The Ter mutation in the dead end gene causes germ cell loss and testicular germ cell tumours

In mice, the Ter mutation causes primordial germ cell (PGC) loss in all genetic backgrounds. Ter is also a potent modifier of spontaneous testicular germ cell tumour (TGCT) susceptibility in the 129 family of inbred strains, and markedly increases TGCT incidence in 129-Ter/Ter males. In 129-Ter/Ter mice, some of the remaining PGCs transform into undifferentiated pluripotent embryonal carcinoma cells, and after birth differentiate into various cells and tissues that compose TGCTs. Here, we report the positional cloning of Ter, revealing a point mutation that introduces a termination codon in the mouse orthologue (Dnd1) of the zebrafish dead end (dnd) gene. PGC deficiency is corrected both with bacterial artificial chromosomes that contain Dnd1 and with a Dnd1-encoding transgene. Dnd1 is expressed in fetal gonads during the critical period when TGCTs originate. DND1 has an RNA recognition motif and is most similar to the apobec complementation factor, a component of the cytidine to uridine RNA-editing complex. These results suggest that Ter may adversely affect essential aspects of RNA biology during PGC development. DND1 is the first protein known to have an RNA recognition motif directly implicated as a heritable cause of spontaneous tumorigenesis. TGCT development in the 129-Ter mouse strain models paediatric TGCT in humans. This work will have important implications for our understanding of the genetic control of TGCT pathogenesis and PGC biology.     

Effect of acetylcholine on melanophores ofRana tigrina

Summary Acetylcholine produced melanin aggregation and blanching of skin colour inRana tigrina, the common Indian frog. The effects were more prolonged in frogs pretreated with an anticholinesterase agent. Acetylcholine effects were not antagonized by eitherm-cholinolytic (atropine) orn-cholinolytic (pentolinium) agents, but were markedly inhibited by procaine. The results have been discussed in the light of the well-known membrane-stabilizing effect of procaine.     

The genome of the protist parasite Entamoeba histolytica

Entamoeba histolytica is an intestinal parasite and the causative agent of amoebiasis, which is a significant source of morbidity and mortality in developing countries. Here we present the genome of E. histolytica, which reveals a variety of metabolic adaptations shared with two other amitochondrial protist pathogens: Giardia lamblia and Trichomonas vaginalis. These adaptations include reduction or elimination of most mitochondrial metabolic pathways and the use of oxidative stress enzymes generally associated with anaerobic prokaryotes. Phylogenomic analysis identifies evidence for lateral gene transfer of bacterial genes into the E. histolytica genome, the effects of which centre on expanding aspects of E. histolytica's metabolic repertoire. The presence of these genes and the potential for novel metabolic pathways in E. histolytica may allow for the development of new chemotherapeutic agents. The genome encodes a large number of novel receptor kinases and contains expansions of a variety of gene families, including those associated with virulence. Additional genome features include an abundance of tandemly repeated transfer-RNA-containing arrays, which may have a structural function in the genome. Analysis of the genome provides new insights into the workings and genome evolution of a major human pathogen.     

Progressive localization of neutral-red positive region with morphogenesis inLimnaea

Résumé Les embryons deLimnaea ont été colorés au neutral rouge suivant la méthode de Janus Verte, signalée parReverberi pour les mitochondries. A un jeune stade (Veliger), l'embryon entier est taché par neutral rouge avec une coloration intense du conduit alimentaire; à un stade plus avancé, la tache se localise dans la partie postérieure et, au stade de l'eclosion à peu près, seuls l'estomac et la région hépatique présentent la tache.     

Bovine TSH-stimulation of fish thyroid peroxidase activity and role of thyroxine thereon

Summary bTSH augmented the fish thyroid peroxidase activity in a dose-response manner. Thyroxine could not modulate the effect of exogenous bTSH, but it decreased the peroxidase activity in a control system when administered alone. The data therefore suggest similar negative feedback control system for TSH-regulation as operative in the case of mammals.Acknowledgment. We are thankful to Prof. A. B. Das, Head of the Department of Zoology, Visva-Bharati University, Santiniketan, for providing laboratory facility. We are greatly indebted to Dr A. G. Dutta for his kind gift of bovine TSH (NIH-B5).     

Stress by restraining potentiates morphine catalepsy in rats

Restraint-induced stress potentiated morphine catalepsy in rats. This potentiation was partially antagonized by pharmacologic treatments decreasing central serotonin, acetylcholine, prostaglandins and by naloxone. Selective increase in central dopamine also inhibited the potentiation.     

Spiranation of phenolic diazoketones: An intermediate towards acorone synthesis

Summary Syntheses of 4-methylspiro [4.5]deca-6, 9-diene-2, 8-dione (IIb) and 1,4-dimethylspiro [4.5]deca-6, 9-diene-2, 8-dione (IIc) by spiranation of phenolic diazoketones (Ib) and (Ic) respectively are reported. Formation of (IIc) illustrates the first aryl participation of phenolic diazoketone prepared from higher homologue of diazomethane.