First published online December 20, 2005
Development 133, 201e (2006)
© The Company of Biologists Limited
Subduing Su(var)3-9
The formation of heterochromatin - tightly packed, transcriptionally
inactive chromosomal DNA - involves a complex arrangement of histone
modifications, including histone H3K9 methylation, which, in flies, is
catalysed by the methyltransferase Su(var)3-9. Having observed that
hypomorphic mutations in JIL-1 (a histone H3S10 kinase) cause
heterochromatin to spread to ectopic chromosomal regions in
Drosophila, Johansen and colleagues set out to explain why (see
p. 229). To do so, they
generated flies that carry both a null and a hypomorphic copy of
JIL-1, which almost never survive to adulthood. But when these flies
carry an additional copy of the Su(var)3-9 gene that has reduced
function, they mostly survive, indicating that Su(var)3-9 and JIL-1 function
in the same pathway and are antagonistic. From their results, the authors
propose that JIL-1 kinase marks transcriptionally active euchromatin -
possibly by phosphorylating histone H3S10 - to prevent Su(var)3-9 from
triggering the formation of heterochromatin at ectopic
locations.
Related articles in Development:
- The JIL-1 histone H3S10 kinase regulates dimethyl H3K9 modifications and heterochromatic spreading in Drosophila
- Weiguo Zhang, Huai Deng, Xiaomin Bao, Stephanie Lerach, Jack Girton, Jørgen Johansen, and Kristen M. Johansen
Development 2006 133: 229-235.
[Abstract]
[Full Text]
