JIL-1 was cloned as a protein that is recognized by a monoclonal antibody mAb2A (Jin et al. 1999). The 1,207-aa protein contains two tandemly arranged serine/threonine kinase domains, and it can phosphorylate histone H3 in vitro (Jin et al. 1999). JIL-1 is required for maintenance of chromatin structure in flies. Null mutation of jil-1 is lethal. Mutant flies have strongly decreased H3S10 phosphorylation and defects in chromatin structure. Interestingly, weak alleles of JIL-1 show distortion of the sex ratio, implicating that male flies are more vulnerable to partial loss of the protein (Wang et al. 2001). In addition to chromosome morphology phenotypes,jil-1 mutant flies have posterior-to-anterior homeotic transformations (Zhang et al. 2003a). Trithorax group (trxG) members brahma and trithorax enhance the homeotic pheno-type, suggesting that JIL-1 participates in regulation of the BX-C locus with trxG genes (Zhang et al. 2003a). Recently, JIL-1 was shown to interact with a splice variant from the lola locus, but it is unknown whether this interaction is significant for dosage compensation (Zhang et al. 2003b).

JIL-1 is enriched approximately two-fold on the male X chromosome (Jin et al. 1999), and this localization coincides with H3S10 phosphorylation and phosphoacetylated (S10P/K14Ac) histone H3 (Wang et al. 2001). Epitope-tagged JIL-1 can be co-immunoprecipitated with MSL-1, MSL-2 and MSL-3 from Drosophila SL2 cells. Furthermore, in vitro pull-down experiments have shown that JIL-1 interaction with MSL-1 and MSL-3 is mediated by its two kinase domains (Jin et al. 2000).

In contrast to other MSL complex members, MSL-2 localization is not disrupted in JIL-1 mutants, suggesting that JIL-1 is not required for targeting, assembly or spreading of the complex (Wang et al. 2001). However, in jil-1 mutants, the X chromosome morphology is more severely affected than that of autosomes (Wang et al. 2001). Taken together, these results indicate that it is a bona fide member of the MSL complex, but as there is no direct evidence linking it to hypertranscription of the X chromosome, further studies need to address this suggestive link.

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