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JIL-1 kinase, a member of the male-specific lethal (MSL) complex, is necessary for proper dosage compensation of eye pigmentation in Drosophila 总被引:2,自引:0,他引:2
Lerach S Zhang W Deng H Bao X Girton J Johansen J Johansen KM 《Genesis (New York, N.Y. : 2000)》2005,43(4):213-215
The upregulation of the JIL-1 kinase on the male X chromosome and its association with the male-specific lethal (MSL) complex suggest that JIL-1 may play a role in regulating dosage compensation. To directly test this hypothesis we measured eye pigment levels of mutants in the X-linked white gene in an allelic series of JIL-1 hypomorphic mutants. We show that dosage compensation of w(a) alleles that normally do exhibit dosage compensation was severely impaired in the JIL-1 mutant backgrounds. As a control we also examined a hypomorphic white allele w(e) that fails to dosage compensate in males due to a pogo element insertion. In this case the relative pigment level measured in males as compared to females remained approximately the same even in the most severe JIL-1 hypomorphic background. These results indicate that proper dosage compensation of eye pigment levels in males controlled by X-linked white alleles requires normal JIL-1 function. 相似文献
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Bao X Cai W Deng H Zhang W Krencik R Girton J Johansen J Johansen KM 《The Journal of biological chemistry》2008,283(47):32741-32750
The JIL-1 histone H3S10 kinase in Drosophila localizes specifically to euchromatic interband regions of polytene chromosomes and is enriched 2-fold on the male X chromosome. JIL-1 can be divided into four main domains including an NH(2)-terminal domain, two separate kinase domains, and a COOH-terminal domain. Our results demonstrate that the COOH-terminal domain of JIL-1 is necessary and sufficient for correct chromosome targeting to autosomes but that both COOH- and NH(2)-terminal sequences are necessary for enrichment on the male X chromosome. We furthermore show that a small 53-amino acid region within the COOH-terminal domain can interact with the tail region of histone H3, suggesting that this interaction is necessary for the correct chromatin targeting of the JIL-1 kinase. Interestingly, our data indicate that the COOH-terminal domain alone is sufficient to rescue JIL-1 null mutant polytene chromosome defects including those of the male X chromosome. Nonetheless, we also found that a truncated JIL-1 protein which was without the COOH-terminal domain but retained histone H3S10 kinase activity was able to rescue autosome as well as partially rescue male X polytene chromosome morphology. Taken together these findings indicate that JIL-1 may participate in regulating chromatin structure by multiple and partially redundant mechanisms. 相似文献
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The JIL-1 kinase localizes to interband regions of Drosophila polytene chromosomes and phosphorylates histone H3 Ser10. Analysis of JIL-1 hypomorphic alleles demonstrated that reduced levels of JIL-1 protein lead to global changes in polytene chromatin structure.
Here we have performed a detailed ultrastructural and cytological analysis of the defects in JIL-1 mutant chromosomes. We show that all autosomes and the female X chromosome are similarly affected, whereas the defects in
the male X chromosome are qualitatively different. In polytene autosomes, loss of JIL-1 leads to misalignment of interband
chromatin fibrils and to increased ectopic contacts between nonhomologous regions. Furthermore, there is an abnormal coiling
of the chromosomes with an intermixing of euchromatic regions and the compacted chromatin characteristic of banded regions.
In contrast, coiling of the male X polytene chromosome was not observed. Instead, the shortening of the male X chromosome
appeared to be caused by increased dispersal of the chromatin into a diffuse network without any discernable banded regions.
To account for the observed phenotypes we propose a model in which JIL-1 functions to establish or maintain the parallel alignment
of interband chromosome fibrils as well as to repress the formation of contacts and intermingling of nonhomologous chromatid
regions.
Electronic Supplementary Material Supplementary material is available for this article at and accessible for authorised users 相似文献
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Dosage compensation refers to the equal expression between the sexes despite the fact that the dosage of the X chromosome
is different in males and females. In Drosophila there is a twofold upregulation of the single male X. In triple X metafemales, there is also dosage compensation, which occurs
by a two-thirds downregulation. There is a concomitant reduction in expression of many autosomal genes in metafemales. The
male specific lethal (MSL) complex is present on the male X chromosome. Evidence is discussed showing that the MSL complex
sequesters a histone acetyltransferase to the X chromosome to mute an otherwise increased expression by diminishing the histone
acetylation on the autosomes. Several lines of evidence indicate that a constraining activity occurs from the MSL complex
to prevent overcompensation on the X that might otherwise occur from the high level of acetylation present. Together, the
evidence suggests that dosage compensation is a modification of a regulatory inverse dosage effect that is a reflection of
intrinsic gene regulatory mechanisms and that the MSL complex has evolved in reaction in order to equalize the expression
on both the X and autosomes of males and females. 相似文献