Genetic and autoradiographic studies of tritiated thymidine in testes ofDrosophila melanogaster

Zusammenfassung Die Aufnahme von H³-Thymidin in 16 h alte männliche Larven vonDrosophila melanogaster wurde autoradiographisch verfolgt und die mutagene Wirkung des einverleibten H³-Thymidin durch die Bestimmung der Häufigkeit der geschlechtsgebundenen rezessiven Mutationen gemessen. Es zeigte sich, dass das der männlichen Larve derDrosophila melanogaster verabreichte H³-Thymidin eine bedeutende Häufigkeit der Mutationen verursacht.

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Supported in part by Grant G-6097 of the National Science Foundation.     

Alterations of the erythrocyte membrane caused by fluorinated dinitrobenzenes

Zusammenfassung Inaktivierung der Acetylcholinesterase in der Erythrozytenmembran mit 1-Fluor-2,4-dinitrobenzol und 1,5-Difluor-2,4-dinitrobenzol konnte durch blutgruppenspezifische Antikörper nicht beeinflusst werden. Nach Difluordinitrobenzol-Behandlung zeigten die Blutkörperchen Verlust der Agglutinabilität und die Membranen eine Herabsetzung ihrer Absorptionsfähigkeit für homologe Antikörper.

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This work was supported by research grant No. HD 01461 from the National Institutes of Health, U.S.P.H.S.     

Neurotrophin signalling pathways regulating neuronal apoptosis

Recent evidence indicates that naturally occurring neuronal death in mammals is regulated by the interplay between receptor-mediated prosurvival and proapoptotic signals. The neurotrophins, a family of growth factors best known for their positive effects on neuronal biology, have now been shown to mediate both positive and negative survival signals, by signalling through the Trk and p75 neurotrophin receptors, respectively. The mechanisms whereby these two neurotrophin receptors interact to determine neuronal survival have been difficult to decipher, largely because both can signal independently or coincidentally, depending upon the cell or developmental context. Nonetheless, the past several years have seen significant advances in our understanding of this receptor signalling system. In this review, we focus on the proapoptotic actions of the p75 neurotrophin receptor (p75NTR), and on the interplay between Trk and p75NTR that determines neuronal survival.     

Effects of tetraphenyboron on erythrocyte enzymes

Rusemen El tratamiento de glóbulos rojos humanos con concentraciones no-hemolíticas de borotetrafenilo causa una reducción irreversible en las activides de la glucosa-6-fosfato dehidrogenasa, una enzima citoplasmática y de la acetilcolinesterasa, ubicada en la superficie externa de la membrana eritrocitaria. El tratamiento casi no tiene efecto alguno sobre la fosfatasa ácida.     

Deficiency of the 50K dystrophin-associated glycoprotein in severe childhood autosomal recessive muscular dystrophy.

X-linked recessive Duchenne muscular dystrophy (DMD) is caused by the absence of dystrophin, a membrane cytoskeletal protein. Dystrophin is associated with a large oligomeric complex of sarcolemmal glycoprotein. The dystrophin-glycoprotein complex has been proposed to span the sarcolemma to provide a link between the subsarcolemmal cytoskeleton and the extracellular matrix component, laminin. In DMD, the absence of dystrophin leads to a large reduction in all of the dystrophin-associated protein. We have investigated the possibility that a deficiency of a dystrophin-associated protein could be the cause of severe childhood autosomal recessive muscular dystrophy (SCARMD) with a DMD-like phenotype. Here we report the specific deficiency of the 50K dystrophin-associated glycoprotein (M(r) 50,000) in sarcolemma of SCARMD patients. Therefore, the loss of this glycoprotein is a common denominator of the pathological process leading to muscle cell necrosis in two forms of muscular dystrophy, DMD and SCARMD.