Molecular changes caused by deficiency of Runx1b and Gfi1/Gfi1b. (A) Cellular constitution of the ventral part of the aortic structure where HSCs are generated in midgestational mouse embryos: Runx1b or Gfi1/Gfi1b heterozygous embryo (left panel) and Runx1b homozygous-knockout (KO) embryo (right panel). Runx1b deletion leads to an extensive change in pre-HE characteristics in addition to the loss of HE, EHT, and intra-aortic hematopoietic cluster cells, as well as alteration of the subaortic niche composition. (B) Expression of the reporters (top 2 lines) and the transcripts of representative markers (lower 6 lines) in different cell populations, including EHT continuum. Gray color indicates very low expression. Note the specific expression of Ace in pre-HE. ENDO, endothelial; IAHC, intra-aortic hematopoietic clusters; MES-PDGFRa, PDGFRa+ mesenchymal; MES-SMA, SMA+ mesenchymal; WT, wild-type. The figure was created by Siyuan Hou (Jinan University, Guangzhou, China).

Molecular changes caused by deficiency of Runx1b and Gfi1/Gfi1b. (A) Cellular constitution of the ventral part of the aortic structure where HSCs are generated in midgestational mouse embryos: Runx1b or Gfi1/Gfi1b heterozygous embryo (left panel) and Runx1b homozygous-knockout (KO) embryo (right panel). Runx1b deletion leads to an extensive change in pre-HE characteristics in addition to the loss of HE, EHT, and intra-aortic hematopoietic cluster cells, as well as alteration of the subaortic niche composition. (B) Expression of the reporters (top 2 lines) and the transcripts of representative markers (lower 6 lines) in different cell populations, including EHT continuum. Gray color indicates very low expression. Note the specific expression of Ace in pre-HE. ENDO, endothelial; IAHC, intra-aortic hematopoietic clusters; MES-PDGFRa, PDGFRa+ mesenchymal; MES-SMA, SMA+ mesenchymal; WT, wild-type. The figure was created by Siyuan Hou (Jinan University, Guangzhou, China).

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