Modulation of Decapentaplegic gradient during haltere specification in Drosophila

Suppression of wing fate and specification of haltere fate in Drosophila by Ultrabithorax is a classical example of Hox regulation of serial homology. However, the mechanism of Ultrabithorax function in specifying haltere size and shape is not well understood. Here we show that Decapentaplegic signaling, which controls wing growth and shape, is a target of Ultrabithorax function during haltere specification. The Decapentaplegic signaling is down-regulated in haltere discs due to a combination of reduced levels of the Dpp, its trapping at the A/P boundary by increased levels of its receptor Thick-vein and its inability to diffuse in the absence of Dally. Results presented here suggest a complex mechanism adopted by Ultrabithorax to modulate Decapentaplegic signaling. We discuss how this complexity may regulate the final form of the adult haltere in the fly, without compromising features such as cell survival, which is also dependent on Decapentaplegic signaling.     

Acute metabolic effects of ammonia on the enzymes of glutamate metabolism in isolated astroglial cells

Enzymes of glutamate metabolism were studied in the astrocytes isolated from rats injected with a large dose of ammonium acetate and compared with those isolated from controls. The activities of glutamate dehydrogenase (GDH) and glutaminase decreased while those of glutamine synthetase (GS) and aspartate aminotransferase (AAT) increased both in convulsive and comatose states. The activity of alanine aminotransferase (A1AT) increased only in convulsive state. The results suggested that glutamate required for the formation of glutamine in astrocytes might have its origin in nerve endings and the depletion of citric acid cycle intermediates might occur in nerve endings at least in acute ammonia toxicity.