Abstract. The existence of a neurofilament-deficient mutant of Japanese quail was recently documented (Yamasaki, H., C. Itakura, and M. Mizutani. 1991. Acta Neuropathol. 82:427--434), but the genetic events leading to the neurofilament deficiency have yet to be determined. Our molecular biological analyses revealed that the expression of neurofilament-L (NF-L) gene was specifically repressed in neurons of this mutant. To search for mutation(s) responsible for the shutdown of this gene expression, we cloned and sequenced the NF-L genes in the wild-type and mutant quails. It is eventually found that the NF-L gene in the mutant includes a nonsense mutation at the deduced amino acid residue 114, indicating that the mutant is incapable of producing even a trace amount of polymerizationcompetent NF-L protein at any situation. The identification of this nonsense mutation provides us with a solid basis on which molecular mechanisms underlying the alteration in the neuronal cytoskeletal architecture in the mutant should be interpreted.
Bifenazate is a novel carbazate acaricide discovered by Uniroyal Chemical (now Chemtura Corporation) for the control of phytophagous mites infesting agricultural and ornamental crops. Its acaricidal activity and that of its principal active metabolite, diazene, were characterized. Bifenazate and diazene had high toxicity and specificity both orally and topically to all life stages of Tetranychus urticae and Panonychus citri. Acute poisoning was observed with no temperature dependency. No cross-resistance was found to mites resistant to several other classes of acaricides, such as tebufenpyrad, etoxazole, fenbutatin oxide and dicofol. Bifenazate remained effective for a long time with only about a 10% loss of efficacy on T. urticae after 1 month of application in the field. All stages of development of the predatory mites, Phytoseiulus persimilis and Neoseiulus californicus, survived treatment by both bifenazate and diazene. When adult females of the two predatory mite species were treated with either bifenazate or diazene, they showed a normal level of fecundity and predatory activity in the laboratory, effectively suppressing spider mite population growth. Even when the predators were fed spider mite eggs that had been treated previously with bifenazate, they survived. These findings indicate that bifenazate is a very useful acaricide giving high efficacy, long-lasting activity and excellent selectivity for spider mites. It is, therefore, concluded that bifenazate is an ideal compound for controlling these pest mites.
The genesis of resting microglia in the gray matter of mouse hippocampus was studied by 3H-thymidine autoradiography in combination with electron microscopy. Newborn mice were injected with 3H-thymidine singly or repeatedly at different postnatal stages, and killed shortly after the injection or after various intervals. Tissue specimens of the hippocampus at CA1 and CA2 were processed for light and electron microscopic autoradiography. The results showed that at least 91% of glial cells in the stratum radiatum of the hippocampus are produced after birth. About three-fourths of astroglia in this area are produced before the sixth postnatal day, and a larger part of resting microglia are formed after the ninth postnatal day. Morphological transition can be traced from either proliferating cells in the stratum radiatum at late postnatal days to resting microglia, or from those in early postnatal days to astroglia. A continuous morphological transition was observed between the proliferating cells at the late postnatal days (microglial production period) and those at the early postnatal days (astroglial production period). The latter retain some fine structural characteristics similar to small glioblasts in the subependymal layer. These findings strongly suggest that resting microglia, as well as astroglia, are derived from glioblasts, and are of neurectodermal origin.
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