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A high-resolution record, covering 9.3–0.2 ka BP, from the sub-arctic Stjernsund (70°N) was studied for benthic foraminiferal faunas and stable isotopes, revealing three informally named main phases during the Holocene. The Early- to Mid-Holocene (9.3–5.0 ka BP) was characterized by the strong influence of the North Atlantic Current (NAC), which prevented the reflection of the Holocene Climatic Optimum (HCO) in the bottom-water temperature. During the Mid-Holocene Transition (5.0–2.5 ka BP), a turnover of benthic foraminiferal faunas occurred, Atlantic Water species decreased while Arctic-Polar species increased, and the oxygen isotope record showed larger fluctuations. Those variations correspond to a period of global climate change, to spatially more heterogeneous benthic foraminiferal faunas in the Nordic Seas region, and to regionally diverging terrestrial temperatures. The Cool Late Holocene (2.5–0.2 ka BP) was characterized by increased abundances of Arctic-Polar species and a steady cooling trend reflected in the oxygen isotopes. In this period, our record differs considerably from those on the SW Barents Sea shelf and locations farther south. Therefore, we argue that regional atmospheric cooling triggered the late Holocene cooling trend. Several cold episodes centred at ∼8.3, ∼7.8, ∼6.5, ∼4.9, ∼3.9 and ∼3.3 ka BP were identified from the benthic foraminiferal faunas and the δ18O record, which correlated with marine and atmospherically driven proxy records. This suggests that short-term cold events may result from reduced heat advection via the NAC or from colder air temperatures.

Summary The dnaK operon of Streptomyces coelicolor encodes the DnaK chaperone machine and HspR, the transcriptional repressor of the operon; HspR confers repression by binding to several inverted repeat sequences in the promoter region, dnaKp. Here, we demonstrate that HspR specifically requires the presence of DnaK protein to retard a dnaKp fragment in gel-shift assays. This requirement is independent of the co-chaperones, DnaJ and GrpE, and it is ATP independent. Furthermore the retarded protein‐DNA complex can be ‘supershifted’ by antiDnaK monoclonal antibody, demonstrating that DnaK forms an integral component of the complex. It was shown in DNase I footprinting experiments that refolding and specific binding of HspR to its DNA target does not require DnaK. We conclude that the formation of the stable DnaK‐HspR‐DNA ternary complex does not depend on the chaperoning activity of DnaK. In affinity chromatography experiments using whole-cell extracts, DnaK was shown to copurify with HspR, providing additional evidence that the two proteins interact in vivo; it was not possible to purify HspR away from DnaK in any experiments unless a powerful denaturant was used. The level of heat shock induction of chromosomal DnaK could be partially suppressed by expressing dnaK extrachromosomally from a heterologous promoter. In addition, it is shown that DnaK confers enhanced HspRmediated repression of transcription in vitro. Taken together, these results suggest that DnaK functions as a transcriptional co-repressor by binding to HspR at its operator sites. In this model, the DnaK‐HspR system would represent a novel example of feedback regulation of gene expression by a molecular chaperone, in which DnaK directly activates a

Potassium ions stabilize the DnaK · ADP complex that forms on incubation of nucleotide-free DnaK with ADP or ATP. Generation of the crystallographically defined Mg2+ cluster [Wilbanks, S. M. & McKay, D. B. (1995) J. Biol. Chem. 270, 2251–2257], in which two K+ and the nucleotide are bound together with Mg2+ in the ATPase site, appears to be essential for the ATP-induced acceleration of binding of peptide ligands, the ATP-induced release of peptide ligands and for the peptide-induced increase in ATPase activity. Thus, K+ is instrumental in signal transmission between the ATPase site and the peptide-binding site.

Durch potentionstatische und potentiokinetische Polarisationsmessungen an verschiedenen 18 Cr-10 Ni-Stahlen mit Molybdangehalten bis zu 4,3% in 25 und 45 proz. Ammoniumrhodanidlosungen wurde festgestellt, das die Ursache der Lochkorrosion im Potentialbereich von –300 bis +250 m V H auf einer unvollstandigen Passivierung beruht. Die Ausbildung stabiler Passivschichten wird hier durch die Bildung und lokale oxidative Wiederauflosung sulfidischer Deckschichten gestort. Oberhalb +250 m V H wirken Rhodanidionen in den schwachsauren Ammoniumrhodanidlosungen ahnlich wie Chloridionen als passivitatszerstorendes Agens. Die Durch potentionstatische Halteversuche ermittelten Grenzpotentiale der stabilen Lochkorrosion werden mit zunehmendem Molybdangehalt von –300 bis nach –150 m V H verschoben. Die geringste Lochkorrosionsneigung zeigte der Stahl mit dem hochsten Molybdangehalt. Pitting corrosion of austenitic CrNiMo-steels in concentrated ammoniumrhodanide solutions Quasipotentiostatic and potentiokinetic polarisation measurements at various 18 Cr-10 Ni steels with molybdenum contents up to 4,3% were performed in 25 and 45% ammoniumrhodanide solutions. It was found that pitting corrosion is caused by incomplete passivation in the potential range of –300 to +250 m V H. At these potentials the formation of stable passive layers is hindered by the formation and local oxidative dissolution of sulfidic layers. Above +250 m V H rhodanide ions act in these weak acidic ammoniumrhodanide solutions as agents which destroy passive layers, comparable with chloride ions. The limiting potentials for stable pitting corrosion, obtained from potentiostatic experiments, are shifted from –300 to –150 m V H with increasing molybdenum content of the steel. The least tendency of pitting corrosion was found for that steel with the highest molybdenum content.