EMBO/soda-nel huggingface dataset:
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 1

Figure 1. Female APP23 mice at 21 months have higher Aβ burden than male APP23 mice.

(A) Quantitative analysis of the Aβ1-40 protein in the TBS (*p=0.0212), Triton-X (p=0.0544) and SDS (**p=0.0063) fractions of brain homogenates from male (n=7) and female (n=10) APP23 mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test.

(B) Stereological analysis of cortical area covered by 4G8-positive plaques in male (n=10) and female (n=8) APP23 mice (left) and representative images (right), scale bar = 500 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, ***p=0.0004.

(C) Fluorescence intensity based analysis of pFTAA-stained Aβ plaques in the cortex of male (n=10) and female (n=8) APP23 mice (left) and representative images (right), scale bar = 1 mm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, **p=0.0011.

(D) Stereological analysis of cortical area covered by Congo Red-positive plaques in male (n=10) and female (n=8) APP23 mice (left) and representative images (right), scale bar = 500 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, ***p=0.0001.

(E) Native filter assay analysis of TBS (p=0.2453), Triton-X (p=0.0604), SDS (*p=0.0196) and formic acid (FA) (**p=0.0057) fractions from male (n=8) and female (n=7) APP23 mouse brain homogenates. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test between the same fractions. Data points were taken from graphs analysing APP23p40+/+ against APP23p40-/- mice.
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 2

Figure 2. Female APP23 mice have higher astrocyte numbers than male mice.

(A) Histological analysis of plaque-associated BACE1 immunoreactivity in male (n=10) and female (n=8) APP23 mice. BACE1 area covered was normalised to 4G8-positive area covered of the same image (left). Right: representative images, scale bar = 50 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.3724.

(B) Stereological quantification of the number of cortical GFAP-positive astrocytes in male (n=10) and female (n=8) APP23 mice (left). Right: representative images of GFAP staining, scale bar = 200 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, *p=0.0134.

(C) Quantification of activated microglia within 30 µm from plaque borders. Top: Numbers of Iba1-positive microglia were normalised to the size of the nearest 4G8-positive plaque and quantified in male (n=10) and female (n=8) APP23 mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.0576. Bottom: Histogram representing Clec7a staining intensity within plaque-associated Iba1-positive microglia in male (n=10) and female (n=8) APP23 mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test with Bonferroni correction for each single bin, p=N.S.. Right: representative images, scale bar = 40 µm. Data points were taken from graphs analysing APP23p40+/+ against APP23p40-/- mice.

(D) Radial intensity profiles of Iba1 and 4G8 around the center of the nucleus of plaque-associated Iba1-positive microglia in male (n=10) and female (n=8) APP23 mice. Iba1 intensity declines until a radius of ~6 µm, marking the cell periphery. 4G8 intensity peaks inside the cell (~4 µm), but stays high outside the cell. This is very likely due to the close proximity to 4G8 positive plaques. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test with Bonferroni correction for the number of binned radii shows no significant difference between both 4G8 traces.
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 3

Figure 3. APP23 mice have increased microglia-specific Il12b/IL12p40 levels in the brain.

(A) Gene expression analysis of IL12b in whole brain (n=3 per gender, Il12b undetected), Cd11b-negative non-microglial cells (n=3 per gender, Il12b undetected) and CD11b-positive microglia (n=5 per gender, p=0.3540) in male and female APP23 mice. Gapdh expression was used as an internal reference gene. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test for each fraction.

(B) ELISA measurements of the IL12p40 concentration in the TBS-soluble protein fraction derived from wild-type (WT) (n=5), APP23p40+/+(n=17) and APP23p40‑/- (n=16) mice. Male mice are depicted by blue squares while female mice are shown as red squares. Mean ± s.e.m., statistical analysis: one-way ANOVA, Tukey post-hoc test, *p=0.0276, ***p=<0.0001.
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 4

Figure 4. In male APP23 mice, IL12p40 deficiency reduces Aβ plaque deposition but not does not affect biochemical characteristics of Aβ.

(A) Mesoscale analysis for the Aβ1-40 protein in the TBS (p=0.2298), Triton-X (p=0.1329) and SDS (p=0.7184) fractions of brain homogenates from male APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice. Total protein concentration of each sample was used as an internal reference. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test.

(B) Stereological analysis of cortical area covered by 4G8-positive plaques (left) and representative images of 4G8-staining in APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice (right), scale bar = 500 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, **p=0.0039.

(C) Fluorescence intensity based analysis of pFTAA-positive area covered in the cortex of APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice (left) and representative images for each genotype (right), scale bar = 1 mm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, **p=0.0051.

(D) Stereological analysis of cortical area covered by Congo Red-positive plaques in APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice (left) and representative images (right), scale bar = 500 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, **p=0.0070.

(E) Native filter assay analysis of TBS (p=0.7124), Triton-X (p=0.3170), SDS (p=0.4833) and formic acid (FA) (p=0.8144) fractions from APP23p40+/+ (n=8) and APP23p40-/- (n=8) mouse brain homogenates. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test between the same fractions.
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 5

Figure 5. Lack of IL12p40 does not affect plaque-associated BACE1 immunoreactivity or glial properties in male APP23 mice.

(A) Histological analysis of plaque-associated BACE1 immunoreactivity in male APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice. BACE1 area covered was normalised to 4G8-positive area covered of the same image (left). Right: representative images, scale bar = 50 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.1780.

(B) Stereological quantification of the number of cortical GFAP-positive astrocytes in male APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice (left). Right: representative images of GFAP staining, scale bar = 200 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.3148.

(C) Quantification of activated microglia within 30 µm from plaque borders. Top: Numbers of Iba1-positive microglia were normalised to the size of the nearest 4G8-positive plaque and quantified in male APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.1925. Bottom: Histogram representing Clec7a staining intensity within plaque-associated Iba1-positive microglia in male APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test with Bonferroni correction for each single bin, p=N.S.. Right: representative images, scale bar = 40 µm.

(D) Radial intensity profiles of Iba1 and 4G8 around the center of the nucleus of plaque-associated Iba1-positive microglia in male APP23p40+/+ (n=10) and APP23p40-/- (n=8) mice. Iba1 intensity declines until a radius of ~6 µm, marking the cell periphery. 4G8 intensity peaks inside the cell (~4 µm), but stays high outside the cell. This is very likely due to the close proximity to 4G8 positive plaques. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test with Bonferroni correction for the number of binned radii shows no significant difference between both 4G8 traces.
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 6

Figure 6. In female APP23 mice, IL12p40 deletion leads to a reduction in soluble Aβ1-40 but not Aβ plaque load.

(A) Mesoscale analysis for the Aβ1-40 protein in the TBS (*p=0.0208), Triton-X (*p=0.0440) and SDS (p=0.0540) fractions of brain homogenates from APP23p40+/+(n=7) and APP23p40-/- (n=8) mice. Total protein concentration of each sample was used as an internal reference. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test.

(B) Stereological analysis of cortical area covered by 4G8-positive plaques (left) and representative images of 4G8-staining in APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice (right), scale bar = 500 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.1831.

(C) Fluorescence intensity based analysis of pFTAA-positive area covered in the cortex of APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice (left) and representative images for each genotype (right), scale bar = 1 mm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.3406.

(D) Stereological analysis of cortical area covered by Congo Red-positive plaques in APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice (left) and representative images (right), scale bar = 500 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.4542.

(E) Native filter assay analysis of TBS (p=0.6823), Triton-X (p=0.1146), SDS (p=0.0508) and formic acid (FA) (p=0.6603) fractions from APP23p40+/+ (n=7) and APP23p40-/- (n=7) mouse brain homogenates. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-tests between the same fractions.
Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice (2020)
Figure 7

Figure 7. Lack of IL12p40 but does not affect plaque-associated BACE1 immunoreactivity or gliosis in female APP23 mice.

(A) Histological analysis of plaque-associated BACE1 immunoreactivity in female APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice. BACE1 area covered was normalised to 4G8-positive area covered of the same image (left). Right: representative images, scale bar = 50 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.5402.

(B) Stereological quantification of the number of cortical GFAP-positive astrocytes in female APP23p40+/+ (n=8) and APP23p40-/- (n=8) mice (left). Right: representative images of GFAP staining, scale bar = 200 µm. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.1579.

(C) Quantification of activated microglia within 30 µm from plaque borders. Top: Numbers of Iba1-positive microglia were normalised to the size of the nearest 4G8-positive plaque and quantified in female APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test, p=0.8240. Bottom: Histogram representing Clec7a staining intensity within plaque-associated Iba1-positive microglia in female APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test with Bonferroni correction for each single bin, p=N.S.. Right: representative images, scale bar = 40 µm.

(D) Radial intensity profiles of Iba1 and 4G8 around the center of the nucleus of plaque-associated Iba1-positive microglia in female APP23p40+/+ (n=8) and APP23p40-/- (n=10) mice. Iba1 intensity declines until a radius of ~6 µm, marking the cell periphery. 4G8 intensity peaks inside the cell (~4 µm), but stays high outside the cell. This is very likely due to the close proximity to 4G8 positive plaques. Mean ± s.e.m., statistical analysis: two-tailed unpaired t-test with Bonferroni correction for the number of binned radii shows no significant difference between both 4G8 traces.

Expanded View Figure Legends
HDACs link the DNA damage response, processing of double-strand breaks and autophagy (2011)
f1

a–c, RFA1::FLAG DDC2::MYC cells were arrested in G2 and released in YP galactose to induce HO endonuclease. After 30 min, the culture was split in two: +VPA and −VPA. a, Samples were processed for western blot using anti-Rad53, Srs2 and Ddc2 antibodies. b, A schematic diagram showing probe locations with respect to the HO cut site. The resection rate was calculated as the rate of HO cut band disappearance. c, Fold enrichment of the 0.2-kb fragment was calculated after ChIP of Rfa1–Flag, Ddc2–Myc. d, VPA effect on ectopic recombination (rec.) in wild-type (WT) cells. Error bars represent standard deviation (s.d.) calculated from four independent experiments.
HDACs link the DNA damage response, processing of double-strand breaks and autophagy (2011)
f2

a, MRE11::MYC cells were treated as in Fig. 1a. Cell samples were processed for ChIP analysis and the fold enrichment of the 0.2-kb fragment after ChIP of Mre11–Myc without (−VPA) or with (+VPA) VPA was calculated. b, EXO1::FLAG SAE2::PK MRE11::MYC cells were grown as in a. Cell samples were taken and processed for western blot analysis using anti-Flag, PK and Myc antibodies.
HDACs link the DNA damage response, processing of double-strand breaks and autophagy (2011)
f3

a, Cherry::APE1 GFP::ATG8 cells were grown and shifted to YPD, nitrogen starvation (SD-N) or YPD+VPA medium for 3 h. Samples were processed for microscopy. The table shows numbers corresponding to the experiment. Percentage of fluorescence signals is presented and error bars represent the s.d. obtained from three independent experiments. DIC, differential interference contrast. Scale bars, 3 &mgr;m. b, pho8&Dgr;60 and pho8&Dgr;60 atg1&Dgr; cells were grown as in a. Pho8&Dgr;60 activity was calculated by measuring alkaline phosphatase levels. Error bars represent s.d. calculated from five independent experiments. c, GFP::ATG8 and GFP::ATG8 atg1&Dgr; cells were grown as in a. Cell samples were processed for western blot using anti-GFP antibody. Quantification is presented in Supplementary Fig. 3.
HDACs link the DNA damage response, processing of double-strand breaks and autophagy (2011)
f4

a, 4HA–Sae2 was immunoprecipitated ± VPA with anti-HA and subsequently ± anti-acetyl-Lysine. Eluate was analysed using anti-HA. Lane 1: input Sae2; 2: input Sae2–HA −VPA; 3: as in 2 but +VPA; 4: 3 &mgr;l elution Sae2–HA −VPA after anti-HA immunoprecipitation (IP; input AcK-IP); 5: double amount of 4; 6: IP anti-AcK elution from anti-HA IP of Sae2–HA −VPA; 7: as in 6 but +VPA. b, SAE2::PK erg6&Dgr; cells were treated as in Fig. 2a. After 30 min induction, VPA and PMSF were added or not. Samples were processed for western blot using anti-PK. c, Wild-type SAE2::PK, SAE2::PK atg1&Dgr; and SAE2::PK atg19&Dgr; cells were grown as in b. After 30 min induction, VPA was added or not and samples treated as in b. d, Wild-type SAE2::PK cells were grown as in b. After 120 min induction, rapamycin (200 ng ml−1) was added or not and samples were treated as in b.
HDACs link the DNA damage response, processing of double-strand breaks and autophagy (2011)
f5

a, Survival of wild-type, rpd3&Dgr;, hda1&Dgr; and rpd3&Dgr; hda1&Dgr; strains after 4NQO, MMS and HU treatment. Error bars represent s.d. calculated from seven independent experiments. b, HO was induced in G2 wild-type, hda1&Dgr;, rpd3&Dgr; and hda1&Dgr; rpd3&Dgr; cells and western and Southern blot analyses were performed. c, Wild-type SAE2::PK and hda1&Dgr; rpd3&Dgr; SAE2::PK cells were grown as in b and western blot was performed as in Fig. 4b. d, e, Wild-type SAE2::PK and gcn5&Dgr; SAE2::PK strains were grown as in b and after 30 min of HO induction either VPA (d) or rapamycin (e) was added or not. Western blot was performed. f, Percentage of viability of wild-type, atg1&Dgr;, rpd3&Dgr; hda1&Dgr; and atg1&Dgr; rpd3&Dgr; hda1&Dgr; strains. Error bars represent s.d. calculated from four independent experiments.
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 1

Figure 1. The protein levels of ARR1/10/12 decrease under salt treatment in a time dependent manner.

A-C ARR1/10/12 protein levels were examined by western blot when five-day-old seedlings of 35S:ARR1:MYC, 35S:ARR10:YFP, and 35S:ARR12:YFP were treated with or without 200 mM NaCl for the indicated time points. Actin was used as the internal reference. The relative intensity of band detected by anti-MYC or anti-GFP antibody to that by anti-Actin antibody without treatment was set to 1.0.

D-F Quantification analysis of the protein levels of ARR1/10/12 in (A-C).

Data information: In (D-F), the statistical analyses of the related density of western blotting bands were performed using ImageJ software based on three independent biological replicates. Values are means ± SD (n=3). **, ***, and **** indicate significant difference to the corresponding controls with P<0.01, P<0.001, and P<0.0001, respectively (student's t-test).
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 2

Figure 2. MPK3/6 interact with ARR1/10/12.

A Yeast two hybrid analysis showing the interaction between MPK3/6 and ARR12. Yeast cells were plated on selection medium: SD-LW (-Leu/Trp) or SD-LWHA (-Leu/Trp/His/Ade) supplemented with AbA (Aureobasidin A) and X-α-gal (5-bromo-4-chloro-3-indolyl-b-d-galactopyranoside). MPK3/4/6 coding sequences were fused with the GAL4 DNA-binding domain (Bait proteins), and ARR1/10/12 coding sequences were fused with the GAL4 activation domain (Prey proteins).

B BiFC analysis of interaction between MPK3/4/6 and ARR1/10/12. Partial yellow fluorescence protein (YFP) constructs were fused to MPK3/4/6 or ARR1/10/12. The fusion constructs were co-expressed transiently in Arabidopsis protoplasts cells. The interaction between MPK3/4/6 and ARR1/10/12 were visualized by fluorescence microscopy. The percentages labelled in the images mean the probability of present cell in cells observed. Scale Bar, 50 μm.

C In vivo Coimmunoprecipitation assay of MPK3/4/6 and ARR1/10/12. MPK3/4/6-YFP and ARR1/10/12-MYC were co-expressed in Arabidopsis protoplast cells. Protein extracts (Input) were immunoprecipitated with GFP Trap magnetic agarose beads. Immunoblots were performed with anti-MYC antibody to detect ARR1/10/12 and with anti-GFP antibody to detect MPK3/4/6.
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 3

Figure 3. MPK3/6-mediated ARR1/10/12 phosphorylation in vitro.

A-C Thiophosphorylation assays of wild type and mutated forms ARR1/10/12 by MPK3/6 in vitro. Potential phosphorylated Ser residues or Thr residues of ARR1, ARR10, and ARR12 were mutated to Ala (ARR1m/ARR10m/ARR12m). Recombinant ARR1/10/12-His and ARR1m/10m/12m-His proteins were incubated with MPK3 and MPK6 which were activated by MKK5DD. Phosphorylated ARR1/10/12, ARR1m/10m/12m, and MPK3/6 were visualized by an anti-thiophosphate ester-specific antibody (α-TPE) (upper panel). Asterisk in (B) indicates non-specific bands. Recombinant MKK5DD, MPK3, MPK6, ARR1/10/12, and ARR1m/10m/12m were detected by comassie brilliant blue (CBB) staining as loading controls (bottom panel).

Data information: Two independent biological repeats showed similar results.
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 4

Figure 4. MPK3/6-mediated ARR1/10/12 phosphorylation in vivo.

A-C Immunoblot analysis with anti-MYC antibody or anti-GFP antibody showing the upshift of ARR1, ARR10, and ARR12 in a phos-tag gel. The phosphorylated ARR1, ARR10, and ARR12 were abolished after treatment with calf intestinal alkaline phosphatase (CIAP). Seven-day-old seedlings of 35S:ARR1:MYC (A), 35S:ARR10:YFP (B), and 35S:ARR12:YFP (C) in Col and MPK3SR backgrounds were treated with or without 200 mM NaCl for indicated time points. Total proteins were extracted and subjected to immunoblot analysis. ARR1, ARR10, and ARR12 proteins separated on SDS-PAGE gel without phos-tag were detected as loading controls.

Data information: Similar results were obtained with three biological repeats.
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 5

Figure 5. Salt stress-induced ARR1/10/12 degradation is dependent on MPK3/6.

A-C Immunoblot analysis the effects of MPK3/6 on salt stress-induced ARR1/10/12 protein degradation. Seven-day-old seedlings of 35S:ARR1:MYC, 35S:ARR10:YFP, and 35S:ARR12:YFP in Col-0 and MPK3SR backgrounds were treated with or without 200 mM NaCl for indicated time points. Actin was used as the internal reference. The relative intensity of band detected by anti-MYC or anti-GFP antibody to that by anti-Actin antibody without treatment was set to 1.0.

D-I Quantification analysis of MPK3/6 effect on salt stress-induced ARR1/10/12 protein degradation in (A-C).

Data information: In (D-I), the statistical analyses of the related density of western blotting bands were performed using ImageJ software based on three independent biological replicates. Values are means ± SD (n=3). **, ***, and **** indicate significant difference to the corresponding controls with P<0.01, P<0.001, and P<0.0001, respectively (student's t-test).
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 6

Figure 6. MPK3/6 promote ARR1/10/12 protein degradation under salt stress.

A-C Immunoblot analysis stability of ARR1/10/12 and ARR1T553A/10S383A/12S323A proteins under salt stress. Seven-day-old seedlings of 35S:ARR1:MYC, 35S:ARR10:YFP, 35S:ARR12:YFP, 35S:ARR1T553A:MYC, 35S:ARR10S383A:YFP, and 35S:ARR12S323A:YFP were treated with or without 200 mM NaCl for indicated time points. Actin was used as the internal reference. The relative intensity of band detected by anti-MYC or anti-GFP antibody to that by anti-Actin antibody without treatment was set to 1.0.

D-I Quantification analysis of stability of ARR1/10/12 and ARR1T553A/10S383A/12S323A proteins under salt stress in (A-C).

Data information: In (D-I), the statistical analyses of the related density of western blotting bands were performed using ImageJ software based on three independent biological replicates. Values are means ± SD (n=3). **, ***, and **** indicate significant difference to the corresponding controls with P<0.01, P<0.001, and P<0.0001, respectively (student's t-test).
MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis (2021)
Figure 7

Figure 7. MPK3/6-mediated ARR1 phosphorylation decreases the ability of ARR1 protein in repressing salt tolerance.

A-D Four-day-old seedlings of 35S:ARR1:MYC, 35S:ARR1T553A:MYC, and 35S:ARR1T553D:MYC were transferred to 1/2 MS medium supplemented with or without 50 mM or 75 mM NaCl. After three days of salt treatment, plant phenotypes (A) and relative primary root lengths (B) were determined. After ten days of salt treatment, changes in survival rates (C) and fresh weights (D) were examined. Scale Bar, 1 cm.

Data information: In (B-D), data are means of three biological replicates ± SD (n=60 for B, and n=12 for C and D). ns indicates no significant difference to the corresponding controls. **, ***, and **** indicate significant difference to the corresponding controls with P<0.01, P<0.001, and P<0.0001, respectively (student's t-test).