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. 2021 Nov 12;7(46):eabk0271. doi: 10.1126/sciadv.abk0271

Fig. 1. Cellular enlargement contributes to DNA damage–induced fitness decline in HSCs.

Fig. 1.

(A) Mean volume (fl) of HSCs obtained from vehicle (n = 6), sublethally irradiated (3 Gy, n = 4), G0/1 2.8 to 3 Gy (n = 11), rapamycin-treated (RAP, n = 4), and RAP + 3 Gy–treated (n = 7) mice 2 weeks after irradiation (∆ = difference). (B) Measurement of DNA damage using CometChip: percentage tail DNA of HSCs (%) isolated from mice 2 weeks after treatment with vehicle, 3 Gy, RAP, or 3 Gy + RAP (n ≥ 166). (C) Reconstitution assay: Donor (CD45.2) mice were pretreated with RAP or vehicle for 2 weeks, sublethally irradiated (3 Gy), and treated with RAP (n; donors = 12, recipients = 8) or vehicle (n; donors = 12, recipients = 15) for another 2 weeks before 1000 CD45.2 HSCs were isolated and transplanted into lethally irradiated recipient mice. Control donor HSCs were not treated (control, n; donors = 6, recipients = 9) or treated with RAP without irradiation (control, n; donors = 3, recipients = 5). Recipient mice were not treated with RAP after reconstitution. Percentage of donor-derived white blood cells in recipients and slope of reconstitution kinetics over time were determined.