithorax group genes results in reduced expression of both Antennapedia Complex and Bithorax Complex genes. Although Enhancer of zeste has been classified as a member of the Polycomb group, in this paper we show that Enhancer of zeste can also be classified as a member of the trithorax group. The requirement for Enhancer of zeste activity as either a trithorax group or Polycomb group gene depends on the homeotic selector gene locus as well as on spatial and temporal cues.

scholarly journals Cross-Regulation among the Polycomb Group Genes in Drosophila melanogaster

2004 ◽  
Vol 24 (17) ◽  
pp. 7737-7747 ◽  
Author(s):  
Janann Y. Ali ◽  
Welcome Bender
Keyword(s):  
Drosophila Melanogaster ◽  
Feedback Regulation ◽  
Polycomb Group ◽  
Negative Feedback Regulation ◽  
Polycomb Group Genes ◽  
Large Size ◽  
Evolutionarily Conserved ◽  
Positive Regulators ◽  
Core Components

ABSTRACT Genes of the Polycomb group in Drosophila melanogaster function as long-term transcriptional repressors. A few members of the group encode proteins found in two evolutionarily conserved chromatin complexes, Polycomb repressive complex 1 (PRC1) and the ESC-E(Z) complex. The majority of the group, lacking clear biochemical functions, might be indirect regulators. The transcript levels of seven Polycomb group genes were assayed in embryos mutant for various other genes in the family. Three Polycomb group genes were identified as upstream positive regulators of the core components of PRC1. There is also negative feedback regulation of some PRC1 core components by other PRC1 genes. Finally, there is positive regulation of PRC1 components by the ESC-E(Z) complex. These multiple pathways of cross-regulation help to explain the large size of the Polycomb group family of genes, but they complicate the genetic analysis of any single member.

scholarly journals Molecular characterisation of the Polycomblike gene of Drosophila melanogaster, a trans-acting negative regulator of homeotic gene expression

Development ◽  
1994 ◽  
Vol 120 (9) ◽  
pp. 2629-2636 ◽  
Author(s):  
A. Lonie ◽  
R. D'Andrea ◽  
R. Paro ◽  
R. Saint
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Polycomb Group ◽  
Negative Regulator ◽  
Homeotic Gene ◽  
Homeotic Genes ◽  
Molecular Characterisation ◽  
Polycomb Group Proteins ◽  
Polycomb Group Genes ◽  
Homeotic Gene Expression

The Polycomblike gene of Drosophila melanogaster, a member of the Polycomb Group of genes, is required for the correct spatial expression of the homeotic genes of the Antennapaedia and Bithorax Complexes. Mutations in Polycomb Group genes result in ectopic homeotic gene expression, indicating that Polycomb Group proteins maintain the transcriptional repression of specific homeotic genes in specific tissues during development. We report here the isolation and molecular characterisation of the Polycomblike gene. The Polycomblike transcript encodes an 857 amino acid protein with no significant homology to other proteins. Antibodies raised against the product of this open reading frame were used to show that the Polycomblike protein is found in all nuclei during embryonic development. Antibody staining also revealed that the Polycomblike protein is found on larval salivary gland polytene chromosomes at about 100 specific loci, the same loci to which the Polycomb and polyhomeotic proteins, two other Polycomb Group proteins, are found. These data add further support for a model in which Polycomb Group proteins form multimeric protein complexes at specific chromosomal loci to repress transcription at those loci.

Patterning of dopaminergic neurotransmitter identity among Caenorhabditis elegans ray sensory neurons by a TGFbeta family signaling pathway and a Hox gene

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5819-5831 ◽  
Author(s):  
R. Lints ◽  
S.W. Emmons
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Signaling Pathway ◽  
Cell Fate ◽  
Sensory Neurons ◽  
Ectopic Expression ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Hox Gene

We have investigated the mechanism that patterns dopamine expression among Caenorhabditis elegans male ray sensory neurons. Dopamine is expressed by the A-type sensory neurons in three out of the nine pairs of rays. We used expression of a tyrosine hydroxylase reporter transgene as well as direct assays for dopamine to study the genetic requirements for adoption of the dopaminergic cell fate. In loss-of-function mutants affecting a TGFbeta family signaling pathway, the DBL-1 pathway, dopaminergic identity is adopted irregularly by a wider subset of the rays. Ectopic expression of the pathway ligand, DBL-1, from a heat-shock-driven transgene results in adoption of dopaminergic identity by rays 3–9; rays 1 and 2 are refractory. The rays are therefore prepatterned with respect to their competence to be induced by a DBL-1 pathway signal. Temperature-shift experiments with a temperature-sensitive type II receptor mutant, as well as heat-shock induction experiments, show that the DBL-1 pathway acts during an interval that extends from two to one cell generation before ray neurons are born and begin to differentiate. In a mutant of the AbdominalB class Hox gene egl-5, rays that normally express EGL-5 do not adopt dopaminergic fate and cannot be induced to express DA when DBL-1 is provided by a heat-shock-driven dbl-1 transgene. Therefore, egl-5 is required for making a subset of rays capable of adopting dopaminergic identity, while the function of the DBL-1 pathway signal is to pattern the realization of this capability.

Altered cellular proliferation and mesoderm patterning in Polycomb-M33-deficient mice

Development ◽  
1997 ◽  
Vol 124 (3) ◽  
pp. 721-729 ◽  
Author(s):  
N. Core ◽  
S. Bel ◽  
S.J. Gaunt ◽  
M. Aurrand-Lions ◽  
J. Pearce ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Hox Genes ◽  
Es Cells ◽  
Embryonic Stem ◽  
Axial Skeleton ◽  
Polycomb Group ◽  
Homeotic Genes ◽  
Loss Of Function ◽  
Polycomb Group Genes

In Drosophila, the trithorax-group and the Polycomb-group genes are necessary to maintain the expression of the homeobox genes in the appropriate segments. Loss-of-function mutations in those groups of genes lead to misexpression of the homeotic genes resulting in segmental homeotic transformations. Recently, mouse homologues of the Polycomb-group genes were identified including M33, the murine counterpart of Polycomb. In this report, M33 was targeted in mice by homologous recombination in embryonic stem (ES) cells to assess its function during development. Homozygous M33 (−/−) mice show greatly retarded growth, homeotic transformations of the axial skeleton, sternal and limb malformations and a failure to expand in vitro of several cell types including lymphocytes and fibroblasts. In addition, M33 null mutant mice show an aggravation of the skeletal malformations when treated to RA at embryonic day 7.5, leading to the hypothesis that, during development, the M33 gene might play a role in defining access to retinoic acid response elements localised in the regulatory regions of several Hox genes.

scholarly journals Differences in temperature-sensitive expression of PcG-regulated genes among natural populations of Drosophila melanogaster

2021 ◽  
Author(s):  
Susanne Voigt ◽  
Luise Kost
Keyword(s):  
Drosophila Melanogaster ◽  
Target Genes ◽  
Natural Populations ◽  
Polycomb Group ◽  
Temperature Sensitive ◽  
Induced Expression ◽  
Temperate Europe ◽  
Transcriptional Output ◽  
Warm Temperate ◽  
Different Climates

Asbstract Environmental temperature can affect chromatin-based gene regulation, in particular in ectotherms such as insects. Genes regulated by the Polycomb group (PcG) vary in their transcriptional output in response to changes in temperature. Expression of PcG-regulated genes typically increases with decreasing temperatures. Here we examined variations in temperature-sensitive expression of PcG target genes in natural populations from different climates of Drosophila melanogaster, and differences thereof across different fly stages and tissues. Temperature-induced expression plasticity was found to be stage- and sex-specific with differences in the specificity between the examined PcG target genes. Some tissues and stages, however, showed a higher number of PcG target genes with temperature-sensitive expression than others. Overall, we found higher levels of temperature-induced expression plasticity in African tropical flies from the ancestral species range than in flies from temperate Europe. We also observed differences between temperate flies, however, with more reduction of expression plasticity in warm-temperate than in cold-temperate populations. Although, in general, temperature sensitive expression appeared to be detrimental in temperate climates, there were also cases in which plasticity was increased in temperate flies, as well as no changes in expression plasticity between flies from different climates.

scholarly journals Evidence of a dual function in fl(2)d, a gene needed for Sex-lethal expression in Drosophila melanogaster.

Genetics ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 597-612 ◽  
Author(s):  
B Granadino ◽  
A San Juán ◽  
P Santamaria ◽  
L Sánchez
Keyword(s):  
Drosophila Melanogaster ◽  
Germ Cells ◽  
Sensitive Period ◽  
Dual Function ◽  
Temperature Sensitive ◽  
Permissive Temperature ◽  
Loss Of Function ◽  
Germline Development ◽  
Suppression Effect ◽  
Pole Cells

Abstract In Drosophila melanogaster, the female sexual development of the soma and the germline requires the activity of the gene Sxl. The somatic cells need the function of the gene fl(2)d to follow the female developmental pathway, due to its involvement in the female-specific splicing of Sxl RNA. Here we report the analysis of both fl(2)d1 and fl(2)d2 mutations: (1) fl(2)d1 is a temperature-sensitive mutation lethal in females and semilethal in males; (2) fl(2)d2 is lethal in both sexes; (3) the fl(2)d1/fl(2)d2 constitution is temperature-sensitive and lethal in females, while semilethal in males. The temperature-sensitive period of fl(2)d1 in females expands the whole development. SxlM1 partially suppresses the lethality of fl(2)d1 homozygous females and that of fl(2)d1/fl(2)d2 constitution, whereas it does not suppress the lethality of fl(2)d2 homozygous females. The addition of extra Sxl+ copies does not increase the suppression effect of SxlM1. The fl(2)d1 mutation in homozygosis and the fl(2)d1/fl(2)d2 constitution, but not the fl(2)d2 in homozygosis, partially suppress the lethality of SxlM1 males. This suppression is not prevented by the addition of extra Sxl+ copies. The semilethality of both fl(2)d1 and fl(2)d1/fl(2)d2 males, and the lethality of fl(2)d2 males, is independent of Sxl function. There is no female synergistic lethality between mutations at fl(2)d and neither at sc or da. However, the female synergistic lethality between mutations at Sxl and either sc or da is increased by fl(2)d mutations. We have analyzed the effect of the fl(2)d mutations on the germline development of both females and males. For that purpose, we carried out the clonal analysis of fl(2)d1 in the germline. In addition, pole cells homozygous for fl(2)d2 were transplanted into wild-type host embryos, and we checked whether the mutant pole cells were capable of forming functional gametes. The results indicated that fl(2)d mutant germ cells cannot give rise to functional oocytes, while they can form functional sperm. Moreover, SxlM1 suppresses the sterility of the fl(2)d1 homozygous females developing at the permissive temperature. Thus, with respect to the development of the germline the fl(2)d mutations mimic the behavior of loss-of-function mutations at the gene Sxl. Females double heterozygous for fl(2)d and snf1621 are fully viable and fertile. fl(2)d2 in heterozygosis partially suppresses the phenotype of female germ cells homozygous for snf1621; however, this is not the case with the fl(2)d1 mutation. The fl(2)d mutations partially suppress the phenotype of the female germ cells homozygous for ovoDIrSI.(ABSTRACT TRUNCATED AT 400 WORDS)

Ten different Polycomb group genes are required for spatial control of the abdA and AbdB homeotic products

Development ◽  
1992 ◽  
Vol 114 (2) ◽  
pp. 493-505 ◽  
Author(s):  
J. Simon ◽  
A. Chiang ◽  
W. Bender
Keyword(s):  
Expression Patterns ◽  
Ectopic Expression ◽  
Specific Pattern ◽  
Polycomb Group ◽  
Polycomb Group Genes ◽  
Sex Combs ◽  
Normal Expression ◽  
Sex Comb ◽  
Regulatory Dna ◽  
Pair Rule

Mutations in genes of the Polycomb (Pc) group cause abnormal segmental development due to ectopic expression of the homeotic products of the Antennapedia and bithorax complexes. Here the requirements for Pc group genes in controlling the abdA and AbdB products of the bithorax complex are described. Embryos containing mutations in the genes Polycomb (Pc), extra sex combs (esc), Enhancer of zeste [E(z)], polyhomeotic (ph), Sex comb on midleg (Scm), Polycomb-like (Pcl), Sex comb extra (Sce), Additional sex combs (Asx), Posterior sex combs (Psc) and pleiohomeotic (pho) were examined. In every case, both abdA and AbdB are expressed outside of their normal domains along the anterior-posterior (A-P) axis, consistent with these Pc group products acting in a single pathway or molecular complex. The earliest detectable ectopic expression is highest in the parasegments immediately adjacent to the normal expression boundary. Surprisingly, in the most severe Pc group mutants, the earliest ectopic AbdB is distributed in a pair-rule pattern. At all stages, ectopic abdA in the epidermis is highest along the anterior edges of the parasegments, in a pattern that mimics the normal abdA cell-specific pattern. These examples of highly patterned mis-expression show that Pc group mutations do not cause indiscriminate activation of homeotic products. We suggest that the ectopic expression patterns result from factors that normally activate abdA and AbdB only in certain parasegments, but that in Pc group mutants these factors gain access to regulatory DNA in all parasegments.

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