Ikaros is a transcription factor that contains an N-terminal domain with multiple zinc fingers that bind to DNA and a C-terminal domain that mediates dimerization. Ikaros is expressed in non-lymphoid leukemia cells and can function both as a transcriptional repressor and activator by binding histone deacetylase complexes and chromatin remodeling complexes. Ikaros represses the TdT gene by displacing the activator Ets-1 and enhancing heterochromatin formation, keeping the gene inactive by recruiting the NURD complex.

3. Introduction

4. Structure N-terminal domain Containing different numbers of zinc fingers. Exhibit DNA binding activity when it has 3 or more zinc fingers . Bind to DNA sites contain the core motif GGGA and ZNFs 2,3 C -terminal domain Oligomerization domain. Containing a bipartite transactivation domain and 2 zinc finger motifs. Mediate hommo or hetrodimerisation between isoforms and iteract in with other molecules .

6. Isoforms

8. ikaros gene expression in human non-lymphoid leukemia cell line

10. Different roles

12. Disease associated with ikaros

13. Function of Ikaros Ikaros appears function both as a transcriptional repressor and as an activator through its ability to bind a large number of nuclear factors: Histon deacetylase repressor complexses SIN3 , NURD (causes gene inactivation ) ATP-dependent chromatin remodeling complexes SW1/SNF (can distrupt histon-DNA –complexes)

15. TdT gene is initially down-regulated when ikaros dislocates the transcriptional activator Ets-1 from the TdT promotor. Down-regulation enhanced by an ikaros –dependent hetrochromatin formation at the TdT locus. Ikaros can keep the gene in an inactive state through recruitment of NURD .