Figure 7. Exit from the cell cycle... | Rockefeller University Press

Figure 7.

$Figure 7. Exit from the cell cycle induces centrosome composition changes. (A) Quantification of centrosomal levels of indicated proteins after serum starvation or Purvalanol A treatment (n ≥ 96 centrosomes from two independent experiments). (B) Western blots of γ-tubulin levels in cytoplasmic and centrosomal fractions from control, serum-starved, or Purvalanol A–treated cells. (C) Western blot of total levels of Nedd1 in control, serum-starved, or Purvalanol A–treated cells. (D) Backskin cryosections from postnatal day 1 K14rtTA TRE-Cdkn1b mice and littermate controls, stained for the proliferation marker Ki67. Dashed line marks the basement membrane. Note the loss of Ki67+ cells is specific to the epidermis. (E) Quantification of the percentage of Ki67+ basal cells in control and K14rtTA TRE-Cdkn1b mice (n = 3 mice of each genotype from two independent litters). (F) Immunofluorescence of γ-tubulin in backskins from control and K14rtTA TRE-Cdkn1b mice. (G) Quantification of the ratio of the fluorescence intensity of γ-tubulin on basal cell centrosomes to dermal centrosomes (n = 3 mice of each genotype from two independent litters). (H) Immunofluorescence of Nedd1 in backskins from control and K14rtTA TRE-Cdkn1b mice. (I) Quantification of the ratio of the fluorescence intensity of Nedd1 on basal cell centrosomes to dermal centrosomes (n = 3 mice each genotype from two independent litters). (J) Diagram of the effects of different levels of Cdk1 activity on centrosome morphology and function. Bars, 10 µm. n.s., not significant; ***, P < 0.001. Data are presented as mean ± SEM.$

Exit from the cell cycle induces centrosome composition changes. (A) Quantification of centrosomal levels of indicated proteins after serum starvation or Purvalanol A treatment (n ≥ 96 centrosomes from two independent experiments). (B) Western blots of γ-tubulin levels in cytoplasmic and centrosomal fractions from control, serum-starved, or Purvalanol A–treated cells. (C) Western blot of total levels of Nedd1 in control, serum-starved, or Purvalanol A–treated cells. (D) Backskin cryosections from postnatal day 1 K14rtTA TRE-Cdkn1b mice and littermate controls, stained for the proliferation marker Ki67. Dashed line marks the basement membrane. Note the loss of Ki67⁺ cells is specific to the epidermis. (E) Quantification of the percentage of Ki67⁺ basal cells in control and K14rtTA TRE-Cdkn1b mice (n = 3 mice of each genotype from two independent litters). (F) Immunofluorescence of γ-tubulin in backskins from control and K14rtTA TRE-Cdkn1b mice. (G) Quantification of the ratio of the fluorescence intensity of γ-tubulin on basal cell centrosomes to dermal centrosomes (n = 3 mice of each genotype from two independent litters). (H) Immunofluorescence of Nedd1 in backskins from control and K14rtTA TRE-Cdkn1b mice. (I) Quantification of the ratio of the fluorescence intensity of Nedd1 on basal cell centrosomes to dermal centrosomes (n = 3 mice each genotype from two independent litters). (J) Diagram of the effects of different levels of Cdk1 activity on centrosome morphology and function. Bars, 10 µm. n.s., not significant; ***, P < 0.001. Data are presented as mean ± SEM.