Temporally restricted expression of transcription factor betaFTZ-F1: significance for embryogenesis, molting and metamorphosis in Drosophila melanogaster

Development ◽  
2000 ◽  
Vol 127 (23) ◽  
pp. 5083-5092 ◽  
Author(s):  
M. Yamada ◽  
T. Murata ◽  
S. Hirose ◽  
G. Lavorgna ◽  
E. Suzuki ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Larval Instar ◽  
Ectopic Expression ◽  
Wild Type ◽  
Specific Expression ◽  
Molting Process ◽  
In The Wild ◽  
Time Specific ◽  
Almost All ◽  
Exact Timing

FTZ-F1, a member of the nuclear receptor superfamily, has been implicated in the activation of the segmentation gene fushi tarazu during early embryogenesis of Drosophila melanogaster. We found that an isoform of FTZ-F1, betaFTZ-F1, is expressed in the nuclei of almost all tissues slightly before the first and second larval ecdysis and before pupation. Severely affected ftz-f1 mutants display an embryonic lethal phenotype, but can be rescued by ectopic expression of betaFTZ-F1 during the period of endogenous betaFTZ-F1 expression in the wild type. The resulting larvae are not able to molt, but this activity is rescued again by forced expression of betaFTZ-F1, allowing progression to the next larval instar stage. On the other hand, premature expression of betaFTZ-F1 in wild-type larvae at mid-first instar or mid-second instar stages causes defects in the molting process. Sensitive periods were found to be around the time of peak ecdysteroid levels and slightly before the start of endogenous betaFTZ-F1 expression. A hypomorphic ftz-f1 mutant that arrests in the prepupal stage can also be rescued by ectopic, time-specific expression of betaFTZ-F1. Failure of salivary gland histolysis, one of the phenotypes of the ftz-f1 mutant, is rescued by forced expression of the ftz-f1 downstream gene BR-C during the late prepupal period. These results suggest that betaFTZ-F1 regulates genes associated with ecdysis and metamorphosis, and that the exact timing of its action in the ecdysone-induced gene cascade is important for proper development.

scholarly journals The hobo Transposable Element Excises and Has Related Elements in Tephritid Species

Genetics ◽  
1996 ◽  
Vol 143 (3) ◽  
pp. 1339-1347
Author(s):  
Alfred M Handler ◽  
Sheilachu P Gomez
Keyword(s):  
Drosophila Melanogaster ◽  
Ceratitis Capitata ◽  
Bactrocera Dorsalis ◽  
Parsimony Analysis ◽  
Wild Type ◽  
Anastrepha Suspensa ◽  
Tephritid Species ◽  
Mutant Strains ◽  
Almost All ◽  
Horizontal Transfers

Abstract Function of the Drosophila melanogaster hobo transposon in tephritid species was tested in transient embryonic excision assays. Wild-type and mutant strains of Anastrepha suspensa, Bactrocera dorsalis, B. cucurbitae, Ceratitis capitata, and Toxotrypana curvicauda all supported hobo excision or deletion both in the presence and absence of co-injected hobo transposase, indicating a permissive state for hobo mobility and the existence of endogenous systems capable of mobilizing hobo. In several strains hobo helper reduced excision. Excision depended on hobo sequences in the indicator plasmid, though almost all excisions were imprecise and the mobilizing systems appear mechanistically different from hobo. hobe-related sequences were identified in all species except T. curvicauda. Parsimony analysis yielded a subgroup including the B. cucurbitae and C. capitata sequences along with hobo and Hermes, and a separate, more divergent subgroup including the A. suspensa and B. dorsalis sequences. All of the sequences exist as multiple genomic elements, and a deleted form of the B. cucurbitae element exists in B. dorsalis. The hobo-related sequences are probably members of the hAT transposon family with some evolving from distant ancestor elements, while others may have originated from more recent horizontal transfers.

scholarly journals Disruption of the RAD52 gene alters the spectrum of spontaneous SUP4-o mutations in Saccharomyces cerevisiae.

Genetics ◽  
1989 ◽  
Vol 122 (3) ◽  
pp. 535-542 ◽  
Author(s):  
B A Kunz ◽  
M G Peters ◽  
S E Kohalmi ◽  
J D Armstrong ◽  
M Glattke ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Base Pair ◽  
Type Strain ◽  
Wild Type Strain ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
Mutator Phenotype ◽  
In The Wild ◽  
Single Base Pair ◽  
Almost All

Abstract Defects in the RAD52 gene of the yeast Saccharomyces cerevisiae confer a mutator phenotype. To characterize this effect in detail, a collection of 238 spontaneous SUP4-o mutations arising in a strain having a disrupted RAD52 gene was analyzed by DNA sequencing. The resulting mutational spectrum was compared to that derived from an examination of 222 spontaneous mutations selected in a nearisogenic wild-type (RAD52) strain. This comparison revealed that the mutator phenotype was associated with an increase in the frequency of base-pair substitutions. All possible types of substitution were detected but there was a reduction in the relative fraction of A.T----G.C transitions and an increase in the proportion of G.C----C.G transversions. These changes were sufficient to cause a twofold greater preference for substitutions at G.C sites in the rad52 strain despite a decrease in the fraction of G.C----T.A transversions. There were also considerable differences between the distributions of substitutions within the SUP4-o gene. Base-pair changes occurred at fewer sites in the rad52 strain but the mutated sites included several that were not detected in the RAD52 background. Only two of the four sites that were mutated most frequently in the rad52 strain were also prominent in the wild-type strain and mutation frequencies at almost all sites common to both strains were greater for the rad52 derivative. Although single base-pair deletions occurred in the two strains with similar frequencies, several classes of mutation that were recovered in the wild-type background including multiple base-pair deletions, insertions of the yeast transposable element Ty, and more complex changes, were not detected in the rad52 strain.(ABSTRACT TRUNCATED AT 250 WORDS)

The development of the sensory neuron pattern in the antennal disc of wild-type and mutant (lz3, ssa) Drosophila melanogaster

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 1063-1075
Author(s):  
M.C. Lienhard ◽  
R.F. Stocker
Keyword(s):  
Drosophila Melanogaster ◽  
Sensory Neuron ◽  
Antennal Segment ◽  
Wild Type ◽  
Homeotic Mutant ◽  
In The Wild ◽  
The Brain ◽  
Antennal Disc ◽  
Antennal Nerve

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.

A genetic and molecular analysis of an invectedDominant mutation in Drosophila melanogaster

Genome ◽  
1998 ◽  
Vol 41 (3) ◽  
pp. 381-390 ◽  
Author(s):  
A J Simmonds ◽  
J B Bell
Keyword(s):  
Drosophila Melanogaster ◽  
Imaginal Disc ◽  
Transcriptional Start Site ◽  
Ectopic Expression ◽  
Careful Analysis ◽  
Wing Imaginal Disc ◽  
Coding Region ◽  
Specific Expression ◽  
Additional Lesion ◽  
Normal Expression

The invected gene of Drosophila melanogaster is a homeobox-containing gene that is closely related to engrailed. A dominant gain of function allele, invectedDominant, was derived from mutagenesis of a dominant allele of vestigial, In(2R)vgW. A careful analysis of the phenotype of invectedDominant shows that it is associated with a transformation of the anterior compartment of the wing to a posterior fate. This transformation is normally limited to the wing blade itself and does not involve the remaining tissues derived from the wing imaginal disc, including the wing hinge and dorsal thorax of the fly. The ectopic expression of invected protein associated with invectedDominant correlates spatially with the normal expression pattern of vestigial in the wing imaginal disc, suggesting that control elements of vestigial are driving ectopic invected expression. This was confirmed by sequence analysis that shows that the dominant vestigial activity was eliminated by a deletion that removes the 3' portion of the vestigial coding region. This leaves a gene fusion wherein the vestigial enhancer elements are still juxtaposed immediately 5' to the invected transcriptional start site, but with the vg sequences harboring an additional lesion. Unlike recessive invected alleles, the invectedDominant allele produces an observable phenotype, and as such, should prove useful in determining the role of invected in patterning the wing imaginal disc. Genetic analysis has shown that mutations of polyhomeotic, a gene involved in regulating engrailed expression, cause a reproducible alteration in the invectedDominant phenotype. Finally, the invectedDominant allele should prove valuable for identifying and characterizing genes that are activated within the posterior compartment. A screen using various lacZ lines that are asymmetrically expressed in an anterior-posterior manner in the wing imaginal disc isolated one line that shows posterior-specific expression within the transformed anterior compartment.Key words: Drosophila, development, dominant mutation, ectopic, wings.

scholarly journals SPO71 Encodes a Developmental Stage-Specific Partner for Vps13 in Saccharomyces cerevisiae

2013 ◽  
Vol 12 (11) ◽  
pp. 1530-1537 ◽  
Author(s):  
Jae-Sook Park ◽  
Yuuya Okumura ◽  
Hiroyuki Tachikawa ◽  
Aaron M. Neiman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
De Novo ◽  
Ectopic Expression ◽  
Membrane Vesicles ◽  
Specific Gene ◽  
Wild Type ◽  
Protein Mutation ◽  
Prospore Membrane ◽  
In The Wild ◽  
Membrane Morphogenesis

ABSTRACT The creation of haploid gametes in yeast, termed spores, requires the de novo formation of membranes within the cytoplasm. These membranes, called prospore membranes, enclose the daughter nuclei generated by meiosis. Proper growth and closure of prospore membranes require the highly conserved Vps13 protein. Mutation of SPO71 , a meiosis-specific gene first identified as defective in spore formation, was found to display defects in membrane morphogenesis very similar to those seen in vps13 Δ cells. Specifically, prospore membranes are smaller than in the wild type, they fail to close, and membrane vesicles are present within the prospore membrane lumen. As in vps13 Δ cells, the levels of phophatidylinositol-4-phosphate are reduced in the prospore membranes of spo71 Δ cells. SPO71 is required for the translocation of Vps13 from the endosome to the prospore membrane, and ectopic expression of SPO71 in vegetative cells results in mislocalization of Vps13. Finally, the two proteins can be coprecipitated from sporulating cells. We propose that Spo71 is a sporulation-specific partner for Vps13 and that they act in concert to regulate prospore membrane morphogenesis.

scholarly journals The abnormal oocyte phenotype is correlated with the presence of blood transposon in Drosophila melanogaster.

Genetics ◽  
1989 ◽  
Vol 123 (3) ◽  
pp. 485-494
Author(s):  
G Lavorgna ◽  
C Malva ◽  
A Manzi ◽  
S Gigliotti ◽  
F Graziani
Keyword(s):  
Drosophila Melanogaster ◽  
Sequence Analysis ◽  
Restriction Enzyme ◽  
Polymorphism Analysis ◽  
Restriction Map ◽  
Dna Rearrangement ◽  
Restriction Enzyme Site ◽  
Wild Type ◽  
Chromosome Walking ◽  
In The Wild

Abstract The abnormal oocyte mutation (2;44) originates in the wild: it confers no visible phenotype on homozygous abo males or females, but homozygous abo females produce defective eggs and the probability of their developing into adults is much lower than that of heterozygous sister females. We isolated by chromosome walking 200 kb of DNA from region 32. This paper reports that a restriction enzyme site polymorphism analysis in wild type and mutant stocks allowed us to identify a DNA rearrangement present only in stocks carrying the abo mutation. The rearrangement is caused by a DNA insert on the abo chromosome in region 32E which, by restriction map and sequence analysis, was identified as copia-like blood transposon. The transposon, in strains that had remained in abo homozygous conditions for several generations and had lost the abo maternal-effect, was no longer present in region 32E. Certain features of the abo mutation, discussed in the light of this finding, may be ascribed to the nature of the particular allele studied.

scholarly journals A Feedback Mechanism Regulates Odorant Receptor Expression in the Malaria Mosquito, Anopheles gambiae

2020 ◽  
Author(s):  
Sarah E. Maguire ◽  
Ali Afify ◽  
Loyal A. Goff ◽  
Christopher J. Potter
Keyword(s):  
Drosophila Melanogaster ◽  
Anopheles Gambiae ◽  
Odorant Receptor ◽  
Ectopic Expression ◽  
Feedback Mechanism ◽  
Receptor Expression ◽  
Rna Seq ◽  
Human Odor ◽  
Mosquito Anopheles Gambiae ◽  
Almost All

ABSTRACTMosquitoes locate and approach humans (‘host-seek’) when specific Olfactory Neurons (ORNs) in the olfactory periphery activate a specific combination of glomeruli in the mosquito Antennal Lobe (AL). We hypothesize that dysregulating proper glomerular activation in the presence of human odor will prevent host-seeking behavior. In experiments aimed at ectopically activating most ORNs in the presence of human odor, we made a surprising finding: ectopic expression of an AgOr (AgOr2) in Anopheles gambiae ORNs dampens the activity of the expressing neuron. This contrasts studies in Drosophila melanogaster, the typical insect model of olfaction, in which ectopic expression of non-native ORs in ORNs confers ectopic neuronal responses without interfering with native olfactory physiology. To gain insight into this dysfunction in mosquitoes, RNA-seq analyses were performed comparing wild-type antennae to those ectopically expressing AgOr2 in ORNs. Remarkably, almost all Or transcripts were significantly downregulated (except for AgOr2), and additional experiments suggest that it is AgOR2 protein rather than mRNA that mediates this downregulation. Our study shows that ORNs of Anopheles mosquitoes (in contrast to Drosophila) employ a currently unexplored regulatory mechanism of OR expression, which may be adaptable as a vector-control strategy.SIGNIFICANCE STATEMENTStudies in Drosophila melanogaster suggest that insect Olfactory Receptor Neurons (ORNs) do not contain mechanisms by which Odorant Receptors (ORs) regulate OR expression. This has proved useful in studies where ectopic expression of an OR in Drosophila ORNs confers responses to the odorants that activate the newly expressed OR. In experiments in Anopheles gambiae mosquitoes, we found that ectopic expression of an OR in most Anopheles ORNs dampened the activity of the expressing neurons. RNA-seq analyses demonstrated that ectopic OR expression in Anopheles ORNs leads to downregulation of endogenous Or transcripts. Additional experiments suggest that this downregulation required ectopic expression of a functional OR protein. These findings reveal that Anopheles mosquitoes, in contrast to Drosophila, contain a feedback mechanism to regulate OR expression. Mosquito ORNs might employ regulatory mechanisms of OR expression previously thought to occur only in non-insect olfactory systems.

scholarly journals The RNA-seq transcriptomic analysis reveals genes mediating salt tolerance through rapid triggering of ion transporters in a mutant barley

2019 ◽  
Author(s):  
Sareh Yousefirad ◽  
Hassan Soltanloo ◽  
Sayad Sanaz Ramezanpour ◽  
Khalil Zaynalinezhad ◽  
Vahid Shariati
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Ion Homeostasis ◽  
High Ratio ◽  
Rna Seq ◽  
Ion Transporters ◽  
Wild Type ◽  
Specific Expression ◽  
Mutant Genotype ◽  
In The Wild

Abstract Regarding the complexity of the mechanisms of salinity tolerance, the use of isogenic lines or mutants that have the same genetic background but show different tolerance to salinity is a suitable method to reduce the analytical complexity to study these mechanisms. In the current study, whole transcriptome analysis was evaluated using RNA-seq method between a salt-tolerant mutant line “73-M4-30” and its wild-type “Zarjou” cultivar at a seedling stage after six hours of exposure to salt stress (300 mM NaCl). Transcriptome sequencing yielded 20 million reads for each genotype. A total number of 7116 transcripts with differential expression were identified, 1586 and 1479 of which were obtained with significantly increased expression in the mutant and the wild-type, respectively. In addition, the families of WRKY, ERF, AP2/EREBP, NAC, CTR/DRE, AP2/ERF, MAD, MIKC, HSF, and bZIP were identified as the important transcription factors with specific expression in the mutant genotype. The RNA-seq results were confirmed in several time points using qRT-PCR of some important salt-responsive genes. In general, the results revealed that the mutant compared to its wild-type via fast stomach closure and consequently transpiration reduction under the salt stress, saved more sodium ion in the root and decreased its transfer to the shoot, and increased the amount of potassium ion leading to the maintenance a high ratio [K+]/­[Na+] in the shoot. Moreover, it caused a reduction in photosynthesis and respiration, resulting in the use of the stored energy and the carbon for maintaining the plant tissues, which is a mechanism of salt tolerance in plants. Up-regulation of catalase, peroxidase, and ascorbate peroxidase genes, which was probably due to the more accumulation of H2O2 in the wild-type compared to the mutant. Therefore, the wild-type initiated rapid ROS signals lead to less oxidative scavenging than the mutant. The mutant increased expression in the ion transporters and the channels related to the salinity to retain the ion homeostasis. Totally, the results demonstrated that the mutant responded better to the salt stress under both the osmotic and the ionic stress phases. Less damage was observed in the mutant compared to its wild-type under the salt stress.

spiel ohne grenzen/pou2is required for zebrafish hindbrain segmentation

Development ◽  
2002 ◽  
Vol 129 (7) ◽  
pp. 1645-1655 ◽  
Author(s):  
Giselbert Hauptmann ◽  
Heinz-Georg Belting ◽  
Uta Wolke ◽  
Karen Lunde ◽  
Iris Söll ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Hox Genes ◽  
Ectopic Expression ◽  
Loss Of Function ◽  
Wild Type ◽  
Specific Expression ◽  
Size And Shape ◽  
Regulatory Cascade ◽  
Normal Expression ◽  
Segmental Identity

Segmentation of the vertebrate hindbrain leads to the formation of a series of rhombomeres with distinct identities. In mouse, Krox20 and kreisler play important roles in specifying distinct rhombomeres and in controlling segmental identity by directly regulating rhombomere-specific expression of Hox genes. We show that spiel ohne grenzen (spg) zebrafish mutants develop rhombomeric territories that are abnormal in both size and shape. Rhombomere boundaries are malpositioned or absent and the segmental pattern of neuronal differentiation is perturbed. Segment-specific expression of hoxa2, hoxb2 and hoxb3 is severely affected during initial stages of hindbrain development in spg mutants and the establishment of krx20 (Krox20 ortholog) and valentino (val; kreisler ortholog) expression is impaired. spg mutants carry loss-of-function mutations in the pou2 gene. pou2 is expressed at high levels in the hindbrain primordium of wild-type embryos prior to activation of krx20 and val. Widespread overexpression of Pou2 can rescue the segmental krx20 and val domains in spg mutants, but does not induce ectopic expression of these genes. This suggests that spg/pou2 acts in a permissive manner and is essential for normal expression of krx20 and val. We propose that spg/pou2 is an essential component of the regulatory cascade controlling hindbrain segmentation and acts before krx20 and val in the establishment of rhombomere precursor territories.

scholarly journals THE α-GLYCEROPHOSPHATE CYCLE IN DROSOPHILA MELANOGASTER

1974 ◽  
Vol 63 (3) ◽  
pp. 864-882 ◽  
Author(s):  
Stephen J. O'Brien ◽  
Yoshio Shimada
Keyword(s):  
Drosophila Melanogaster ◽  
Oxidative Phosphorylation ◽  
Adult Life ◽  
Respiratory Control ◽  
Premature Mortality ◽  
Pyridine Nucleotide ◽  
Null Alleles ◽  
Wild Type ◽  
Relative Viability ◽  
In The Wild

"Null" mutations previously isolated at the αGpdh-1 locus of Drosophila melanogaster, because of disruption of the energy-producing α-glycerophosphate cycle, severely restrict the flight ability and relative viability of affected individuals. Two "null" alleles, αGpdh-1BO-1-4, and αGpdh-1BO-1-5, when made hemizygous with a deficiency of the αGpdh-1 locus, Df(2L)GdhA, were rendered homozygous by recombination with and selective elimination of the Df(2L)GdhA chromosome. After over 25 generations, a homozygous αGpdh-1BO-1-4 stock regained the ability to fly despite the continued absence of measurable αGPDH activity. Inter se heterozygotes of three noncomplementing αGpdh-1 "null" alleles and the "adapted" αGpdh-1BO-1-4 homozygotes were examined for metabolic enzymatic activities related to the energy-producing and pyridine nucleotide-regulating functions of the α-glycerophosphate cycle in Drosophila. The enzyme functions tested included glyceraldehyde-3-phosphate dehydrogenase, cytoplasmic and soluble malate dehydrogenase, lactate dehydrogenase, mitochondrial NADH oxidation, oxidative phosphorylation, and respiratory control with the substrates α-glycerophosphate, succinate, and pyruvate. These activities in any of the mutant genotypes in early adult life were indistinguishable from those in the wild type. There was, however, a premature deterioration and atrophy of the ultrastructural integrity of flight muscle sarcosomes observed by electron microscopy in the "null" mutants. These observations were correlated with a decrease in state 3 mitochondrial oxidation with α-glycerophosphate, succinate, and pyruvate, as well as with loss of respiratory control in adults as early as 2 wk after eclosion. Such observations, which normally are seen in aged dipterans, were accompanied by premature mortality of the mutant heterozygotes. The adapted αGpdh-1BO-1-4 was identical with wild type in each of the aging characters with the single exception of lowered rates of mitochondrial oxidative phosphorylation.

Sign in / Sign up

Export Citation Format

Share Document