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. 2014 Aug 21;3:e02236. doi: 10.7554/eLife.02236

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Copyright © 2014, Xiong et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 7. — (A) Deletion of Trp53 rescues postnatal death by Rps27l disruption. Lower than expected number of mice with Trp53^−/− genotype (regardless of Rps27l genotype) is due to high frequency of developmental abnormalities during embryonic and neonatal stages which cause the premature death (Armstrong et al., 1995; Sah et al., 1995). (B–D) Deletion of Trp53 rescues growth retardation and organ hypocellularity. Representative mice at P18 of three genotypes were photographed (B). The bodies (C) were weighed; and the total cell numbers (D) of bone marrow (femur and tibia from two hind limbs), spleen, and thymus were counted from P18 mice with genotypes of Rps27l^+/+;Trp53^+/+ (n = 3), Rps27l^−/−;Trp53^+/+ (n = 7), Rps27l^−/−-;Trp53^+/− (n = 10), Rps27l^−/−;Trp53^−/− (n = 5). Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001. (E) Representative H&E staining of bone marrows in femurs from P18 mice. Scale bars represent 200 µm (top) or 40 µm (bottom). (F and G) Deletion of Trp53 rescues HSPCs depletion in Rps27l^−/− bone marrow. The percentage of LSK, MPP, ST-HSC, and LT-HSC (F); and the percentage of MP, CMP, GMP, and MEP (G) in bone marrow from P18 mice with genotypes of Rps27l^+/+;Trp53^+/+ (n = 4), Rps27l^−/−;Trp53^+/+ (n = 5), Rps27l^−/−;Trp53^+/− (n = 7), and Rps27l^−/−;Trp53^−/− (n = 5). LSK: Lin⁻/Sca-1⁻/c-Kit⁺; MPP: Lin⁻/Sca-1⁻/c-Kit⁺/CD48⁺/CD150⁻; ST-HSC: Lin⁻/Sca-1⁻/c-Kit⁺/CD48⁺/CD150⁺; LT-HSC: Lin⁻/Sca-1⁻/c-Kit⁺/CD48⁻/CD150⁺. Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001. (H) Deletion of Trp53 rescues defects in Rps27l^−/− peripheral blood. CBC classification of peripheral blood from Rps27l^+/+;Trp53^+/+ (n = 3), Rps27l^−/−;Trp53^+/+ (n = 7), Rps27l^−/−;Trp53^+/− (n = 10), Rps27l^−/−;Trp53^−/− (n = 5) mice at P18 was performed. WBC, white blood cells; NE, neutrophils; LY, lymphocytes; MO, monocytes; HCT, hematocrit; RBC, red blood cells; Hb, hemoglobin; PLT, platelets. Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001. (I and J) Deletion of Trp53 rescues HSPCs depletion in Rps27l^−/− fetal livers. Flow cytometry analysis was performed to measure the percentage of HSPCs including LSK (I), MP, CMP, GMP, and MEP (J) in E14.5 fetal livers with genotypes of Rps27l^−/−;Trp53^+/+ (n = 5), Rps27l^−/−;Trp53^+/− (n = 7), and Rps27l^−/−;Trp53^−/− (n = 6). Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001, as compared to Rps27l^−/−;Trp53^+/+. (K) Kaplan–Meier survival curves of recipient mice after transplantation. Fetal liver cells (2 × 10⁶ cells) from E14.5 embryos with indicated genotypes were respectively injected into lethally irradiated recipient mice (n = 7 for each genotype). p < 0.0001.

DOI: http://dx.doi.org/10.7554/eLife.02236.015

Figure 7—figure supplement 1. — (A) Deletion of Trp53 rescues postnatal death by Rps27l disruption. Lower than expected number of mice with Trp53^−/− genotype (regardless of Rps27l genotype) is due to high frequency of developmental abnormalities during embryonic and neonatal stages which cause the premature death (Armstrong et al., 1995; Sah et al., 1995). (B–D) Deletion of Trp53 rescues growth retardation and organ hypocellularity. Representative mice at P18 of three genotypes were photographed (B). The bodies (C) were weighed; and the total cell numbers (D) of bone marrow (femur and tibia from two hind limbs), spleen, and thymus were counted from P18 mice with genotypes of Rps27l^+/+;Trp53^+/+ (n = 3), Rps27l^−/−;Trp53^+/+ (n = 7), Rps27l^−/−-;Trp53^+/− (n = 10), Rps27l^−/−;Trp53^−/− (n = 5). Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001. (E) Representative H&E staining of bone marrows in femurs from P18 mice. Scale bars represent 200 µm (top) or 40 µm (bottom). (F and G) Deletion of Trp53 rescues HSPCs depletion in Rps27l^−/− bone marrow. The percentage of LSK, MPP, ST-HSC, and LT-HSC (F); and the percentage of MP, CMP, GMP, and MEP (G) in bone marrow from P18 mice with genotypes of Rps27l^+/+;Trp53^+/+ (n = 4), Rps27l^−/−;Trp53^+/+ (n = 5), Rps27l^−/−;Trp53^+/− (n = 7), and Rps27l^−/−;Trp53^−/− (n = 5). LSK: Lin⁻/Sca-1⁻/c-Kit⁺; MPP: Lin⁻/Sca-1⁻/c-Kit⁺/CD48⁺/CD150⁻; ST-HSC: Lin⁻/Sca-1⁻/c-Kit⁺/CD48⁺/CD150⁺; LT-HSC: Lin⁻/Sca-1⁻/c-Kit⁺/CD48⁻/CD150⁺. Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001. (H) Deletion of Trp53 rescues defects in Rps27l^−/− peripheral blood. CBC classification of peripheral blood from Rps27l^+/+;Trp53^+/+ (n = 3), Rps27l^−/−;Trp53^+/+ (n = 7), Rps27l^−/−;Trp53^+/− (n = 10), Rps27l^−/−;Trp53^−/− (n = 5) mice at P18 was performed. WBC, white blood cells; NE, neutrophils; LY, lymphocytes; MO, monocytes; HCT, hematocrit; RBC, red blood cells; Hb, hemoglobin; PLT, platelets. Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001. (I and J) Deletion of Trp53 rescues HSPCs depletion in Rps27l^−/− fetal livers. Flow cytometry analysis was performed to measure the percentage of HSPCs including LSK (I), MP, CMP, GMP, and MEP (J) in E14.5 fetal livers with genotypes of Rps27l^−/−;Trp53^+/+ (n = 5), Rps27l^−/−;Trp53^+/− (n = 7), and Rps27l^−/−;Trp53^−/− (n = 6). Shown are mean ± SD. *p < 0.05, **p < 0.01, and ***p < 0.001, as compared to Rps27l^−/−;Trp53^+/+. (K) Kaplan–Meier survival curves of recipient mice after transplantation. Fetal liver cells (2 × 10⁶ cells) from E14.5 embryos with indicated genotypes were respectively injected into lethally irradiated recipient mice (n = 7 for each genotype). p < 0.0001.

DOI: http://dx.doi.org/10.7554/eLife.02236.015