Fig. 2: LCM regulate HSC quiescence.

a Gating strategy for BM progenitors (LSK, Lin^-Sca-1⁺c-Kit⁺, representative plot). b Frequency of LSK in endosteal (e) and central (c) MK-LCM^WT/WT and MK-LCM^Δ/Δ BM. c Absolute number of LSK in the eBM and cBM regions within a single hind limb. d Gating strategy for HSC: gating continued from a (Lin^-Sca-1⁺c-Kit⁺CD150⁺CD48^-, representative plot). e Frequency of MK-LCM^WT/WT and MK-LCM^Δ/Δ HSC in eBM and cBM. f Absolute number of HSC in eBM and cBM regions from one hind limb. b, e (eLCM^WT/WT n = 22, eMK-LCM^Δ/Δ n = 28, cLCM^WT/WT n = 16, cMK-LCM^Δ/Δ n = 20, biological replicates, from ≥5 independent experiments), c, f (eLCM^WT/WT n = 26, eMK-LCM^Δ/Δ n = 36, cLCM^WT/WT n = 20, cMK-LCM^Δ/Δ n = 28, biological replicates, from ≥5 independent experiments). g Absolute number of HSC in MK-LCM^WT/WT and MK-LCM^Δ/Δ PB (LCM^WT/WT n = 6, MK-LCM^Δ/Δ n = 9, biological replicates, from ≥3 independent experiments). h Number of HSC in MK-LCM^WT/WT and MK-LCM^Δ/Δ spleen (LCM^WT/WT n = 11, MK-LCM^Δ/Δ n = 26, biological replicates, from ≥4 independent experiments). i Frequency of VWF⁺CD41⁺ HSC in the BM of MK-LCM^WT/WT and MK-LCM^Δ/Δ mice (n = 4, biological replicates, from an experiment). j TPO concentration within the cBM fluid of MK-LCM^WT/WT and MK-LCM^Δ/Δ mice determined by ELISA (LCM^WT/WT n = 6, MK-LCM^Δ/Δ n = 5, biological replicates, from 2 independent experiments). k PF4 concentration within the cBM fluid of MK-LCM^WT/WT and MK-LCM^Δ/Δ mice as determined by ELISA (LCM^WT/WT n = 4, MK-LCM^Δ/Δ n = 4, biological replicates from 2 independent experiments). l ELISA data: TGFβ1 concentration within the cBM fluid of MK-LCM^WT/WT and MK-LCM^Δ/Δ mice (LCM^WT/WT n = 8, MK-LCM^Δ/Δ n = 8, biological replicates, from 2 independent experiments). m ELISA data: The concentration of tcOPN within MK-LCM^WT/WT and MK-LCM^Δ/Δ eBM lysates (LCM^WT/WT n = 6, MK-LCM^Δ/Δ n = 6, biological replicates, from 2 independent experiments). n Expression of α₄ integrin on MK-LCM^WT/WT and MK-LCM^Δ/Δ e and c hematopoietic stem and progenitors. o Expression of α₉ integrin on MK-LCM^WT/WT and MK-LCM^Δ/Δ e and c hematopoietic stem and progenitors. p Ability of MK-LCM^WT/WT and MK-LCM^Δ/Δ e and c hematopoietic stem and progenitors to bind R-BC154 (rB) and the ability of BOP (B) to outcomplete rB. q The contribution of α₉ to rB binding on MK-LCM^WT/WT and MK-LCM^Δ/Δ e and c hematopoietic stem and progenitors, calculated based on rB binding, rB binding in the presence of the selective and potent α₄β₁ antagonist BIO5192 (Bio) and rB binding in the presence of B. n–q LCM^WT/WT n = 4, MK-LCM^Δ/Δ n = 4, biological replicates, from one experiment. r Degree of endogenous integrin activation on MK-LCM^WT/WT and MK-LCM^Δ/Δ e and c hematopoietic stem and progenitors (LCM^WT/WT n = 4, MK-LCM^Δ/Δ n = 3, biological replicates, from one experiment). s Expression of CXCR-4 on MK-LCM^WT/WT and MK-LCM^Δ/Δ e and c hematopoietic stem and progenitors (LCM^WT/WT n = 4, MK-LCM^Δ/Δ n = 4, biological replicates, from one experiment). Percentages shown in flow plots are current gate as a percentage of the parent. Statistical analysis used unpaired two-sided Student’s t-test, p values indicated for (b, e, g, i–q, s), two-sided Mann–Whitney test (c, f, h), Kruskal–Wallis test, p = 0.003 (overall) with individual groups compared using Dunn’s multiple comparisons test, p values indicated for (r). Source data are provided as a Source Data File. Error bars = SEM.