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The RUNX genes encode conserved transcription factors, which play vital roles in the development of various animals and human diseases. Drosophila runt is a secondary pair-rule gene, which regulates embryo segmentation. Human RUNX1, previously known as AML1, is essential for hematopoiesis. C. elegans rnt-1 is co-orthologous to the human RUNX genes. We found that RNT-1: :GFP is expressed in the H0-2, V1-6, and T blast cells in the embryo, and predominantly in the seam cells during larval to adult stages, rnt-1 mutants exhibit a loss of polarity in the asymmetrical T cell division in hermaphrodites and abnormal ray morphology in the male tail. Genetic and molecular analysis revealed that rnt-1 is allelic to mab-2. Mutant analysis suggested that rnt-1/rnab-2 is involved in regulating T blast cell polarity in cooperation with the Wnt signaling pathway. Expression studies of GFP: :POP-1 and TLP-1: :GFP reporters in rnt-1/mab-2 mutants indicated that this gene functions upstream of tlp-1 and downstream, or in parallel to, pop-1 in the genetic cascade that controls asymmetry of the T cell division. All our data suggest that RNT-1/ MAB-2 functions with POP-1 to control the asymmetry of the T cell division. Keywords: rnt-1; mab-2; RUNX; T blast cell; Seam cell; Asymmetrical cell division; Wnt signal; Caenorhabditis elegans

Caenorhabditis elegans has four members of the Six/sine oculis class of homeobox genes, ceh-32, ceh-33, ceh-34, and ceh-35. Proteins encoded by this gene family are transcription factors sharing two conserved domains, the homeodomain and the Six/sine oculis domain, both involved in DNA binding, ceh-32 expression was detected during embryogenesis in hypodermal and neuronal precursor cells and later in descendants of these cells as well as in gonadal sheath cells. RNAi inactivation studies suggest that ceh-32 plays a role in head morphogenesis, like vab-3, the C. elegans Pax-6 orthologue. ceh-32 and vab-3 are coexpressed in head hypodermal cells and ceh-32 mRNA levels are reduced in vab-3 mutants. Moreover, ectopic expression of VAB-3 in transgenic worms is able to induce ceh-32 ectopically. In addition, we demonstrate that VAB-3 is able to bind directly to the ceh-32 upstream regulatory region in vitro and to activate reporter gene transcription in a yeast one-hybrid system. Our results suggest that VAB-3 acts upstream of ceh-32 during head morphogenesis and directly induces ceh-32. Thus, ceh-32 appears to be the first target gene of VAB-3 identified so far. Key Words: ceh-32; homeobox gene; Six/so class; Caenorhabditis elegans; head morphogenesis; vab-3; Pax-6.