Aberrant phase transition of FUS impairs HSCs. (A) This schematic diagram shows the components of each FUS variants, including FUS^ΔRGG123, FLL2^PLD-FUS^ΔRGG123, and ELF3^PLD-FUS^ΔRGG123. (B-C) Freshly isolated 10⁵ LSK cells from 2-month-old young WT mice were infected by lentivirus carrying FUS^FL, FUS^ΔRGG123, FLL2^PLD-FUS^ΔRGG123, ELF3^PLD-FUS^ΔRGG123, and 3 days later, GFP⁺ cells were purified and treated with 0.5 mM ARS. (B) These representative images show the FUS condensates in the nucleoplasm of indicated groups upon 0.5 mM ARS treatment for 4 hours, Scale bar represents 5 μm. (C) Representative FRAP images show the fluorescence recovery of FUS condensates in the nucleoplasm of the indicated groups in response to 0.5 mM ARS treatment for 4 hours. Scale bar represents 1 μm. (D) The line plot shows the recovery rate of FUS condensates in panel C at indicated time points. N = 9-32 condensates per group. (E) The histograms depict the mobile fraction and T-half of FRAP assay of panel C. Data are shown as mean ± SEM. (F-G) These line plots depict the percentage of donor-derived cells (overall, B cell, T cell, myeloid cell) in the peripheral blood of the recipients at the indicated time points. Freshly isolated 10⁵ LSK cells from 2-month-old young WT mice were infected by lentivirus carrying FUS and indicated FUS variants. Three days later, 2000 GFP⁺Sca-1⁺CD48^– cells were purified and transplanted into lethally irradiated recipients (CD45.2) together with 3.5 × 10⁵ competitor cells (CD45.1). Chimera in peripheral blood was evaluated every 4 weeks until the 16th week. N = 5-6 (F) and N = 6-9 (G) recipients per group, data are shown as mean ± SEM.