Reproduced with permission from Forrester AM. Furthermore, loss of rprml also increases the activity of caspase-3 in endothelial cells within the caudal hematopoietic tissue (CHT), the first perivascular niche where HSPCs reside during zebrafish embryonic development. EGFP enhanced green fluorescent protein, ALPM anterior lateral paraxial mesoderm, PBI posterior blood island. Later in development there is a significant reduction in erythroid-myeloid precursors (EMP) at the posterior blood island (PBI) and a significant decline of definitive hematopoietic stem/progenitor cells (HSPCs). Functional knockdown of miR-126 by MO126MB or c-mybTP miR126 resulted in increased erythrocytes and decreased. The formation of hemangioblasts and the primitive wave of hematopoiesis occur normally in absence of rprml. All images depict the posterior blood island of zebrafish larvae at 96 h.p.f. Here, using CRISPR-Cas9 and antisense morpholino oligonucleotides, we disrupt the expression of rprml in zebrafish and demonstrate that its loss leads to impaired definitive hematopoiesis. Importantly, RPRML expression pattern is conserved between zebrafish and human species. Another family member, Reprimo-like (RPRML), has not yet an established role in physiology or pathology. Using this system, we traced the hematopoietic potential of hemogenic endothelium (HE) in the posterior blood island (PBI) of zebrafish embryo and found that HEs in the PBI are heterogeneous, which contains at least myeloid unipotent and myeloid-lymphoid bipotent subtypes. Heretofore, mammalian Reprimo (RPRM) has been described as a putative p53-dependent tumor suppressor gene that functions at the G2/M cell cycle checkpoint. The Reprimo gene family comprises a group of single-exon genes for which their physiological function remains poorly understood.
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