We studied the structure of ocellar photoreceptor cells of Drosophila melanogaster, particularly the subrhabdomeric cisternae which our previous studies have shown to be essential structures for turnover of photoreceptive membranes in compound eyes. Each ocellus contained elongated photoreceptor cells with rhabdomeres positioned distally. In the subrhabdomeric regions, endocytotic invaginations were frequently observed, suggesting active turnover of photoreceptive membranes. In the vicinity of the photoreceptive microvilli, membranous structures similar to the subrhabdomeric cisternae in compound eyes were observed. These membranous structures were immunopositive for the rdgB protein, a phosphatidylinositol transfer protein that is localized to the subrhabdomeric cisternae in compound eyes. The ocellar photoreceptor cells of the retinal degeneration mutants (rdgA,B) were also studied. In these mutants, retinal degeneration has been reported to start, in compound eyes, with the disappearance of the subrhabdomeric cisternae. We found that the ocellar subrhabdomeric cisternae also disappear during the initial stage of retinal degeneration. From these observations, we conclude that the mechanism of photoreceptive membrane turnover in ocellar photoreceptor cells involves the rdgB and probably the rdgA proteins which are associated with subrhabdomeric cisternae, as is the case for photoreceptive membrane turnover in compound eyes.
The toxic effect of benomyl on the embryogenesis of Xenopus laevis was investigated, and the tissues most affected by benomyl were identified. The toxicity of benomyl at various concentrations (5-20 microM) was tested with the Xenopus frog embryo teratogenesis assay (FETAX), used with slight modification. All test embryos subjected to 20 microM of benomyl died, and exposure to 10 and 15 microM benomyl produced growth inhibition and 11 types of severe external malformations. Histological examination of the test embryos showed dysplasia of the brain, eyes, intestine, otic vesicle, and muscle and swelling of the pronephric ducts and integuments. Among the tissues and organs affected, malformation of neural tissue was the most severe. The presumptive ectoderm isolated from st. 9 embryo was cultured in 10 ng/mL of activin A to induce neural tissue and mesoderm. When it was cultured with 10 ng/mL of activin A in the presence of 1 and 10 microM of benomyl, neural tissue induction was inhibited more severely than that of any other tissue. The gene expression of cultivated explants was investigated by reverse transcription-polymerase chain reaction (RT-PCR) assay in order to study the inhibition of neural tissue by benomyl. The results showed that with increasing benomyl concentration, the expression of the neural-specific marker NCAM (neural cell adhesion molecule), was more strongly inhibited than the muscle-specific marker muscle actin. Electron micrographs of test explants showed many residual yolk platelets and mitochondrial degeneration. In the present investigation the most severe toxic effects of benomyl were seen in the nerve tissues of the Xenopus embryo. This inhibition of neural development may have been caused by the inhibition of the assembly of neural microtubules and by the effect of benomyl on neuronal proliferation and migration.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.