The JIL-1 tandem kinase mediates histone H3 phosphorylation and is required for maintenance of chromatin structure in Drosophila

To analyze the function of the chromosomal kinase JIL-1, we generated an al lelic series of hypomorphic and null mutations. JIL-1 is an essential kinas e for viability, and reduced levels of JIL-1 kinase activity lead to a glob al change in chromatin structure. in JIL-1 hypomorphs, euchromatic regions of polytene chromosomes are severely reduced and the chromosome arms conden sed. This is correlated with decreased levels of histone H3 Ser10 phosphory lation. These levels can be restored by a JIL-1 transgene placing JIL-1 dir ectly in the pathway mediating histone H3 phosphorylation. We propose a mod el where JIL-1 kinase activity is required for maintaining the structure of the more open chromatin regions that facilitate gene transcription.