Jack Girton

A developmentally regulated splice variant from the complex lola locus encoding multiple different zinc finger domain proteins interacts with the chromosomal kinase JIL-1.

The Drosophila pleiohomeotic mutation enhances the Polycomblike and Polycomb mutant phenotypes during embryogenesis and in the adult.

Genetic and phenotypic analysis of alleles of the Drosophila chromosomal JIL-1 kinase reveals a functional requirement at multiple developmental stages.

Megator, an essential coiled-coil protein that localizes to the putative spindle matrix during mitosis in Drosophila.

Chromator, a novel and essential chromodomain protein interacts directly with the putative spindle matrix protein skeletor.

D-Hillarin, a novel W180-domain protein, affects cytokinesis through interaction with the septin family member Pnut.

EAST interacts with Megator and localizes to the putative spindle matrix during mitosis in Drosophila.

The JIL-1 kinase regulates the structure of Drosophila polytene chromosomes.

The JIL-1 kinase interacts with lamin Dm0 and regulates nuclear lamina morphology of Drosophila nurse cells.

JIL-1 kinase, a member of the male-specific lethal (MSL) complex, is necessary for proper dosage compensation of eye pigmentation in Drosophila.

The JIL-1 histone H3S10 kinase regulates dimethyl H3K9 modifications and heterochromatic spreading in Drosophila.

Loss-of-function alleles of the JIL-1 kinase are strong suppressors of position effect variegation of the wm4 allele in Drosophila.

The chromodomain protein, Chromator, interacts with JIL-1 kinase and regulates the structure of Drosophila polytene chromosomes.

The lamin Dm0 allele Ari3 acts as an enhancer of position effect variegation of the wm4 allele in Drosophila.

Loss-of-function alleles of the JIL-1 histone H3S10 kinase enhance position-effect variegation at pericentric sites in Drosophila heterochromatin.

Reduced levels of Su(var)3-9 but not Su(var)2-5 (HP1) counteract the effects on chromatin structure and viability in loss-of-function mutants of the JIL-1 histone H3S10 kinase.

Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila.

Chromatin structure and the regulation of gene expression: the lessons of PEV in Drosophila.

RNA polymerase II-mediated transcription at active loci does not require histone H3S10 phosphorylation in Drosophila.

The COOH-terminal domain of the JIL-1 histone H3S10 kinase interacts with histone H3 and is required for correct targeting to chromatin.

Polytene chromosome squash methods for studying transcription and epigenetic chromatin modification in Drosophila using antibodies.

Chromator is required for proper microtubule spindle formation and mitosis in Drosophila.

Asator, a tau-tubulin kinase homolog in Drosophila localizes to the mitotic spindle.

JIL-1 and Su(var)3-7 interact genetically and counteract each other's effect on position-effect variegation in Drosophila.

Do nuclear envelope and intranuclear proteins reorganize during mitosis to form an elastic, hydrogel-like spindle matrix?

A balance between euchromatic (JIL-1) and heterochromatic [SU(var)2-5 and SU(var)3-9] factors regulates position-effect variegation in Drosophila.

The pleiohomeotic functions as a negative regulator of Drosophila even-skipped gene during embryogenesis.

The chromodomain-containing NH(2)-terminus of Chromator interacts with histone H1 and is required for correct targeting to chromatin.

The epigenetic H3S10 phosphorylation mark is required for counteracting heterochromatic spreading and gene silencing in Drosophila melanogaster.