Genetic organization of the ci-M-pan region on chromosome IV in Drosophila melanogaster

Genome ◽  
1999 ◽  
Vol 42 (6) ◽  
pp. 1144-1149
Author(s):  
Jesper Kronhamn ◽  
Åsa Rasmuson-Lestander
Keyword(s):  
Drosophila Melanogaster ◽  
Ribosomal Protein ◽  
P Element ◽  
Gene Encoding ◽  
Regulatory Regions ◽  
Cubitus Interruptus ◽  
First Intron ◽  
Enhancer Trap Line ◽  
Mutant Lines ◽  
Trap Line

The genes cubitus interruptus (ci), ribosomal protein S3A (RpS3A), and pangolin (pan) are localized within 73 kb in the cytological region 101F-102A on chromosome IV in Drosophila melanogaster. A region of 13 kb harbours the regulatory regions of both ci and pan, transcribed in opposite directions, and a 1.1-kb gene encoding RpS3A. This dense clustering gives rise to very complicated complementation patterns between different alleles in these loci. We investigated this region genetically and molecularly by use of an enhancer trap line (IA5), where the P-element was found to be inserted into the first intron of pan. Screens for imprecise excisions of the P-element were performed, and complementations between new and old established mutant lines were investigated. We found that when mutated or deleted the RpS3A gene gives rise to a Minute phenotype, and we conclude that M(4)101 encodes the ribosomal protein S3A.Key words: Drosophila melanogaster, Minute(4)101, ribosomal protein, RpS3A gene, P-element mutagenesis.

Engrailed expression in the anterior lineage compartment of the developing wing blade of Drosophila

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 21-33 ◽  
Author(s):  
S.S. Blair
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Polyclonal Antiserum ◽  
Small Distance ◽  
Pupal Development ◽  
Cubitus Interruptus ◽  
Compartment Boundary ◽  
Enhancer Trap Line ◽  
Trap Line ◽  
Anterior Posterior

The developing wing of Drosophila melanogaster was examined at larval and pupal stages of development to determine whether the anterior-posterior lineage boundary, as identified by lineage restrictions, was congruent with the boundaries defined by the expression of posterior-specific (engrailed, invected), and anterior-specific (cubitus interruptus-D) genes. The lineage boundary was identified by marking mitotic recombinant clones, using an enhancer trap line with ubiquitous beta-gal expression in imaginal tissues; clones of +/+ cells were identified by their lack of beta-gal expression. Domains of gene expression were localized using antibodies and gene specific lacZ constructs. Surprisingly, it was found that engrailed expression extended a small distance into the anterior lineage compartment of the wing blade, as identified with anti-en/inv mAb, anti-en polyclonal antiserum, or an en-promoter-lacZ insert, ryxho25. This anterior expression was not present in early third instar discs, but appeared during subsequent larval and pupal development. In contrast, the expression of cubitus interruptus-D, as identified using the ci-Dplac insert, appeared to be limited to the anterior lineage compartment. Thus, en expression is not limited to cells from the posterior lineage compartment, and en and ci-D activities can overlap in a region just anterior to the lineage compartment boundary in the developing wing. The lineage boundary could also be identified by a line of aligned cells in the prospective wing blade region of wandering third instar discs. A decapentaplegic-lacZ construct was expressed in a stripe several cells anterior to the lineage boundary, and did not define or overlap into the posterior lineage compartment.

scholarly journals Mutations in the Drosophila gene encoding ribosomal protein S6 cause tissue overgrowth.

1993 ◽  
Vol 13 (4) ◽  
pp. 2524-2535 ◽  
Author(s):  
M J Stewart ◽  
R Denell
Keyword(s):  
Ribosomal Protein ◽  
Regulatory Region ◽  
Transcript Abundance ◽  
P Element ◽  
Gene Encoding ◽  
Drosophila Gene ◽  
Ribosomal Protein S6 ◽  
Melanotic Tumors ◽  
Cellular Immune ◽  
Insect Immune Response

We have characterized two P-element-induced, lethal mutations in Drosophila melanogaster which affect the larval hemocytes, mediators of the insect immune response. Each mutant displays larval melanotic tumors characteristic of mutations affecting the insect cellular immune system, and the moribund animals develop grossly hypertrophied hematopoietic organs because of increased cell proliferation and extra rounds of endoreduplication in some hematopoietic cells. Surprisingly, these mutations are due to P element insertions in the 5' regulatory region of the Drosophila gene encoding ribosomal protein S6 and cause a reduction of S6 transcript abundance in mutant larvae.

Sequence and expression of a gene encoding a ribosomal protein S4 homolog from Drosophila melanogaster

Gene ◽  
1993 ◽  
Vol 132 (2) ◽  
pp. 251-254 ◽  
Author(s):  
Yokokura Takakazu ◽  
Tei Hajime ◽  
Yamamoto Daisuke
Keyword(s):  
Drosophila Melanogaster ◽  
Ribosomal Protein ◽  
Gene Encoding ◽  
Ribosomal Protein S4

Ribosomal Protein Insufficiency and the Minute Syndrome in Drosophila: A Dose-Response Relationship

Genetics ◽  
1998 ◽  
Vol 148 (3) ◽  
pp. 1215-1224 ◽  
Author(s):  
Stein Sæbøe-Larssen ◽  
May Lyamouri ◽  
John Merriam ◽  
Morten P Oksvold ◽  
Andrew Lambertsson
Keyword(s):  
Ribosomal Protein ◽  
Insertion Site ◽  
Gene Mutations ◽  
Extreme Case ◽  
P Element ◽  
Mrna Levels ◽  
Gene Encoding ◽  
Slow Development ◽  
Ribosomal Protein S3 ◽  
The Individual

AbstractMinutes comprise >50 phenotypically similar mutations scattered throughout the genome of Drosophila, many of which are identified as mutations in ribosomal protein (rp) genes. Common traits of the Minute phenotype are short and thin bristles, slow development, and recessive lethality. By mobilizing a P element inserted in the 5′ UTR of M(3)95A, the gene encoding ribosomal protein S3 (RPS3), we have generated two homozygous viable heteroalleles that are partial revertants with respect to the Minute phenotype. Molecular characterization revealed both alleles to be imprecise excisions, leaving 40 and 110 bp, respectively, at the P-element insertion site. The weaker allele (40 bp insert) is associated with a ~15% decrease in RPS3 mRNA abundance and displays a moderate Minute phenotype. In the stronger allele (110 bp insert) RPS3 mRNA levels are reduced by ~60%, resulting in an extreme Minute phenotype that includes many morphological abnormalities as well as sterility in both males and females due to disruption of early gametogenesis. The results show that there is a correlation between reduced RPS3 mRNA levels and the severity of the Minute phenotype, in which faulty differentiation of somatic tissues and arrest of gametogenesis represent the extreme case. That heteroalleles in M(3)95A can mimic the phenotypic variations that exist between different Minute/rp-gene mutations strongly suggests that all phenotypes primarily are caused by reductions in maximum protein synthesis rates, but that the sensitivity for reduced levels of the individual rp-gene products is different.

An enhancer trap line identifies the Drosophila homolog of the L37a ribosomal protein

Gene ◽  
1999 ◽  
Vol 239 (1) ◽  
pp. 137-143 ◽  
Author(s):  
Peter Gaines ◽  
Craig T Woodard ◽  
John R Carlson
Keyword(s):  
Ribosomal Protein ◽  
Enhancer Trap ◽  
Enhancer Trap Line ◽  
Drosophila Homolog ◽  
Trap Line

The Drosophila melanogaster RPS17 gene encoding ribosomal protein S17

Gene ◽  
1989 ◽  
Vol 79 (2) ◽  
pp. 289-298 ◽  
Author(s):  
Carl Maki ◽  
Douglas D. Rhoads ◽  
Mary J. Stewart ◽  
Barbara Van Slyke ◽  
Donald J. Roufa
Keyword(s):  
Drosophila Melanogaster ◽  
Ribosomal Protein ◽  
Gene Encoding

scholarly journals The bereft Gene, a Potential Target of the Neural Selector Gene cut, Contributes to Bristle Morphogenesis

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 231-247 ◽  
Author(s):  
Kirsten E Hardiman ◽  
Rachel Brewster ◽  
Shaema M Khan ◽  
Monika Deo ◽  
Rolf Bodmer
Keyword(s):  
Chromosomal Location ◽  
Insertion Site ◽  
Protein Product ◽  
Enhancer Trap ◽  
P Element ◽  
Deletion Mutants ◽  
Sensory Organs ◽  
Enhancer Trap Line ◽  
Homeobox Transcription Factor ◽  
Trap Line

Abstract The neural selector gene cut, a homeobox transcription factor, is required for the specification of the correct identity of external (bristle-type) sensory organs in Drosophila. Targets of cut function, however, have not been described. Here, we study bereft (bft) mutants, which exhibit loss or malformation of a majority of the interommatidial bristles of the eye and cause defects in other external sensory organs. These mutants were generated by excising a P element located at chromosomal location 33AB, the enhancer trap line E8-2-46, indicating that a gene near the insertion site is responsible for this phenotype. Similar to the transcripts of the gene nearest to the insertion, reporter gene expression of E8-2-46 coincides with Cut in the support cells of external sensory organs, which secrete the bristle shaft and socket. Although bft transcripts do not obviously code for a protein product, its expression is abolished in bft deletion mutants, and the integrity of the bft locus is required for (interommatidial) bristle morphogenesis. This suggests that disruption of the bft gene is the cause of the observed bristle phenotype. We also sought to determine what factors regulate the expression of bft and the enhancer trap line. The correct specification of individual external sensory organ cells involves not only cut, but also the lineage genes numb and tramtrack. We demonstrate that mutations of these three genes affect the expression levels at the bft locus. Furthermore, cut overexpression is sufficient to induce ectopic bft expression in the PNS and in nonneuronal epidermis. On the basis of these results, we propose that bft acts downstream of cut and tramtrack to implement correct bristle morphogenesis.

scholarly journals Mutations in the Drosophila gene encoding ribosomal protein S6 cause tissue overgrowth

1993 ◽  
Vol 13 (4) ◽  
pp. 2524-2535
Author(s):  
M J Stewart ◽  
R Denell
Keyword(s):  
Ribosomal Protein ◽  
Regulatory Region ◽  
Transcript Abundance ◽  
P Element ◽  
Gene Encoding ◽  
Drosophila Gene ◽  
Ribosomal Protein S6 ◽  
Melanotic Tumors ◽  
Cellular Immune ◽  
Insect Immune Response

We have characterized two P-element-induced, lethal mutations in Drosophila melanogaster which affect the larval hemocytes, mediators of the insect immune response. Each mutant displays larval melanotic tumors characteristic of mutations affecting the insect cellular immune system, and the moribund animals develop grossly hypertrophied hematopoietic organs because of increased cell proliferation and extra rounds of endoreduplication in some hematopoietic cells. Surprisingly, these mutations are due to P element insertions in the 5' regulatory region of the Drosophila gene encoding ribosomal protein S6 and cause a reduction of S6 transcript abundance in mutant larvae.

The DSC1 Channel, Encoded by the smi60E Locus, Contributes to Odor-Guided Behavior in Drosophila melanogaster

Genetics ◽  
2002 ◽  
Vol 161 (4) ◽  
pp. 1507-1516 ◽  
Author(s):  
Nalini H Kulkarni ◽  
Akihiko H Yamamoto ◽  
Kellie O Robinson ◽  
Trudy F C Mackay ◽  
Robert R H Anholt
Keyword(s):  
Drosophila Melanogaster ◽  
Neuronal Excitability ◽  
Insertion Site ◽  
Antennal Segment ◽  
P Element ◽  
Gene Encoding ◽  
Olfactory Organs ◽  
Nested Gene ◽  
Maxillary Palps

Abstract Previously, we generated P-element insert lines in Drosophila melanogaster with impaired olfactory behavior. One of these smell-impaired (smi) mutants, smi60E, contains a P[lArB] transposon in the second intron of the dsc1 gene near a nested gene encoding the L41 ribosomal protein. The dsc1 gene encodes an ion channel of unknown function homologous to the paralytic (para) sodium channel, which mediates neuronal excitability. Complementation tests between the smi60E mutant and several EP insert lines map the smellimpaired phenotype to the P[lArB] insertion site. Wild-type behavior is restored upon P-element excision. Evidence that reduction in DSC1 rather than in L41 expression is responsible for the smell-impaired phenotype comes from a phenotypic revertant in which imprecise P-element excision restores the DSC1 message while further reducing L41 expression. Behavioral assays show that a threefold decrease in DSC1 mRNA is accompanied by a threefold shift in the dose response for avoidance of the repellent odorant, benzaldehyde, toward higher odorant concentrations. In situ hybridization reveals widespread expression of the dsc1 gene in the major olfactory organs, the third antennal segment and the maxillary palps, and in the CNS. These results indicate that the DSC1 channel contributes to processing of olfactory information during the olfactory avoidance response.

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