Phenotypic interactions of spinster with the genes encoding proteins for cell death control in Drosophila melanogaster

2010 ◽  
Vol 73 (3) ◽  
pp. 119-127 ◽  
Author(s):  
Akira Sakurai ◽  
Yoshiro Nakano ◽  
Masayuki Koganezawa ◽  
Daisuke Yamamoto
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Genes Encoding

scholarly journals A Cluster of Cuticle Protein Genes of Drosophila melanogaster at 65A: Sequence, Structure and Evolution

Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1213-1224
Author(s):  
Jean-Philippe Charles ◽  
Carol Chihara ◽  
Shamim Nejad ◽  
Lynn M Riddiford
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Dna ◽  
Multiple Copy ◽  
Sequence Structure ◽  
Coding Regions ◽  
The Third ◽  
Genetic Complexity ◽  
Genes Encoding ◽  
Cuticle Protein ◽  
Cuticle Proteins

A 36-kb genomic DNA segment of the Drosophila melanogaster genome containing 12 clustered cuticle genes has been mapped and partially sequenced. The cluster maps at 65A 5-6 on the left arm of the third chromosome, in agreement with the previously determined location of a putative cluster encompassing the genes for the third instar larval cuticle proteins LCP5, LCP6 and LCP8. This cluster is the largest cuticle gene cluster discovered to date and shows a number of surprising features that explain in part the genetic complexity of the LCP5, LCP6 and LCP8 loci. The genes encoding LCP5 and LCP8 are multiple copy genes and the presence of extensive similarity in their coding regions gives the first evidence for gene conversion in cuticle genes. In addition, five genes in the cluster are intronless. Four of these five have arisen by retroposition. The other genes in the cluster have a single intron located at an unusual location for insect cuticle genes.

A Family of Genes Clustered at the Triplo-lethal Locus of Drosophila melanogaster Has an Unusual Evolutionary History and Significant Synteny With Anopheles gambiae

Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 613-621 ◽  
Author(s):  
Douglas R Dorer ◽  
Jamie A Rudnick ◽  
Etsuko N Moriyama ◽  
Alan C Christensen
Keyword(s):  
Phylogenetic Analysis ◽  
Drosophila Melanogaster ◽  
Anopheles Gambiae ◽  
Evolutionary History ◽  
Codon Bias ◽  
Good Target ◽  
The Family ◽  
Genes Encoding ◽  
And Function ◽  
Gambiae Genome

Abstract Within the unique Triplo-lethal region (Tpl) of the Drosophila melanogaster genome we have found a cluster of 20 genes encoding a novel family of proteins. This family is also present in the Anopheles gambiae genome and displays remarkable synteny and sequence conservation with the Drosophila cluster. The family is also present in the sequenced genome of D. pseudoobscura, and homologs have been found in Aedes aegypti mosquitoes and in four other insect orders, but it is not present in the sequenced genome of any noninsect species. Phylogenetic analysis suggests that the cluster evolved prior to the divergence of Drosophila and Anopheles (250 MYA) and has been highly conserved since. The ratio of synonymous to nonsynonymous substitutions and the high codon bias suggest that there has been selection on this family both for expression level and function. We hypothesize that this gene family is Tpl, name it the Osiris family, and consider possible functions. We also predict that this family of proteins, due to the unique dosage sensitivity and the lack of homologs in noninsect species, would be a good target for genetic engineering or novel insecticides.

Differential elimination of rDNA genes in bobbed mutants of Drosophila melanogaster

1986 ◽  
Vol 6 (4) ◽  
pp. 1023-1031
Author(s):  
R Terracol ◽  
N Prud'homme
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Copy Number ◽  
Rdna Locus ◽  
Gene Copy ◽  
Specific Gene ◽  
Type I ◽  
28S Rrna ◽  
Wild Type ◽  
Y Chromosomes ◽  
Genes Encoding

In Drosophila melanogaster, the multiply repeated genes encoding 18S and 28S rRNA are located on the X and Y chromosomes. A large percentage of these repeats are interrupted in the 28S region by insertions of two types. We compared the restriction patterns from a subcloned wild-type Oregon R strain to those of spontaneous and ethyl methanesulfonate-induced bobbed mutants. Bobbed mutations were found to be deficiencies that modified the organization of the rDNA locus. Genes without insertions were deleted about twice as often as genes with type I insertions. Type II insertion genes were not decreased in number, except in the mutant having the most bobbed phenotype. Reversion to wild type was associated with an increase in gene copy number, affecting exclusively genes without insertions. One hypothesis which explains these results is the partial clustering of genes by type. The initial deletion could then be due either to an unequal crossover or to loss of material without exchange. Some of our findings indicated that deletion may be associated with an amplification phenomenon, the magnitude of which would be dependent on the amount of clustering of specific gene types at the locus.

scholarly journals Cells differentiating into neuroectoderm undergo apoptosis in the absence of functional retinoblastoma family proteins.

1995 ◽  
Vol 129 (3) ◽  
pp. 779-788 ◽  
Author(s):  
R S Slack ◽  
I S Skerjanc ◽  
B Lach ◽  
J Craig ◽  
K Jardine ◽  
...  
Keyword(s):  
Cell Death ◽  
P19 Cells ◽  
Adenovirus E1a ◽  
Genes Encoding ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Early Mouse ◽  
Dying Cells ◽  
Related Proteins ◽  
E1a Protein

The retinoblastoma (RB) protein is present at low levels in early mouse embryos and in pluripotent P19 embryonal carcinoma cells; however, the levels of RB rise dramatically in neuroectoderm formed both in embryos and in differentiating cultures of P19 cells. To investigate the effect of inactivating RB and related proteins p107 and p130, we transfected P19 cells with genes encoding mutated versions of the adenovirus E1A protein that bind RB and related proteins. When these E1A-expressing P19 cells were induced to differentiate into neuroectoderm, there was a striking rise in the expression of c-fos and extensive cell death. The ultrastructural and biochemical characteristics of the dying cells were indicative of apoptosis. The dying cells were those committed to the neural lineages because neurons and astrocytes were lost from differentiating cultures. Cell death was dependent on the ability of the E1A protein to bind RB and related proteins. Our results suggest that proteins of the RB family are essential for the development of the neural lineages and that the absence of functional RB activity triggers apoptosis of differentiating neuroectodermal cells.

The development of fused− embryos of Drosophila melanogaster

Development ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 99-114
Author(s):  
Alfonso Martinez-Arias
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Mature Embryo ◽  
Lethal Mutations ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Secondary Consequence

The mutant fused (1–59·5) belongs to a class of lethal mutations in Drosophila melanogaster that produce pattern duplications in every segment of the mature embryo. A study of the embryonic development of fused'− embryos derived horn fused− mothers shows that extensive cell death occurs early in development. This cell death accounts for the smaller size of the segments in fused− embryos. The pattern duplication observed is, probably, a secondary consequence of the pattern deletion.

Studies on the female-sterile phenotype of 1(1)su(f) ts76a, a temperature-sensitive allele of the suppressor of forked mutation in Drosophila melanogaster

Development ◽  
1980 ◽  
Vol 55 (1) ◽  
pp. 247-256
Author(s):  
Thomas G. Wilson
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Follicle Cell ◽  
Lethal Mutation ◽  
Female Sterility ◽  
Temperature Sensitive ◽  
Egg Chambers ◽  
A Cell ◽  
Sensitive Allele

A new allele of the suppressor of forked [su(f)] mutation in Drosophila melanogaster has been found and designated 1(1)su(f)ts76a. It is temperature-sensitive for suppression of forked (f) and has additional temperature-sensitive phenotypes of lethality, female sterility, and abnormal bristle formation at 29 °C. It closely resembles two other conditional alleles of su(f), 1(1)su(f)ts67g and 1(1)ts726. Female sterility at 29 °C is characterized by both disorganized egg chambers in the ovarioles and also chorion-deficient oocytes. Both of these abnormalities may be the result of premature follicle cell death. The observations on 1(1)su(f)ts76a are consistent with the proposal that the similar allele, 1(1)ts726, is a cell-lethal mutation specifically affecting mitotically active cells.

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