Jackson Laboratory ddit3 null alleles

A Longitudinal intraocular pressure (IOP) measurements from D2 and D2. <t>Ddit3/Jun</t> −/− eyes ( n listed respectively here and throughout figure legends) at 5 M ( n = 60, 63), 9 M ( n = 60, 63), 10.5 M ( n = 66, 63), and 12 M ( n = 62, 61). Both genotype groups had significantly elevated IOPs at 9 M, 10.5 M, and 12 M compared to 5 M (* P < 0.001). At these timepoints, D2. Ddit3/Jun −/− eyes did not have a statistically significant reduction in IOP compared to WT, although D2. Ddit3/Jun −/− eyes had slightly higher IOPs at 9 M of age compared to D2 (* P = 0.004). Two-way ANOVA, Holm-Sidak’s post hoc . B Examples of optic nerve cross sections with no or early (noe) and severe (sev) glaucomatous damage from D2 and D2. Ddit3/Jun −/− mice and percentages of optic nerves with noe ( n = 23, 16), moderate (mod; n = 3, 11) and sev ( n = 31, 27) glaucomatous damage. Ddit3/Jun deletion did not afford protection to RGC axons and in fact slightly worsened axonal degeneration (* P = 0.049). Chi square test. C Representative retinal flat mounts immunoassayed for RBPMS and quantification of RBPMS+ cells from 12 M D2 and D2. Ddit3/Jun −/− retinas with corresponding noe ( n = 6, 6) or sev ( n = 6, 6) optic nerves. Sev D2. Ddit3/Jun −/− retinas had 77.0 ± 3.1% improved RGC survival compared to D2 controls (* P < 0.001). RBPMS+ cells/mm 2 ± SEM for D2 and D2. Ddit3/Jun −/− respectively: Noe: 2899.6 ± 111.0, 2765.4 ± 49.8; Sev: 226.7 ± 20.8, 2151.5 ± 83.0. Two-way ANOVA, Holm-Sidak post-hoc . Scale bars, 50 μm.

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A Longitudinal intraocular pressure (IOP) measurements from D2 and D2. Ddit3/Jun −/− eyes ( n listed respectively here and throughout figure legends) at 5 M ( n = 60, 63), 9 M ( n = 60, 63), 10.5 M ( n = 66, 63), and 12 M ( n = 62, 61). Both genotype groups had significantly elevated IOPs at 9 M, 10.5 M, and 12 M compared to 5 M (* P < 0.001). At these timepoints, D2. Ddit3/Jun −/− eyes did not have a statistically significant reduction in IOP compared to WT, although D2. Ddit3/Jun −/− eyes had slightly higher IOPs at 9 M of age compared to D2 (* P = 0.004). Two-way ANOVA, Holm-Sidak’s post hoc . B Examples of optic nerve cross sections with no or early (noe) and severe (sev) glaucomatous damage from D2 and D2. Ddit3/Jun −/− mice and percentages of optic nerves with noe ( n = 23, 16), moderate (mod; n = 3, 11) and sev ( n = 31, 27) glaucomatous damage. Ddit3/Jun deletion did not afford protection to RGC axons and in fact slightly worsened axonal degeneration (* P = 0.049). Chi square test. C Representative retinal flat mounts immunoassayed for RBPMS and quantification of RBPMS+ cells from 12 M D2 and D2. Ddit3/Jun −/− retinas with corresponding noe ( n = 6, 6) or sev ( n = 6, 6) optic nerves. Sev D2. Ddit3/Jun −/− retinas had 77.0 ± 3.1% improved RGC survival compared to D2 controls (* P < 0.001). RBPMS+ cells/mm 2 ± SEM for D2 and D2. Ddit3/Jun −/− respectively: Noe: 2899.6 ± 111.0, 2765.4 ± 49.8; Sev: 226.7 ± 20.8, 2151.5 ± 83.0. Two-way ANOVA, Holm-Sidak post-hoc . Scale bars, 50 μm.

Journal: Cell Death Discovery

Article Title: MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury

doi: 10.1038/s41420-025-02842-w

Figure Lengend Snippet: A Longitudinal intraocular pressure (IOP) measurements from D2 and D2. Ddit3/Jun −/− eyes ( n listed respectively here and throughout figure legends) at 5 M ( n = 60, 63), 9 M ( n = 60, 63), 10.5 M ( n = 66, 63), and 12 M ( n = 62, 61). Both genotype groups had significantly elevated IOPs at 9 M, 10.5 M, and 12 M compared to 5 M (* P < 0.001). At these timepoints, D2. Ddit3/Jun −/− eyes did not have a statistically significant reduction in IOP compared to WT, although D2. Ddit3/Jun −/− eyes had slightly higher IOPs at 9 M of age compared to D2 (* P = 0.004). Two-way ANOVA, Holm-Sidak’s post hoc . B Examples of optic nerve cross sections with no or early (noe) and severe (sev) glaucomatous damage from D2 and D2. Ddit3/Jun −/− mice and percentages of optic nerves with noe ( n = 23, 16), moderate (mod; n = 3, 11) and sev ( n = 31, 27) glaucomatous damage. Ddit3/Jun deletion did not afford protection to RGC axons and in fact slightly worsened axonal degeneration (* P = 0.049). Chi square test. C Representative retinal flat mounts immunoassayed for RBPMS and quantification of RBPMS+ cells from 12 M D2 and D2. Ddit3/Jun −/− retinas with corresponding noe ( n = 6, 6) or sev ( n = 6, 6) optic nerves. Sev D2. Ddit3/Jun −/− retinas had 77.0 ± 3.1% improved RGC survival compared to D2 controls (* P < 0.001). RBPMS+ cells/mm 2 ± SEM for D2 and D2. Ddit3/Jun −/− respectively: Noe: 2899.6 ± 111.0, 2765.4 ± 49.8; Sev: 226.7 ± 20.8, 2151.5 ± 83.0. Two-way ANOVA, Holm-Sidak post-hoc . Scale bars, 50 μm.

Article Snippet: Ddit3 null alleles [ ] (Jackson Laboratory, Stock# 005530), floxed alleles of Jun [ ] ( Jun fl ), and the Six3-cre transgene [ ] (Jackson Laboratory, Stock# 019755) were backcrossed >10 times to both the C57BL/6 J genetic background (>99% C57BL/6J) and the DBA/2J background (>99% DBA/2J).

Techniques:

A Representative pattern electroretinography (PERG) traces and amplitude quantification ( B ) from D2. Gpnmb + , D2, D2. Ddit3 −/− , D2. Jun −/− , and D2. Ddit3/Jun −/− mice at 5 M ( n = 20, 34, 38, 34, 39), 9 M ( n = 22, 34, 38, 39, 36), and 12 M ( n = 21, 34, 36, 35, 35). Normotensive D2. Gpnmb + mice did not have significant decline in PERG amplitude at 9 M ( P = 0.220), but had a slight but significant decline in PERG amplitude by 12 M compared to 5 M (* P = 0.001), Ocular hypertensive mice of all genotype groups had significant PERG amplitude decline at 9 M and 12 M compared to 5 M (* P < 0.001). At 9 M and 12 M, each ocular hypertensive group’s PERG amplitude was significantly lower than normotensive D2, Gpnmb + controls (* P < 0.001). No increase in PERG amplitude was observed between D2 and D2. Ddit3 −/− , D2. Jun −/− , or D2. Ddit3/Jun −/− groups at any timepoint measured. Scale bar: Y: 5 μV, X: 100 ms. Mixed effects analysis, Holm-Sidak’s post hoc . C Quantification of full-field ERG a-wave and b-wave ( D ) amplitudes in D2. Gpnmb + , D2, D2. Ddit3 −/− , D2. Jun −/− , and D2. Ddit3/Jun −/− eyes. By 12 M ( n = 21, 36, 35, 33, 37), each ocular hypertensive group had a slight but significant decline of electroretinography (ERG) a and b-wave amplitudes compared to 5 M ( n = 20, 38, 30, 34, 30) (* P < 0.001), but not nearly to the same extent as PERG amplitude decline ( A ). Two-way ANOVA, Holm-Sidak’s post hoc . Percentage of PERG and ERG amplitude declines at 9 and 12 M are listed for each group in Table . E PERG amplitude quantifications from 12 M D2 and D2. Ddit3/Jun -/- retinas with noe ( n = 6, 7) and sev ( n = 8, 17) optic nerve damage. Neither genotype nor optic nerve damage level influenced PERG amplitude ( P > 0.05, Two-way ANOVA). Of note, PERG amplitudes were significantly reduced compared with 12 M D2. Gpnmb + ( n = 21, 7.2 ± 0.6) regardless of genotype or level of axonal damage (* P < 0.001, One-way ANOVA, Holm-Sidak’s post hoc ). PERG amplitude (μV) ± SEM from D2 and D2. Ddit3/Jun −/− retinas, respectively: noe: 2.0 ± 0.4, 1.8 ± 0.2; sev: 2.3 ± 0.3; 1.9 ± 0.2. Scale bar: Y: 5 μV, X: 100 ms. F High-resolution images of retinal flat mounts immunoassayed for RBPMS (scale bar, 50μm) and quantification of average RGC soma size from D2 and D2. Ddit3/Jun −/− retinas with noe ( n = 7, 5) and sev ( n = 6, 6) glaucomatous damage. Both genotype groups had significant reductions in RGC soma size in sev glaucoma compared to respective noe controls (* P < 0.001). While D2. Ddit3/Jun −/− noe retinas had slightly smaller RGCs (* P = 0.044), Ddit3/Jun deletion did not attenuate RGC soma shrinkage in sev retinas. Soma size (μm 2 ) ± SEM from D2 and D2. Ddit3/Jun −/− retinas, respectively: noe: 143.1 ± 3.9, 131.7 ± 2.9; sev: 87.6 ± 2.5, 78.3 ± 3.0. Two-way ANOVA, Holm-Sidak’s post hoc .

Journal: Cell Death Discovery

Article Title: MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury

doi: 10.1038/s41420-025-02842-w

Figure Lengend Snippet: A Representative pattern electroretinography (PERG) traces and amplitude quantification ( B ) from D2. Gpnmb + , D2, D2. Ddit3 −/− , D2. Jun −/− , and D2. Ddit3/Jun −/− mice at 5 M ( n = 20, 34, 38, 34, 39), 9 M ( n = 22, 34, 38, 39, 36), and 12 M ( n = 21, 34, 36, 35, 35). Normotensive D2. Gpnmb + mice did not have significant decline in PERG amplitude at 9 M ( P = 0.220), but had a slight but significant decline in PERG amplitude by 12 M compared to 5 M (* P = 0.001), Ocular hypertensive mice of all genotype groups had significant PERG amplitude decline at 9 M and 12 M compared to 5 M (* P < 0.001). At 9 M and 12 M, each ocular hypertensive group’s PERG amplitude was significantly lower than normotensive D2, Gpnmb + controls (* P < 0.001). No increase in PERG amplitude was observed between D2 and D2. Ddit3 −/− , D2. Jun −/− , or D2. Ddit3/Jun −/− groups at any timepoint measured. Scale bar: Y: 5 μV, X: 100 ms. Mixed effects analysis, Holm-Sidak’s post hoc . C Quantification of full-field ERG a-wave and b-wave ( D ) amplitudes in D2. Gpnmb + , D2, D2. Ddit3 −/− , D2. Jun −/− , and D2. Ddit3/Jun −/− eyes. By 12 M ( n = 21, 36, 35, 33, 37), each ocular hypertensive group had a slight but significant decline of electroretinography (ERG) a and b-wave amplitudes compared to 5 M ( n = 20, 38, 30, 34, 30) (* P < 0.001), but not nearly to the same extent as PERG amplitude decline ( A ). Two-way ANOVA, Holm-Sidak’s post hoc . Percentage of PERG and ERG amplitude declines at 9 and 12 M are listed for each group in Table . E PERG amplitude quantifications from 12 M D2 and D2. Ddit3/Jun -/- retinas with noe ( n = 6, 7) and sev ( n = 8, 17) optic nerve damage. Neither genotype nor optic nerve damage level influenced PERG amplitude ( P > 0.05, Two-way ANOVA). Of note, PERG amplitudes were significantly reduced compared with 12 M D2. Gpnmb + ( n = 21, 7.2 ± 0.6) regardless of genotype or level of axonal damage (* P < 0.001, One-way ANOVA, Holm-Sidak’s post hoc ). PERG amplitude (μV) ± SEM from D2 and D2. Ddit3/Jun −/− retinas, respectively: noe: 2.0 ± 0.4, 1.8 ± 0.2; sev: 2.3 ± 0.3; 1.9 ± 0.2. Scale bar: Y: 5 μV, X: 100 ms. F High-resolution images of retinal flat mounts immunoassayed for RBPMS (scale bar, 50μm) and quantification of average RGC soma size from D2 and D2. Ddit3/Jun −/− retinas with noe ( n = 7, 5) and sev ( n = 6, 6) glaucomatous damage. Both genotype groups had significant reductions in RGC soma size in sev glaucoma compared to respective noe controls (* P < 0.001). While D2. Ddit3/Jun −/− noe retinas had slightly smaller RGCs (* P = 0.044), Ddit3/Jun deletion did not attenuate RGC soma shrinkage in sev retinas. Soma size (μm 2 ) ± SEM from D2 and D2. Ddit3/Jun −/− retinas, respectively: noe: 143.1 ± 3.9, 131.7 ± 2.9; sev: 87.6 ± 2.5, 78.3 ± 3.0. Two-way ANOVA, Holm-Sidak’s post hoc .

Techniques:

A Representative sections and quantification of IPL length from B6, B6. Ddit3/Jun −/− , and B6. Mkk4/7 −/− retinas 35 days post-Sham ( n = 6, 5, 7) or CONC ( n = 6, 5, 8) procedures. B6 IPL length significantly decreased 35 days post-CONC (by 22.7 ± 11%, * P = 0.030), while B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− IPL lengths did not significantly change after CONC ( P = 0.883 and P = 0.925, respectively). B6. Mkk4/7 −/− IPLs were significantly longer than B6 IPLs post-CONC (* P = 0.020). Note, in this experiment, Jun fl alleles were recombined from the retina using bilateral intravitreal delivery of AAV2.2-CMV-Cre-GFP. IPL length (µm) ± SEM for B6, B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− mice, respectively: Sham: 50.1 ± 3.6, 51.8 ± 4.3, 52.8 ± 2.8; CONC: 38.7 ± 5.5, 51.0 ± 2.7, 52.4 ± 1.7. Two-way ANOVA, Holm-Sidak’s post hoc . Scale bar, 50 μm. B Representative PERG traces and quantification of PERG amplitudes from B6, B6. Ddit3/Jun −/− , and B6. Mkk4/7 −/− retinas 14 days post- Sham ( n = 33, 17, 20) or CONC ( n = 35, 17, 20) procedures. B6 and B6. Ddit3/Jun −/− PERG amplitudes significantly declined 14 days post-CONC (by 52.6 ± 5.7%, * P < 0.001 and 57.9 ± 7.9%, * P = 0.002, respectively), while B6. Mkk4/7 −/− PERG amplitudes did not significantly decline ( P = 0.108). Two-way ANOVA, Holm-Sidak’s post-hoc . Scale bar: Y: 5 μV, X: 100 ms. C Representative high-resolution images of retinal flat mounts immunoassayed for RBPMS and quantification of RGC soma size from B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− retinas 14 days post-Sham ( n = 8, 9) or CONC ( n = 7, 9) procedures. After CONC, B6. Ddit3/Jun −/− RGC somas were reduced to 65.5 ± 4.6% (* P < 0.001) the size of respective RGCs after Sham procedures. B6. Mkk4/7 −/− RGC soma sizes did not change after CONC compared to Sham ( P = 0.439). B6. Mkk4/7 −/− RGCs were significantly larger compared to B6. Ddit3/Jun −/− (* P < 0.001) RGCs after CONC. Soma size (μm 2 ) ± SEM from B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− mice, respectively: Sham: 137.0 ± 7.3, 155.8 ± 3.2; CONC: 89.7 ± 6.3, 147.5 ± 7.8. Two-way ANOVA, Holm-Sidak’s post hoc . Scale bar, 50 μm.

Journal: Cell Death Discovery

Article Title: MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury

doi: 10.1038/s41420-025-02842-w

Figure Lengend Snippet: A Representative sections and quantification of IPL length from B6, B6. Ddit3/Jun −/− , and B6. Mkk4/7 −/− retinas 35 days post-Sham ( n = 6, 5, 7) or CONC ( n = 6, 5, 8) procedures. B6 IPL length significantly decreased 35 days post-CONC (by 22.7 ± 11%, * P = 0.030), while B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− IPL lengths did not significantly change after CONC ( P = 0.883 and P = 0.925, respectively). B6. Mkk4/7 −/− IPLs were significantly longer than B6 IPLs post-CONC (* P = 0.020). Note, in this experiment, Jun fl alleles were recombined from the retina using bilateral intravitreal delivery of AAV2.2-CMV-Cre-GFP. IPL length (µm) ± SEM for B6, B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− mice, respectively: Sham: 50.1 ± 3.6, 51.8 ± 4.3, 52.8 ± 2.8; CONC: 38.7 ± 5.5, 51.0 ± 2.7, 52.4 ± 1.7. Two-way ANOVA, Holm-Sidak’s post hoc . Scale bar, 50 μm. B Representative PERG traces and quantification of PERG amplitudes from B6, B6. Ddit3/Jun −/− , and B6. Mkk4/7 −/− retinas 14 days post- Sham ( n = 33, 17, 20) or CONC ( n = 35, 17, 20) procedures. B6 and B6. Ddit3/Jun −/− PERG amplitudes significantly declined 14 days post-CONC (by 52.6 ± 5.7%, * P < 0.001 and 57.9 ± 7.9%, * P = 0.002, respectively), while B6. Mkk4/7 −/− PERG amplitudes did not significantly decline ( P = 0.108). Two-way ANOVA, Holm-Sidak’s post-hoc . Scale bar: Y: 5 μV, X: 100 ms. C Representative high-resolution images of retinal flat mounts immunoassayed for RBPMS and quantification of RGC soma size from B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− retinas 14 days post-Sham ( n = 8, 9) or CONC ( n = 7, 9) procedures. After CONC, B6. Ddit3/Jun −/− RGC somas were reduced to 65.5 ± 4.6% (* P < 0.001) the size of respective RGCs after Sham procedures. B6. Mkk4/7 −/− RGC soma sizes did not change after CONC compared to Sham ( P = 0.439). B6. Mkk4/7 −/− RGCs were significantly larger compared to B6. Ddit3/Jun −/− (* P < 0.001) RGCs after CONC. Soma size (μm 2 ) ± SEM from B6. Ddit3/Jun −/− and B6. Mkk4/7 −/− mice, respectively: Sham: 137.0 ± 7.3, 155.8 ± 3.2; CONC: 89.7 ± 6.3, 147.5 ± 7.8. Two-way ANOVA, Holm-Sidak’s post hoc . Scale bar, 50 μm.

Techniques:

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