RESUMEN
Paired carbon-14 ((14)C) and thorium-230((230)Th) ages were determined on fossil corals from the Huon Peninsula, Papua New Guinea. The ages were used to calibrate part of the (14)C time scale and to estimate rates of sea-level rise during the last deglaciation. An abrupt offset between the (14)C and (230)Th ages suggests that the atmospheric (14)C/(12)C ratio dropped by 15 percent during the latter part of and after the Younger Dryas (YD). This prominent drop coincides with greatly reduced rates of sea-level rise. Reduction of melting because of cooler conditions during the YD may have caused an increase in the rate of ocean ventilation, which caused the atmospheric (14)C/(12)C ratio to fall. The record of sea-level rise also shows that globally averaged rates of melting were relatively high at the beginning of the YD. Thus, these measurements satisfy one of the conditions required by the hypothesis that the diversion of meltwater from the Mississippi to the St. Lawrence River triggered the YD event.
RESUMEN
A series of Mud1 and Tn10 insertions were identified in the pncA chromosome region of Salmonella typhimurium which is responsible for the production of nicotinamide deamidase. Both pncA (resulting in no nicotinamide deamidase activity) and pncX (resulting in lowered nicotinamide deamidase activity) insertions were constructed. In addition, mutants which could utilize nicotinamide as a sole source of nitrogen were isolated. These mutants, designated pncH, hyperproduce nicotinamide deamidase. Genetic studies utilizing pncX--lacZ and pncA--lacZ operon fusions indicate that pncX::Tn10 insertions reduce transcription of pncA--lac while pncH mutations increase the expression of both pncA--lacZ and pncX-lacZ. The gene order was determined as purB--pncA--pncX--gdh with transcription of both pncA and pncX occurring in the counterclockwise direction. Merodiploid studies suggest a model whereby pncX and pncA form an operon with the major promoter occurring upstream from pncX. A second, weaker promoter for pncA must be situated between pncX and pncA. The pncH mutations appear to occur in the pncX promoter (pncXp) increasing promoter activity.