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1.
FIGURE 3.

FIGURE 3. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

Hog1 localization is regulated uniquely during ER stress. A–D, cells expressing HOG1-GFP were treated with 0.4 m NaCl, 0.8 units/ml of zymolyase, 2 mm DTT, or 1 μg/ml of Tm, then collected for microscopy and phospho-Hog1 immunoblot analysis. E, cells expressing HOG1-GFP were treated with 0.4 m NaCl alone (left panel) or following 3 h of preincubation with 2 mm DTT (middle panel) or 1 μg/ml of Tm (right panel). DAPI, 4′,6-diamidino-2-phenylindole.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.
2.
FIGURE 7.

FIGURE 7. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

Cellular effects of the role of Hog1 in Atg8 induction. A, alkaline phosphatase activity of cells bearing the pho8Δ60 mutation following a 6-h Tm treatment (compared with untreated cells). Error bars represent S.D. of three replicates. B, 5-fold serial dilutions of wild type and atg8Δ cells grown on medium alone, or medium containing 0.4 μg/ml of Tm.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.
3.
FIGURE 4.

FIGURE 4. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

Hog1 regulates mRNA expression during ER stress. A, HSP12 Northern blots of WT and hog1Δ cells treated with 2 mm DTT or 1 μg/ml of Tm. B and C, following 2 h of DTT treatment, the levels of HSP12, YMR103C, and YPL088W in wild type (WT) and hog1Δ cells were measured by Northern blot, normalized to actin, and presented as fold-increase compared with untreated cells. Error bars represent S.D. of three repeats.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.
4.
FIGURE 2.

FIGURE 2. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

ER stress activates Hog1 through a unique mechanism mediated by SSK1 and the UPR. A–C, phospho-Hog1 immunoblots of cells treated with 4 mm DTT for 3 h, 0.4 m NaCl for 5 min, or 0.8 units/ml of zymolyase for 1 h. D, 5-fold serial dilutions of cells grown with or without 0.1 μg/ml of Tm. E, schematic depicting the overlapping but non-identical pathways of Hog1 activation during ER stress (shaded gray), osmotic stress, and cell wall stress. WT, wild type.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.
5.
FIGURE 1.

FIGURE 1. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

During ER stress Hog1 is phosphorylated and promotes stress recovery. A, phospho-Hog1 immunoblots of wild type cells treated with 2 mm DTT or 1 μg/ml of Tm. B, Northern analysis with HAC1-specific probe shows conversion of unspliced HAC1 (HAC1(U)) to spliced HAC1 (HAC1(S)) within 15 min of 2 mm DTT treatment, or 45 min of 1 μg/ml of Tm treatment. C and D, HAC1 Northern analysis during sustained 2 mm DTT treatment (C) or 45 min of 1 μg/ml of Tm treatment followed by removal of the drug from the medium (D) in wild type (WT) and hog1Δ cells. Graphs depict HAC1(S)/[HAC1(U) + HAC1(S)]. Error bars represent S.D. of three repeats. E, 5-fold serial dilutions of wild type and hog1Δ cells grown on medium alone, or medium containing 0.1 μg/ml of Tm or 8 mm DTT.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.
6.
FIGURE 5.

FIGURE 5. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

Induction of Atg8 protein during ER stress requires HOG1. A, the schematic shows parallel pathways that converge to induce autophagy. PAS formation and increases in Atg8 protein levels are both necessary for appropriate levels of autophagy. Hog1 specifically regulates the increase in Atg8 protein levels and induction of autophagy downstream. B, cells expressing the GFP-ATG8 reporter were subjected to 4 h of 2 mm DTT or 1 μg/ml of Tm treatment before microscopic visualization to assess PAS formation. C, following 6 h of 1 μg/ml of Tm treatment, fluorescence intensity of Atg8-GFP puncta was quantified (n = 300). D, E, and G, GFP immunoblots of cells bearing the GFP-ATG8 reporter, treated with 1 μg/ml of Tm or 3 mm DTT. The top GFP band represents the GFP-Atg8 fusion protein, and the bottom GFP band represents free GFP. F and H, quantitation of GFP immunoblots. GFP-Atg8 + free GFP signal was normalized to Pgk1 (loading control). Error bars represent S.E. of at least three replicates.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.
7.
FIGURE 6.

FIGURE 6. From: Late Phase of the Endoplasmic Reticulum Stress Response Pathway Is Regulated by Hog1 MAP Kinase.

Hog1 acts from the cytoplasm and regulates Atg8 protein stability during ER stress. A, GFP immunoblots of cells bearing the GFP-ATG8 reporter following nitrogen deprivation. B, ATG8 Northern blots of wild type and hog1Δ cells treated with 1 μg/ml of Tm. C and D, following 6 h of 1 μg/ml of Tm treatment, 50 μg/ml of CHX was added to cells for 12 h. The GFP-Atg8 band was quantified and normalized to Asc1 levels. The protein level at each time point was divided by the level at the time of CHX addition to determine the % protein remaining. E, strains expressing Hog1-GFP or Hog1-GFP-CCAAX (PM-anchored) were visualized following 2 h of 2 mm DTT treatment or 1 μg/ml of Tm treatment. F, GFP immunoblots of a hog1Δ strain, a strain expressing Hog1-GFP (WT), and a strain expressing Hog1-GFP-CCAAX (PM-anchored) following treatment with 1 μg/ml of Tm. Each strain expressed the GFP-Atg8 marker. Note that in this strain background, GFP-Atg8 cleavage occurs less efficiently than in the strain background used for Fig. 5, and that additional GFP degradation products are observed (*). G, quantitation of F. GFP-Atg8 + free GFP bands were normalized to Pgk1. Error bars represent S.E. of three replicates.

Alicia A. Bicknell, et al. J Biol Chem. 2010 June 4;285(23):17545-17555.

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