Timing of mitosis in Physarum polycephalum: effects of agents affecting cyclic AMP concentrations.

Cultures of Physarum polycephalum incubated with caffeine or theophylline for over 100 min prior to mitosis exhibited mitotic delay proportional to the time of treatment before 100 min. Starved cultures exhibited mitotic delay at times of starvation longer than 180 min and slight stimulation from 100-180 min. Dibutyryl cAMP appeared to accelerate reconstruction of the nucleus following mitosis.     

Lipogenesis in rats adapted to intermittent starvation or continuous underfeeding

Zusammenfassung Albinoratten, bei denen zwischen die Fütterungstage 1–2tägige Hungerperioden eingesetzt wurden, zeigten nach 3 Wochen eine wesentlich erhöhte Inkorporation von 1-C¹⁴-Acetat in die Fettsäuren der Leberschnitte. Selbst bei Herabsetzung der Kalorienzufuhr um ca. 50% stieg hier, im Gegensatz zu kontinuierlich unterernährten Tieren, der prozentuale Körperfettgehalt. Die Resultate sprechen für eine Steigerung der Lipogenese.     

Changes in the distribution of gamma-glutamyl transferase in the organs of the mouse as a function of development]

In the Mouse, gamma-glutamyl transferase distribution changes with development in the kidney and the liver; on the contrary, its activity remains almost equal and low in other organs. In the liver, a low activity is observed in the fetus and the new-born up to the 3rd day of life; then it is no more measurable. In the kidney, the low enzyme activity of the fetus is multiplied by 10 in the 10 first days of life and by 50 in the 6 first weeks.     

Study on the distribution of methyl-mercury (203Hg) by whole body autoradiography of macaque monkeys (Macaca irus)]

The distribution of methyl-mercury labelled with mercury-203 has been studied in Monkeys by whole body autoradiography technique. The mercury is rapidly absorbed. It is localized in all the body and mainly in well defined areas of the central nervous system.     

The genome sequence of the filamentous fungus Neurospora crassa

Neurospora crassa is a central organism in the history of twentieth-century genetics, biochemistry and molecular biology. Here, we report a high-quality draft sequence of the N. crassa genome. The approximately 40-megabase genome encodes about 10,000 protein-coding genes--more than twice as many as in the fission yeast Schizosaccharomyces pombe and only about 25% fewer than in the fruitfly Drosophila melanogaster. Analysis of the gene set yields insights into unexpected aspects of Neurospora biology including the identification of genes potentially associated with red light photobiology, genes implicated in secondary metabolism, and important differences in Ca2+ signalling as compared with plants and animals. Neurospora possesses the widest array of genome defence mechanisms known for any eukaryotic organism, including a process unique to fungi called repeat-induced point mutation (RIP). Genome analysis suggests that RIP has had a profound impact on genome evolution, greatly slowing the creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related genes.     

Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination

Myelination of axons by oligodendrocytes enables rapid impulse propagation in the central nervous system. But long-term interactions between axons and their myelin sheaths are poorly understood. Here we show that Cnp1, which encodes 2',3'-cyclic nucleotide phosphodiesterase in oligodendrocytes, is essential for axonal survival but not for myelin assembly. In the absence of glial cyclic nucleotide phosphodiesterase, mice developed axonal swellings and neurodegeneration throughout the brain, leading to hydrocephalus and premature death. But, in contrast to previously studied myelin mutants, the ultrastructure, periodicity and physical stability of myelin were not altered in these mice. Genetically, the chief function of glia in supporting axonal integrity can thus be completely uncoupled from its function in maintaining compact myelin. Oligodendrocyte dysfunction, such as that in multiple sclerosis lesions, may suffice to cause secondary axonal loss.