TY - JOUR
T1 - The JIL-1 tandem kinase mediates histone H3 phosphorylation and is required for maintenance of chromatin structure in Drosophila
AU - Wang, Yanming
AU - Zhang, Weiguo
AU - Jin, Ye
AU - Johansen, Jorgen
AU - Johansen, Kristen M.
N1 - Funding Information:
We wish to thank Drs. Linda Ambrosio and Jack Girton for advice, discussion, and for providing the w; Δ2-3/TM2 Ubx stock, Dr. Todd Laverty and the Berkeley Drosophila Genome Project for providing the EP(3)3657 stock, Drs. Mitzi Kuroda, Harold Saumweber, and Michael Paddy for their generous gifts of anti-MSL1,-2,-3 antisera (M.K.) and anti-lamin (H.S. and M.P.) antibodies, and the ISU Cell and Hybridoma Facility for assistance in antibody production. We also wish to thank Ms. Anna Yeung for expert technical assistance and Ms. Virginia Lephart for maintenance of fly stocks. This work was supported by grants from NSF (MCB-9600587) and NIH (GM62916) and by Fung and Stadler graduate fellowship awards (Y.J.).
PY - 2001/5/18
Y1 - 2001/5/18
N2 - To analyze the function of the chromosomal kinase JIL-1, we generated an allelic series of hypomorphic and null mutations. JIL-1 is an essential kinase for viability, and reduced levels of JIL-1 kinase activity lead to a global change in chromatin structure. In JIL-1 hypomorphs, euchromatic regions of polytene chromosomes are severely reduced and the chromosome arms condensed. This is correlated with decreased levels of histone H3 Ser10 phosphorylation. These levels can be restored by a JIL-1 transgene placing JIL-1 directly in the pathway mediating histone H3 phosphorylation. We propose a model where JIL-1 kinase activity is required for maintaining the structure of the more open chromatin regions that facilitate gene transcription.
AB - To analyze the function of the chromosomal kinase JIL-1, we generated an allelic series of hypomorphic and null mutations. JIL-1 is an essential kinase for viability, and reduced levels of JIL-1 kinase activity lead to a global change in chromatin structure. In JIL-1 hypomorphs, euchromatic regions of polytene chromosomes are severely reduced and the chromosome arms condensed. This is correlated with decreased levels of histone H3 Ser10 phosphorylation. These levels can be restored by a JIL-1 transgene placing JIL-1 directly in the pathway mediating histone H3 phosphorylation. We propose a model where JIL-1 kinase activity is required for maintaining the structure of the more open chromatin regions that facilitate gene transcription.
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U2 - 10.1016/S0092-8674(01)00325-7
DO - 10.1016/S0092-8674(01)00325-7
M3 - Article
C2 - 11371341
AN - SCOPUS:0035906859
SN - 0092-8674
VL - 105
SP - 433
EP - 443
JO - Cell
JF - Cell
IS - 4
ER -