Chromatin remodeling is an essential step for many chromatin-related fundamental cellular processes, such as gene replication, transcription, recombination and gene silencing. Two classes of protein complexes contribute to chromatin remodeling: protein complexes with ATPase activity and protein complexes capable of enzymatic modifications of chromosomal proteins, especially histones. Compared to well-studied histone acetylation which has been directly linked to gene transcription, the role of histone phosphorylation in chromatin remodeling for gene transcription is still poorly understood although there is some correlation between histone phosphorylation and gene transcription;A novel nuclear tandem protein kinase JIL-1 was cloned and identified in Kristen Johansen's lab. Initial functional analysis indicated JIL-1 is associated with chromosomes throughout the cell cycle as revealed by green fluorescence protein tagged JIL-1 fusion protein. In interphase nuclei, JIL-1 is found to associate with numerous sites on Drosophila salivary polytene chromosomes by antibody immunostaining. These sites are complementary to the bands of Hoechst 33258 and correspond to interbands of polytene chromosomes that are gene rich regions. Furthermore, JIL-1 binds to the male X chromosome with an almost two-fold increased level compared with autosomal and female X chromosome staining. The JIL-1 immunostaining pattern on polytene chromosomes suggests that JIL-1 may be implicated in up-regulation of gene expression through chromatin remodeling possibly by phosphorylation of histone H3 based on the observation that JIL-1 is able to phosphorylate histone H3 in vitro. The approximately two-fold higher level of JIL-1 on male X chromosomes implies that JEL-1 is involved in gene dosage compensation. This hypothesis is further supported by the observations that JIL-1 is colocalized with H4Ac 16 and the MSL complex on male X chromosomes, that MSL1 and MSL3 can be co-immunoprecipitated with JIL-1, and that the preferential association with male X chromosomes is dependent on the MSL complex. A series of deficiency mapping and rescue experiments suggests JIL-1 is likely to be a redundant gene mapping in the 68A4-5 region.