The dopamine antagonist flupentixol does not alter ghrelin-induced food intake in rats.

It has been shown that dopamine antagonists suppress the ghrelin-induced increased motivation to work for food. The aim of this study was to investigate the influence of the dopamine antagonist flupentixol on ghrelin-induced food intake. Ad libitum fed male Sprague-Dawley (SD) rats were injected intraperitoneally (ip) with vehicle plus vehicle, vehicle plus ghrelin (13 μg/kg), 0.

Characterization of lamin mutation phenotypes in Drosophila and comparison to human laminopathies.

Lamins are intermediate filament proteins that make up the nuclear lamina, a matrix underlying the nuclear membrane in all metazoan cells that is important for nuclear form and function. Vertebrate A-type lamins are expressed in differentiating cells, while B-type lamins are expressed ubiquitously. Drosophila has two lamin genes that are expressed in A- and B-type patterns, and it is assumed that similarly expressed lamins perform similar functions.

Woc (without children) gene control of ecdysone biosynthesis in Drosophila melanogaster.

The first step in ecdysteroidogenesis, i.e. the 7,8-dehydrogenation of dietary cholesterol (C) to 7-dehydrocholesterol (7dC), is blocked in Drosophila melanogaster homozygous woc (without children) third instar larval ring glands (source of ecdysone).

The mutation without children(rgl) causes ecdysteroid deficiency in third-instar larvae of Drosophila melanogaster.

Larvae homozygous for the recessive lethal allele without children(rgl) (woc(rgl)) fail to pupariate. Application of exogenous 20-hydroxyecdysone elicits puparium formation and pupation. Ecdysteroid titer measurements on mutant larvae show an endocrine deficiency in the brain-ring gland complex, which normally synthesizes ecdysone, resulting in a failure of the larvae to achieve a threshold whole body hormone titer necessary for molting.

Insertional mutation of the Drosophila nuclear lamin Dm0 gene results in defective nuclear envelopes, clustering of nuclear pore complexes, and accumulation of annulate lamellae.

Nuclear lamins are thought to play an important role in disassembly and reassembly of the nucleus during mitosis. Here, we describe a Drosophila lamin Dm0 mutant resulting from a P element insertion into the first intron of the Dm0 gene. Homozygous mutant animals showed a severe phenotype including retardation in development, reduced viability, sterility, and impaired locomotion.

Functional analysis of Drosophila developmental genes instrumental in tumor suppression.

Of the 28 presently known Drosophila tumor suppressor genes we present the status of the functional analysis of the following three genes: (a) lethal (3) malignant brain tumor [1(3)mbt], which by homology belongs to the Pc-G gene family and may be involved in the stable silencing of specific developmental genes by changing the chromatin structure, and thus establishing and maintaining the differentiated state; (b) lethal (3) malignant blood neoplasm-1 [1(3)mbn-1], for whose function only vague predictions can be made; 4) benign (2) gonial cell neoplasm [b(2)gcn], which may function as a splice factor. Each Drosophila tumor suppressor gene transforms in the homozygously mutated state either one or two specific cell-types in a single step, and is thus the primary cause for tumorigenesis. For one of the genes a putative human homologue has been found.

Drosophila differentiation genes instrumental in tumor suppression.

Tumor suppressor genes of Drosophila are developmental genes which, in the homozygously mutated state, induce in one step malignant or benign neoplastic transformation of specific cell types. They act early in development and by this set the stage for cell specific differentiation of imaginal discs, adult optic neuroblasts, blood and gonial cells. The structure, expression and possible function of the following four tumor suppressor genes are discussed: tumorous imaginal disc, lethal (3) malignant brain tumor, lethal (3) malignant blood neoplasm-1 and benign (2) gonial cell neoplasm.

The Drosophila melanogaster tumor suppressor gene lethal(3)malignant brain tumor encodes a proline-rich protein with a novel zinc finger.

The lethal(3)malignant brain tumor [t(3)mbt] gene causes, when mutated, malignant growth of the adult optic neuroblasts and ganglion mother cells in the larval brain and imaginal disc overgrowth. Via overlapping deficiencies a genomic region of approximately 6.0 kb was identified, containing l(3)mbt+ gene sequences.

A temperature-sensitive brain tumor suppressor mutation of Drosophila melanogaster: developmental studies and molecular localization of the gene.

The recessive-lethal, temperature-sensitive (ts) mutation of the tumor suppressor gene lethal(3)malignant brain tumor (l(3)mbt) causes in a single step the malignant transformation of the adult optic neuroblasts and ganglion mother cells in the larval brain at the restrictive temperature of 29 degrees C. The transformed cells are differentiation-incompetent and grow autonomously in a lethal and invasive fashion in situ in the brain as well as after transplantation in vivo into wild-type adult hosts. The imaginal discs show epithelial overgrowth.

Genetic and molecular analysis of six tumor suppressor genes in Drosophila melanogaster.

Six Drosophila melanogaster tumor suppressor genes causing malignant or benign tumors in specific cell types are described. The wild-type alleles of these genes are instrumental in the differentiation of particular cell types. In the homozygous state, recessive mutations in the genes interrupt the differentiation of the cells and thus cause their uncontrolled, autonomous, lethal proliferation.