Induction of the ferritin gene (ftnA) of Escherichia coli by Fe2+–Fur is mediated by reversal of H-NS silencing and is RyhB independent

FtnA is the major iron-storage protein of Escherichia coli accounting for < or = 50% of total cellular iron. The FtnA gene (ftnA) is induced by iron in an Fe(2+)-Fur-dependent fashion. This effect is reportedly mediated by RyhB, the Fe(2+)-Fur-repressed, small, regulatory RNA. However, results presented here show that ftnA iron induction is independent of RyhB and instead involves direct interaction of Fe(2+)-Fur with an 'extended' Fur binding site (containing five tandem Fur boxes) located upstream (-83) of the ftnA promoter. In addition, H-NS acts as a direct repressor of ftnA transcription by binding at multiple sites (I-VI) within, and upstream of, the ftnA promoter. Fur directly competes with H-NS binding at upstream sites (II-IV) and consequently displaces H-NS from the ftnA promoter (sites V-VI) which in turn leads to derepression of ftnA transcription. It is proposed that H-NS binding within the ftnA promoter is facilitated by H-NS occupation of the upstream sites through H-NS oligomerization-induced DNA looping. Consequently, Fur displacement of H-NS from the upstream sites prevents cooperative H-NS binding at the downstream sites within the promoter, thus allowing access to RNA polymerase. This direct activation of ftnA transcription by Fe(2+)-Fur through H-NS antisilencing represents a new mechanism for iron-induced gene expression.

Response of the Atlantic meridional overturning circulation to a reversal of greenhouse gas increases

The reversibility of the Atlantic meridional overturning circulation (AMOC) is investigated in multi-model experiments using global climate models (GCMs) where CO2 concentrations are increased by 1 or 2 % per annum to 2× or 4× preindustrial conditions. After a period of stabilisation the CO2 is decreased back to preindustrial conditions. In most experiments when the CO2 decreases, the AMOC recovers before becoming anomalously strong. This "overshoot" is up to an extra 18.2Sv or 104 % of its preindustrial strength, and the period with an anomalously strong AMOC can last for several hundred years. The magnitude of this overshoot is shown to be related to the build up of salinity in the subtropical Atlantic during the previous period of high CO2 levels. The magnitude of this build up is partly related to anthropogenic changes in the hydrological cycle. The mechanisms linking the subtropical salinity increase to the subsequent overshoot are analysed, supporting the relationship found. This understanding is used to explain differences seen in some models and scenarios. In one experiment there is no overshoot because there is little salinity build up, partly as a result of model differences in the hydrological cycle response to increased CO2 levels and partly because of a less aggressive scenario. Another experiment has a delayed overshoot, possibly as a result of a very weak AMOC in that GCM when CO2 is high. This study identifies aspects of overshoot behaviour that are robust across a multi-model and multi-scenario ensemble, and those that differ between experiments. These results could inform an assessment of the real-world AMOC response to decreasing CO2.