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Critical Modulation of Hematopoietic Lineage Fate by Hepatic Leukemia Factor

Wahlestedt, Martin, Ladopoulos, Vasileios, Hidalgo, Isabel, Sanchez Castillo, Manuel, Hannah, Rebecca, Säwén, Petter, Wan, Haixia, Dudenhöffer-Pfeifer, Monika, Magnusson, Mattias, Norddahl, Gudmundur L., Göttgens, Berthold, Bryder, David·2017·Cell Reports
DOI 10.1016/j.celrep.2017.10.112PMC PMC5714592
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Graphical abstract CC BY-NC-ND · PubMed Central
Figure 1 Identification of Hlf as a Candidate Regulator of Early Hematopoiesis (A) Schematic depiction of the progenitor subsets that underlie the early stages of hematopoiesis. (B) Heatmap showing the expression levels of TFs displaying 2-fold or higher expression in HSCs and GMLPs compared with downstream progenitor cell types (mean values of three replicate arrays per cell type, except for HSCs and pMegEs, for which six and five replicate arrays were used, respectively). See also Table S1. (C) Schematic depiction of the different lentiviral constructs used for OP9 stromal co-cultures. (D) The lineage output relative to controls of B cells, NK cells, and myeloid cells produced from Hlf/Hlf, Hlf/Dbp, Hlf/Tef, Hlf/Nfil3, Hlf, Nfil3, and M33-Hlf transduced GMLPs in OP9 stroma co-cultures (n = 6, 6, 6, 6, 6, 3, 6, and 45 cultures, respectively, from two independent experiments). (E) B, NK, and myeloid cell generation in OP9 co-culture experiments and T cell generation in OP9-DL1 co-cultures using Hlf-inducible GMLPs cultured in the absence or presence of DOX. Shown are representative FACS plots as well as bar graphs showing the frequency relative to untreated controls of CD19+ B cells, NK1.1+ NK cells, CD11b+ myeloid cells, and CD90+ T cells in the cultures from three independent experiments (n = 5 for the B, NK, and myeloid experiments, and n = 9 for the T cell experiments). Error bars denote SEM. CFU-erythroid, colony-forming unit-erythroid; MkP, megakaryocyte progenitor; pCFU-erythroid, pre-colony-forming unit-erythroid; pGM, pre-granulocyte-monocyte progenitor; pMeg/erythroid, pre-megakaryocyte-erythroid progenitor. See also Figures S1 and S2.
Figure 1 Identification of Hlf as a Candidate Regulator of Early Hematopoiesis (A) Schematic depiction of the progenitor subsets that underlie the early stages of hematopoiesis. (B) Heatmap showing the expression levels of TFs displaying 2-fold or higher expression in HSCs and GMLPs compared with downstream progenitor cell types (mean values of three replicate arrays per cell type, except for HSCs and pMegEs, for which six and five replicate arrays were used, respectively). See also Table S1. (C) Schematic depiction of the different lentiviral constructs used for OP9 stromal co-cultures. (D) The lineage output relative to controls of B cells, NK cells, and myeloid cells produced from Hlf/Hlf, Hlf/Dbp, Hlf/Tef, Hlf/Nfil3, Hlf, Nfil3, and M33-Hlf transduced GMLPs in OP9 stroma co-cultures (n = 6, 6, 6, 6, 6, 3, 6, and 45 cultures, respectively, from two independent experiments). (E) B, NK, and myeloid cell generation in OP9 co-culture experiments and T cell generation in OP9-DL1 co-cultures using Hlf-inducible GMLPs cultured in the absence or presence of DOX. Shown are representative FACS plots as well as bar graphs showing the frequency relative to untreated controls of CD19+ B cells, NK1.1+ NK cells, CD11b+ myeloid cells, and CD90+ T cells in the cultures from three independent experiments (n = 5 for the B, NK, and myeloid experiments, and n = 9 for the T cell experiments). Error bars denote SEM. CFU-erythroid, colony-forming unit-erythroid; MkP, megakaryocyte progenitor; pCFU-erythroid, pre-colony-forming unit-erythroid; pGM, pre-granulocyte-monocyte progenitor; pMeg/erythroid, pre-megakaryocyte-erythroid progenitor. See also Figures S1 and S2.CC BY-NC-ND · PubMed Central
Figure 2 Hlf Induction In Vivo Negatively Influences Lymphopoiesis at the Expense of Enhanced Myelopoiesis Hlf-inducible mice were given DOX via their food pellets for 0, 3, 7, 11, and 14 days (n = 7, 7, 7, 3, and 4 mice in each group, respectively, from two independent experiments) and 38 weeks (n = 5 mice, from one experiment). (A) Bar charts showing the amount of HSCs, GMLPs, pGMs, GMPs, all lymphoid progenitors (ALPs), and B cell-biased lymphoid progenitors (BLPs) in the BM of the analyzed mice (relative to uninduced mice). (B) Relative cell numbers of the analyzed B cell subsets in the BM and relative frequencies of the indicated splenic B cell fractions among all splenocytes in the analyzed mice (relative to uninduced mice). See also Figure S5. (C) Photographs depicting thymi after 0, 3, 7, 11, and 14 days of enforced Hlf expression (four thymi per time point, representative of one of three experiments). The scale bar represents 1 cm. (D) The amount of CD4+CD8+ double-positive, single-positive CD4+, single-positive CD8+ thymocytes, and DN1, DN2, and DN3 thymocytes following the different number of days of DOX administration (relative to uninduced mice). See also Table S1. Error bars denote SEM. ALP, all lymphoid progenitor; BM, bone marrow; BLP, B cell biased lymphoid progenitor; DN, double negative. See also Figures S3 and S4.
Figure 2 Hlf Induction In Vivo Negatively Influences Lymphopoiesis at the Expense of Enhanced Myelopoiesis Hlf-inducible mice were given DOX via their food pellets for 0, 3, 7, 11, and 14 days (n = 7, 7, 7, 3, and 4 mice in each group, respectively, from two independent experiments) and 38 weeks (n = 5 mice, from one experiment). (A) Bar charts showing the amount of HSCs, GMLPs, pGMs, GMPs, all lymphoid progenitors (ALPs), and B cell-biased lymphoid progenitors (BLPs) in the BM of the analyzed mice (relative to uninduced mice). (B) Relative cell numbers of the analyzed B cell subsets in the BM and relative frequencies of the indicated splenic B cell fractions among all splenocytes in the analyzed mice (relative to uninduced mice). See also Figure S5. (C) Photographs depicting thymi after 0, 3, 7, 11, and 14 days of enforced Hlf expression (four thymi per time point, representative of one of three experiments). The scale bar represents 1 cm. (D) The amount of CD4+CD8+ double-positive, single-positive CD4+, single-positive CD8+ thymocytes, and DN1, DN2, and DN3 thymocytes following the different number of days of DOX administration (relative to uninduced mice). See also Table S1. Error bars denote SEM. ALP, all lymphoid progenitor; BM, bone marrow; BLP, B cell biased lymphoid progenitor; DN, double negative. See also Figures S3 and S4.CC BY-NC-ND · PubMed Central
Figure 3 Cell-Autonomous Alterations Underlie the Altered Hematopoiesis Following Enforced Hlf Expression In Vivo Hlf-inducible GMLPs (CD45.1+) were transplanted into sublethally irradiated WT recipient hosts (CD45.2+) maintained on a DOX food diet (n = 6 and 7 mice for the control and DOX groups, respectively, from one of three experiments with similar results). (A) Magnitudes of myeloid B, and T cell reconstitution in the BM of the recipient mice. (B) FACS plots showing the appearance of CD45.1+c-Kit+IL7Ra+CD19+ cells in the BM of mice transplanted with Hlf-induced GMLPs. (C and D) Donor-derived reconstitution of myeloid, B, and T cells in the spleen (C) and the PB (D). (E) The thymi of recipient mice were assessed for donor-derived reconstitution of the indicated thymocyte subsets. Error bars denote SEM. See also Figure S5.
Figure 3 Cell-Autonomous Alterations Underlie the Altered Hematopoiesis Following Enforced Hlf Expression In Vivo Hlf-inducible GMLPs (CD45.1+) were transplanted into sublethally irradiated WT recipient hosts (CD45.2+) maintained on a DOX food diet (n = 6 and 7 mice for the control and DOX groups, respectively, from one of three experiments with similar results). (A) Magnitudes of myeloid B, and T cell reconstitution in the BM of the recipient mice. (B) FACS plots showing the appearance of CD45.1+c-Kit+IL7Ra+CD19+ cells in the BM of mice transplanted with Hlf-induced GMLPs. (C and D) Donor-derived reconstitution of myeloid, B, and T cells in the spleen (C) and the PB (D). (E) The thymi of recipient mice were assessed for donor-derived reconstitution of the indicated thymocyte subsets. Error bars denote SEM. See also Figure S5.CC BY-NC-ND · PubMed Central
Figure 4 Acute Hlf Depletion and Modulation of Hlf into a Transcriptional Repressor Lead to Enhanced Lymphopoiesis Hlf-inducible GMLPs (CD45.1+) were transplanted into sublethally irradiated WT recipients (CD45.2+) on DOX food. After 14 days, one group of mice was shifted to normal food and kept for another 8 days prior to analysis (“Hlf depleted”), while control mice were treated with DOX throughout the experiment (“Hlf induced,” n = 7 and 6 mice, respectively, from one experiment). (A) Data show the percentage of the indicated donor-derived cell types out of all CD45+ cells. (B and C) The impact of Hlf target gene silencing on differentiation was studied by culturing control or M33-Hlf retrovirus infected WT GMLPs in B/NK and T cell permissive conditions (n = 6 replicates per group from two experiments). Shown is the lineage output relative to controls of indicated subsets in OP9 cultures (B) and OP9-DL1 cultures (C), respectively. Error bars denote SEM.
Figure 4 Acute Hlf Depletion and Modulation of Hlf into a Transcriptional Repressor Lead to Enhanced Lymphopoiesis Hlf-inducible GMLPs (CD45.1+) were transplanted into sublethally irradiated WT recipients (CD45.2+) on DOX food. After 14 days, one group of mice was shifted to normal food and kept for another 8 days prior to analysis (“Hlf depleted”), while control mice were treated with DOX throughout the experiment (“Hlf induced,” n = 7 and 6 mice, respectively, from one experiment). (A) Data show the percentage of the indicated donor-derived cell types out of all CD45+ cells. (B and C) The impact of Hlf target gene silencing on differentiation was studied by culturing control or M33-Hlf retrovirus infected WT GMLPs in B/NK and T cell permissive conditions (n = 6 replicates per group from two experiments). Shown is the lineage output relative to controls of indicated subsets in OP9 cultures (B) and OP9-DL1 cultures (C), respectively. Error bars denote SEM.CC BY-NC-ND · PubMed Central
Figure 5 The Genome-wide Binding Characteristics of Hlf WT LSK cells were transduced with either a control retroviral vector or a vector encoding an N-terminal FLAG-tagged variant of Hlf/Hlf and were subjected to ChIP-seq analysis. (A) The Hlf peaks were ranked in a decreasing peak height order, and H3K27Ac signal intensity (Lara-Astiaso et al., 2014) was plotted around the summit of the Hlf peaks and is shown as heatmaps. The histograms at the top of each heatmap depict the average signal intensity around the Hlf peaks for each cell type. (B) Correlation analysis of the putative Hlf targets with those of other hematopoiesis associated TFs. (C) BM resident B cells were subjected to transdifferentiation experiments by transduction with retroviral vectors encoding Cebpb or Hlf and cultured for 4 days on OP9 stromal cells prior to FACS analysis (representative FACS plots from two independent experiments). ChIP, chromatin immunoprecipitation. See also Figure S6.
Figure 5 The Genome-wide Binding Characteristics of Hlf WT LSK cells were transduced with either a control retroviral vector or a vector encoding an N-terminal FLAG-tagged variant of Hlf/Hlf and were subjected to ChIP-seq analysis. (A) The Hlf peaks were ranked in a decreasing peak height order, and H3K27Ac signal intensity (Lara-Astiaso et al., 2014) was plotted around the summit of the Hlf peaks and is shown as heatmaps. The histograms at the top of each heatmap depict the average signal intensity around the Hlf peaks for each cell type. (B) Correlation analysis of the putative Hlf targets with those of other hematopoiesis associated TFs. (C) BM resident B cells were subjected to transdifferentiation experiments by transduction with retroviral vectors encoding Cebpb or Hlf and cultured for 4 days on OP9 stromal cells prior to FACS analysis (representative FACS plots from two independent experiments). ChIP, chromatin immunoprecipitation. See also Figure S6.CC BY-NC-ND · PubMed Central
Figure 6 Hlf Instructs GMLPs to Adopt a Myeloid Fate by Upregulation of a Myeloid-Associated Transcriptional Program and a Concomitant Downregulation of Lymphoid-Affiliated Genes (A) Single Hlf-inducible GMLPs were maintained on OP9 stromal cells for 14 days. The lineage potential of each seeded GMLP was determined using FACS, by scoring each well for the presence of B cells, NK cells, and myeloid cells. Shown is the distribution of the different colony types among the positive wells of the control and DOX treated groups. (B) Venn diagrams depicting the number of shared up- and downregulated genes following Hlf induction using the two complementary approaches (compared with controls). (C) Up- and downregulated genes, their fold changes compared with controls using both experimental strategies, and whether they were identified also using ChIP-seq. See also Table S2. (D) GSEA in which the commonly up- and downregulated genes were used as gene sets and correlated against the whole transcriptomes of pGMs and CLPs. Error bars denote SEM. GSEA, gene set enrichment analysis. See also Figure S7.
Figure 6 Hlf Instructs GMLPs to Adopt a Myeloid Fate by Upregulation of a Myeloid-Associated Transcriptional Program and a Concomitant Downregulation of Lymphoid-Affiliated Genes (A) Single Hlf-inducible GMLPs were maintained on OP9 stromal cells for 14 days. The lineage potential of each seeded GMLP was determined using FACS, by scoring each well for the presence of B cells, NK cells, and myeloid cells. Shown is the distribution of the different colony types among the positive wells of the control and DOX treated groups. (B) Venn diagrams depicting the number of shared up- and downregulated genes following Hlf induction using the two complementary approaches (compared with controls). (C) Up- and downregulated genes, their fold changes compared with controls using both experimental strategies, and whether they were identified also using ChIP-seq. See also Table S2. (D) GSEA in which the commonly up- and downregulated genes were used as gene sets and correlated against the whole transcriptomes of pGMs and CLPs. Error bars denote SEM. GSEA, gene set enrichment analysis. See also Figure S7.CC BY-NC-ND · PubMed Central
Figure 7 Identification of Nfic as a Direct Hlf Target with Pronounced Functional Effects on Hematopoietic Differentiation (A) UCSC Genome Browser track depicting the genomic context of Nfic with regard to accessible chromatin and histone modifications of indicated cell types (assay for transposase-accessible chromatin using sequencing [ATAC-seq] and histone modification data from Lara-Astiaso et al. (2014). The region occupied by Hlf is highlighted. (B) Luciferase reporter assay of the candidate Nfic enhancer using Hlf-inducible ESCs. Bars denote the mean firefly luciferase signal (±SEM) after normalization against Renilla using the +6.5 kb, a minimal (Min) enhancer construct, or an empty reporter construct, with or without Hlf induction (triplicate cultures from one of three representative experiments). (C and D) Frequency of myeloid and B cells generated as a consequence of enforced Nfic expression. Shown are the ratios of percentage GFP+ Gr1+ myeloid cells over GFP+CD19+ B cells for the indicated groups. Data are from one of three experiments with similar results (n = 6 cultures per group for all cultures except day 14 Nfic, for which five cultures were analyzed). Enforced Nfic expression leads to a general loss of hematopoietic cells over time. Hlf-inducible GMLPs were maintained in the absence (C) or presence (D) of DOX and were transduced with either a control (Migr1) or Nfic retroviral vector and were subsequently cultured on OP9 stroma cells with monitoring every 2 days for frequency of GFP+ cells (n = 1 replicate for days 0, 2, and 4 and n = 5 replicates for days 6, 8, 10, 12, and 14 for the groups in both C and D). Error bars denote SEM. See also Figure S7.
Figure 7 Identification of Nfic as a Direct Hlf Target with Pronounced Functional Effects on Hematopoietic Differentiation (A) UCSC Genome Browser track depicting the genomic context of Nfic with regard to accessible chromatin and histone modifications of indicated cell types (assay for transposase-accessible chromatin using sequencing [ATAC-seq] and histone modification data from Lara-Astiaso et al. (2014). The region occupied by Hlf is highlighted. (B) Luciferase reporter assay of the candidate Nfic enhancer using Hlf-inducible ESCs. Bars denote the mean firefly luciferase signal (±SEM) after normalization against Renilla using the +6.5 kb, a minimal (Min) enhancer construct, or an empty reporter construct, with or without Hlf induction (triplicate cultures from one of three representative experiments). (C and D) Frequency of myeloid and B cells generated as a consequence of enforced Nfic expression. Shown are the ratios of percentage GFP+ Gr1+ myeloid cells over GFP+CD19+ B cells for the indicated groups. Data are from one of three experiments with similar results (n = 6 cultures per group for all cultures except day 14 Nfic, for which five cultures were analyzed). Enforced Nfic expression leads to a general loss of hematopoietic cells over time. Hlf-inducible GMLPs were maintained in the absence (C) or presence (D) of DOX and were transduced with either a control (Migr1) or Nfic retroviral vector and were subsequently cultured on OP9 stroma cells with monitoring every 2 days for frequency of GFP+ cells (n = 1 replicate for days 0, 2, and 4 and n = 5 replicates for days 6, 8, 10, 12, and 14 for the groups in both C and D). Error bars denote SEM. See also Figure S7.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Wahlestedt, M., Ladopoulos, V., Hidalgo, I., Sanchez Castillo, M., Hannah, R., Säwén, P., Wan, H., Dudenhöffer-Pfeifer, M., Magnusson, M., Norddahl, G. L., Göttgens, B., & Bryder, D.
Venue
Cell Reports
Publisher
Elsevier BV
Published
2017-11
Volume
21
Issue
8
Pages
2251-2263
ISSN
2211-1247
DOI
10.1016/j.celrep.2017.10.112
PMC
PMC5714592
Cited by
75
References
9
Language
en
Licence
Funders
  • Swedish Cancer Society
  • Swedish Medical Research Council
  • Swedish Pediatric Leukemia Foundation
  • Knut and Alice Wallenberg Foundation
  • European Research Council (615068)
  • Wellcome Trust
  • CRUK
  • Bloodwise
  • MRC
  • NIH-NIDDK
  • National Cancer Institute
  • NCI (P30 CA91842, UL1TR000448)
  • National Center for Research Resources

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Wahlestedt, M., Ladopoulos, V., Hidalgo, I., Sanchez Castillo, M., Hannah, R., Säwén, P., Wan, H., Dudenhöffer-Pfeifer, M., Magnusson, M., Norddahl, G. L., Göttgens, B., & Bryder, D. (2017). Critical Modulation of Hematopoietic Lineage Fate by Hepatic Leukemia Factor. Cell Reports. https://doi.org/10.1016/j.celrep.2017.10.112