The Effects of Lamin B Receptor knockdown on a Myeloid Leukemia Cell
A variety of mutations of the Lamin B Receptor gene (LBR) have been associated with human and mouse genetic diseases; heterozygous mutations in LBR result in the absence of nuclear lobulation of blood neutrophils and homozygosity results in skeletal malformations and fetal death. The diversity of phenotypes resulting from LBR mutations has stimulated research analyses into the multiple functions of LBR. We examined the effect of a stable RNAi knockdown of LBR gene on the transcriptome of an immortalized multipotential human myeloid leukemic cell line (HL-60/S4) either induced to granulocytic form with retinoic acid or left undifferentiated. Aside from chromatin related GO terms, the most surprising finding was a significant downregulation of Golgi Apparatus related genes. This opens the question of the role of LBR in the control of Golgin gene expression.