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Different parts of the genome occupy specific compartments of the cell nucleus based on the gene content and the transcriptional activity. An example of this is the altered nuclear positioning of the  HLXB9  gene in leukaemia cells observed in association with its over-expression. This phenomenon was attributed to the presence of a chromosomal translocation with breakpoint proximal to the  HLXB9  gene. Before becoming an interesting gene in cancer biology,  HLXB9  was studied as a developmental gene. This homeobox gene is also known as  MNX1  (motor neuron and pancreas homeobox 1) and it is relevant for both motor neuronal and pancreatic beta cells development. A spectrum of mutations in this gene are causative of sacral agenesis and more broadly, of what is known as the Currarino Syndrome, a constitutional autosomal dominant disorder. Experimental work on animal models has shown that  HLXB9  has an essential role in motor neuronal differentiation. Here we present data to show that, upon treatment with retinoic acid, the  HLXB9  gene becomes over-expressed during the early stages of neuronal differentiation and that this corresponds to a reposition of the gene in the nucleus. More precisely, we used the SK-N-BE human neuroblastoma cell line as an  in   vitro  model and we demonstrated a transient transcription of  HLXB9  at the 4 th  and 5 th  days of differentiation that corresponded to the presence, predominantly in the cell nuclei, of the encoded protein HB9. The nuclear positioning of the  HLXB9  gene was monitored at different stages: a peripheral location was noted in the proliferating cells whereas a more internal position was noted during differentiation, that is while  HLXB9  was transcriptionally active. Our findings suggest that  HLXB9  can be considered a marker of early neuronal differentiation, possibly involving chromatin remodeling pathways.

HLXB9 Gene Expression, and Nuclear Location during In Vitro Neuronal Differentiation in the SK-N-BE Neuroblastoma Cell Line