Poster Presentation 25th Lorne Cancer Conference 2013

The homeobox transcription factor Hhex regulates haematopoietic stem cell cycling and emergency haematopoiesis. (#218)

Jacob T Jackson 1 , Benjamin J Shields 1 , Chayanica Nasa 1 , Donald Metcalf 1 , Warren S Alexander 1 , Clifford W Bogue 2 , Matthew P McCormack 1
  1. Walter & Eliza Hall Institute of Medical Research, Parkville, VIC, Australia
  2. Department of Pediatrics, Yale University, New Haven, Connecticut, USA

The Haematopoietically-expressed homeobox gene, Hhex, is a transcription factor that is important for the maturation and proliferation of definitive haematopoietic progenitors and B-cell development during embryonic haematopoiesis12 . However, whether Hhex plays similar roles in adult haematopoiesis is currently unknown. To study this we employed an Hhex Inducible Knock-Out (iKO) mouse. Following Hhex deletion using Mx-Cre, mice displayed normal long-term myeloid cell development. However competitive serial transplants of iKO donor Bone Marrow (BM) revealed a defect in Haematopoietic Stem Cell (HSC) self-renewal with a progressive reduction in contribution of Hhex-null HSCs to haematopoiesis. Although, Hhex-null donor BM contained normal numbers of haematopoietic progenitors, there was a striking absence of blast colony recloning in vitro. Thus, whilst Hhex is dispensable for normal steady state myeloid development, it plays crucial roles in the self-renewal of HSCs in vitro and in vivo. To study the response of Hhex-null HSCs to haematopoietic stress, we performed sub-lethal myelo-ablation of Hhex iKO mice. This demonstrated a dramatically impaired ability of the HSCs to regenerate the myeloid compartment. RNAseq analysis of Hhex iKO LSK cells, verified by RT-PCR, showed that the deletion of Hhex lead to altered expression of cell cycle regulators, including a reduction in expression of Cyclin D1. These results demonstrate that Hhex is a key transcriptional mediator of HSC self-renewal and stress haematopoiesis and suggest it mediates these effects via regulation of cell cycling.

  1. Bogue CW, et al. Proc Natl Acad Sci USA. 2003 Jan 21;100(2):556-61.
  2. Paz H, et al. Blood. 2010 Aug 26;116(8):1254-62.