Cells respond to salt stress by osmolyte synthesis and by increase of K⁺ uptake and Na⁺ efflux at the plasma membrane and of Na⁺ accumulation at the vacuole. This cellular level of response has been approached by the molecular genetics of Saccharomyces cerevisiae. Two plasma membrane proteins, Sln1 and Sho1, operate as sensors for turgor loss under mild osmotic stress. They activate the Hog1 MAP kinase which induces several defence genes, including the ENA1 Na⁺-efflux pump. Hog1-mediated induction occurs by inactivation of the Sko1 repressor. High concentrations of Na⁺ activate the calcium-dependent protein phosphatase calcineurin, which induces the ENA1 gene via the positive transcription factor Hal8/Crz1/Tcn1. Vacuoles could operate as Na⁺ sensors through a Na⁺-Ca²⁺ exchange mechanism. The electrical potential of the plasma membrane is a major determinant of the uptake of toxic cations, including Na⁺, by non-specific leakage pathways. This biophysical parameter is modulated by the concerted activities of the proton pumping Pma1 ATPase and the Trk1,2 K⁺ uptake system. Both calcineurin and the protein kinase Hal4,5 modulate Trk1,2 and, indirectly, the membrane potential and salt tolerance. The limiting role of vacuolar cation accumulation in salt tolerance has been demonstrated by expression in yeast vacuoles of the bacterial antiporter NhaA.

Exposure of yeast to increases in extracellular osmolarity activates the Hog1 mitogen‐activated protein kinase (MAPK), which is essential for the induction of gene expression required for cell survival upon osmotic stress. Several genes are regulated in response to osmotic stress by Sko1, a transcriptional repressor of the ATF/CREB family. We show by in vivo coprecipitation and phosphorylation studies that Sko1 and Hog1 interact and that Sko1 is phosphorylated upon osmotic stress in a Hog1‐dependent manner. Hog1 phosphorylates Sko1 in vitro at multiple sites within the N‐terminal region. Phosphorylation of Sko1 disrupts the Sko1–Ssn6–Tup1 repressor complex, and consistently, a mutant allele of Sko1, unphosphorylatable by Hog1, exhibits less derepression than the wild type. Interestingly, Sko1 repressor activity is further enhanced in strains with high protein kinase A (PKA) activity. PKA phosphorylates Sko1 near the bZIP domain and mutation of these sites eliminates modulation of Sko1 responses to high PKA activity. Thus, Sko1 transcriptional repression is controlled directly by the Hog1 MAPK in response to stress, and this effect is further modulated by an independent signaling mechanism through the PKA pathway.

A major part of the transcriptional response of yeast cells to osmotic shock is controlled by the HOG pathway and several downstream transcription factors. Sko1p is a repressor that mediates HOG pathway‐dependent regulation by binding to CRE sites in target promoters. Here, we report five target genes of Hog1p–Sko1p: GRE2, AHP1, SFA1, GLR1 and YML131w. The two CREs in the GRE2 promoter function as activating sequences and, hence, bind (an) activator protein(s). However, the two other yeast CRE‐binding proteins, Aca1p and Aca2p, are not involved in regulation of the GRE2 promoter under osmotic stress. In the absence of the co‐repressor complex Tup1p–Ssn6p/Cyc8p, which is recruited by Sko1p, stimulation by osmotic stress is still observed. These data indicate that Sko1p is not only required for repression, but also involved in induction upon osmotic shock. All five Sko1p targets encode oxidoreductases with demonstrated or predicted roles in repair of oxidative damage. Altered basal expression levels of these genes in hog1Δ and sko1Δ mutants may explain the oxidative stress phenotypes of these mutants. All five Sko1p target genes are induced by oxidative stress, and induction involves Yap1p. Although Sko1p and Yap1p appear to mediate osmotic and oxidative stress responses independently, Sko1p may affect Yap1p promoter access or activity. The five Sko1p target genes described here are suitable models for studying the interplay between osmotic and oxidative responses at the molecular and physiological levels.

Growing evidence suggests substantial quantities of particulate organic carbon (POC) produced in surface waters reach abyssal depths within days during episodic flux events. A 29-year record of in situ observations was used to examine episodic peaks in POC fluxes and sediment community oxygen consumption (SCOC) at Station M (NE Pacific, 4,000-m depth). From 1989 to 2017, 19% of POC flux at 3,400 m arrived during high-magnitude episodic events (≥mean + 2 σ), and 43% from 2011 to 2017. From 2011 to 2017, when high-resolution SCOC data were available, time lags between changes in satellite-estimated export flux (EF), POC flux, and SCOC on the sea floor varied between six flux events from 0 to 70 days, suggesting variable remineralization rates and/or particle sinking speeds. Half of POC flux pulse events correlated with prior increases in EF and/or subsequent SCOC increases. Peaks in EF overlying Station M frequently translated to changes in POC flux at abyssal depths. A power-law model (Martin curve) was used to estimate abyssal fluxes from EF and midwater temperature variation. While the background POC flux at 3,400-m depth was described well by the model, the episodic events were significantly underestimated by ∼80% and total flux by almost 50%. Quantifying episodic pulses of organic carbon into the deep sea is critical in modeling the depth and intensity of POC sequestration and understanding the global carbon cycle. Significance Ignoring temporal fluctuations in the oceanic carbon budget leads to a significant misrepresentation of the cycling of organic matter from production in surface waters to consumption and sequestration in the abyssal ocean. A 29-year time series (1989 to 2017) of particulate organic carbon (POC) fluxes and sea-floor measurements of sediment community oxygen consumption (SCOC) revealed episodic, high-magnitude events over the past 7 years. Time lags between changes in satellite-estimated export flux, POC flux and SCOC varied from 0 to 70 days. A commonly used model to estimate carbon flux through the water column significantly underestimated the measured carbon fluxes by almost 50%. Episodic pulses of organic carbon into the deep sea must be accounted for to balance the oceanic carbon budget.