Branchless and Hedgehog operate in a positive feedback loop to regulate the initiation of neuroblast division in the Drosophila larval brain.

The Drosophila central nervous system is produced by two rounds of neurogenesis: one during embryogenesis to form the larval brain and one during larval stages to form the adult central nervous system. Neurogenesis caused by the activation of neural stem division in the larval brain is essential for the proper patterning and functionality of the adult central nervous system. Initiation of neuroblast proliferation requires signaling by the Fibroblast Growth Factor homolog Branchless and by the Hedgehog growth factor. We show here that the Branchless and Hedgehog pathways form a positive feedback loop to regulate the onset of neuroblast division. This feedback loop is initiated during embryogenesis. Our genetic and molecular studies demonstrate that the absolute level of Branchless and Hedgehog signaling is critical to fully activate stem cell division. Furthermore, over-expression and mutant studies establish that signaling by Branchless is the crucial output of the feedback loop that stimulates neuroblast division and that Branchless signaling is necessary for initiating the division of all mitotically regulated neuroblasts in the brain lobes. These studies establish the molecular mechanism through which Branchless and Hedgehog signaling interface to regulate the activation of neural stem cell division.

Depression of sodium, chloride and calcium ions in the plasma of goldfish (Carassius auratus) and immature freshwater- and seawater-adapted eels (Anguilla anguilla L.) after acute administration of salmon calcitonin.

Goldfish showed a significant reduction in their plasma sodium and calcium levels 1 h after receiving 50 i.u. calcitonin per kg body weight. When 100 i.u. calcitonin were injected there was a significant fall in circulating levels of both sodium and calcium and also of chloride ions compared with those found in untreated control animals. Administration of calcitonin to immature eels adapted to either freshwater or seawater conditions showed no significant change in plasma ion composition at doses of 10 i.u. per kg body weight or less. However, doses of 50 and 100 i.u. caused significant reductions in plasma sodium, chloride and calcium ion levels compared with sham-injected control animals. When immature eels were given 100 i.u. calcitonin per kg body weight there were significant reductions in the plasma levels of sodium, chloride and calcium ions but the timing of these changes was slightly different. In freshwater-adapted eels, the depression of plasma sodium was seen after 30 min and lasted for up to 2 h, whilst depression of plasma chloride and calcium was not seen until 1 h after injection. In addition, whilst the lowering of plasma chloride ions lasted up to 2 h after injection, the plasma calcium had returned to the preinjection control level by this time. In seawater-adapted eels the depression of sodium, chloride and calcium levels was seen at 30 min and the effect continued for up to 2 h after injection when the depression was no longer apparent.