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. 2022 Jan 13;41(4):e106825. doi: 10.15252/embj.2020106825

Figure 1. Rb∆K4 knock‐in mice develop normally but exhibit telomere attrition.

Figure 1

  1. Schematic structure of pRb, location of the 14 CDK sites, and the four Ser/Thr‐to‐Ala substitutions (denoted by *) in Rb∆K4 knock‐in mice in exon 23. Clustering of phosphorylation sites is as per Sanidas et al (2019), based on protein interaction profiles of monophosphorylated pRb species. N, N terminus; A‐B, pocket domain; L, spacer/linker; C, C terminus which includes exon 23.
  2. Western blot analysis of Rb∆K4 thymocytes with an antibody that recognizes both hyper‐phosphorylated (ppRb) and hypo‐phosphorylated pRb species.
  3. Representative flow cytometric profiles of thymocytes from 6‐week‐old Rb∆K4 and control mice for CD3‐, CD4‐ and CD8‐positive cell populations. Bottom, average of CD3, CD4, and CD8 single‐ and double‐positive cells in Rb∆K4 vs. control thymocytes showing no significant (n.s.) difference by Student’s t‐test. Bars represent mean ± SD (standard deviation); n = 6 biological replicates.
  4. Short telomeres in Rb∆K4 mice. Images of splenocyte metaphase spreads hybridized with the telomere repeat probe (pink). Note shorter telomeres in Rb∆K4 splenocytes (arrows). Bottom, quantitative analysis of 10 splenocyte metaphases from one pair of Rb∆K4 and control littermate; all five pairs are shown in Appendix Fig S2 (P < 0.001 by two‐tailed Mann–Whitney–Wilcoxon test).

Source data are available online for this figure.