20 research outputs found

    Corals record long-term Leeuwin current variability including Ningaloo Niño/Niña since 1795

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    Variability of the Leeuwin current (LC) off Western Australia is a footprint of interannual and decadal climate variations in the tropical Indo-Pacific. La Niña events often result in a strengthened LC, high coastal sea levels and unusually warm sea surface temperatures (SSTs), termed Ningaloo Niño. The rarity of such extreme events and the response of the southeastern Indian Ocean to regional and remote climate forcing are poorly understood owing to the lack of long-term records. Here we use well-replicated coral SST records from within the path of the LC, together with a reconstruction of the El Niño-Southern Oscillation to hindcast historical SST and LC strength from 1795 to 2010. We show that interannual and decadal variations in SST and LC strength characterized the past 215 years and that the most extreme sea level and SST anomalies occurred post 1980. These recent events were unprecedented in severity and are likely aided by accelerated global ocean warming and sea-level rise. © 2014 Macmillan Publishers Limited

    Croll revisited: Why is the northern hemisphere warmer than the southern hemisphere?

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    The question of why, in the annual-mean, the northern hemisphere (NH) is warmer than the southern hemisphere (SH) is addressed, revisiting an 1870 paper by James Croll. We first show that ocean is warmer than land in general which, acting alone, would make the SH, with greater ocean fraction, warmer. Croll was aware of this and thought it was caused by greater specific humidity and greenhouse trapping over ocean than over land. However, for any given temperature, it is shown that greenhouse trapping is actually greater over land. Instead, oceans are warmer than land because of the smaller surface albedo. However, hemispheric differences in planetary albedo are negligible because the impact of differences in land-sea fraction are offset by the SH ocean and land reflecting more than their NH counterparts. In the absence of a role for albedo differences it is shown that, in agreement with Croll, northward cross-equatorial ocean heat transport (X-OHT) is critical for the warmer NH. This is examined in a simple box model based on the energy budget of each hemisphere. The hemispheric difference forced by X-OHT is enhanced by the positive water vapor-greenhouse feedback, and is partly compensated by the southward atmospheric energy transport. Due to uncertainties in the ocean data, a range of X-OHT is considered. A X-OHT of larger than 0.5 PW is needed to explain the warmer NH solely by X-OHT. For smaller X-OHT, a larger basic state greenhouse trapping in the NH, conceived as imposed by continental geometry, needs to be imposed. Numerical experiments with a GCM coupled to a slab ocean provide evidence that X-OHT is fundamentally important in determining the hemispheric differences in temperature. Therefore, despite some modifications to his theory, analysis of modern data confirms Croll's 140-year-old theory that the warmer NH is partly because of northward X-OHT.close1

    Ixr1 is required for the expression of the ribonucleotide reductase Rnr1 and maintenance of dNTP pools

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    The Saccharomyces cerevisiae Dun1 protein kinase is a downstream target of the conserved Mec1-Rad53 checkpoint pathway. Dun1 regulates dNTP pools during an unperturbed cell cycle and after DNA damage by modulating the activity of ribonucleotide reductase (RNR) by multiple mechanisms, including phosphorylation of RNR inhibitors Sml1 and Dif1. Dun1 also activates DNA-damage-inducible genes by inhibiting the Crt1 transcriptional repressor. Among the genes repressed by Crt1 are three out of four RNR genes: RNR2, RNR3, and RNR4. The fourth RNR gene, RNR1, is also DNA damage-inducible, but is not controlled by Crt1. It has been shown that the deletion of DUN1 is synthetic lethal with the deletion of IXR1, encoding an HMG-box-containing DNA binding protein, but the reason for this lethality is not known. Here we demonstrate that the dun1 ixr1 synthetic lethality is caused by an inadequate RNR activity. The deletion of IXR1 results in decreased dNTP levels due to a reduced RNR1 expression. The ixr1 single mutants compensate for the reduced Rnr1 levels by the Mec1-Rad53-Dun1-Crt1-dependent elevation of Rnr3 and Rnr4 levels and downregulation of Sml1 levels, explaining why DUN1 is indispensible in ixr1 mutants. The dun1 ixr1 synthetic lethality is rescued by an artificial elevation of the dNTP pools. We show that Ixr1 is phosphorylated at several residues and that Ser366, a residue important for the interaction of HMG boxes with DNA, is required for Ixr1 phosphorylation. Ixr1 interacts with DNA at multiple loci, including the RNR1 promoter. Ixr1 levels are decreased in Rad53-deficient cells, which are known to have excessive histone levels. A reduction of the histone gene dosage in the rad53 mutant restores Ixr1 levels. Our results demonstrate that Ixr1, but not Dun1, is required for the proper RNR1 expression both during an unperturbed cell cycle and after DNA damage
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