1987 Fiscal Year Final Research Report Summary
Signals and their reception in the regulation of mouse X chromosome activity
| Project/Area Number |
61480438
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Human genetics
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
TAKAGI Nobuo Research Center for Molecular Genetics, 遺伝子実験施設, 助教授 (20001852)
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| Co-Investigator(Kenkyū-buntansha) |
佐々木 本道 北海道大学, 理学部, 教授 (70000817)
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| Project Period (FY) |
1986 – 1987
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| Keywords | X chromosome / X-inactivation / Enbryonal carcinoma / DNA methylation / Inactivation center |
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| Research Abstract |
Several points of interest emerged from our cytogenetic. somatic cell henetic, biochemical and molecular biological studies on cultured murine embryonal carcinoma cell (ECC) lines and early mouse embryos. Among other, our study raised a serious question about the varidity of the belief that DNA methylation is involved in the initiation of X inactivation. DNA sequences in the first intron of the mouse Hprt gene are methylalted on the inactive X but not the active X chromosome. We found that these sequences are unmethylated before X-inactivation and do not become methylated on the inactive X in most fetal cells until several days postinactivation.
Further significant progress we have would be isolation of two ECC clones(C4 and D2) with two active X chromosomes from M-MuLV infected MC12 cells having an inactivated X chromosome. It is likely that M-MuLV insertion into X inactivation center or Xce was responsible for the reactivation of the inactive X. If this is the case, these clones may be particularly useful for the study of primary events in X inactivation.
The clear-cut differences in the nuclear protein profile between C4 and MC12 is another promising finding. Further characterization of non-histone proteins specific to the inactive X chromosome may hilp understand the mechanism of spreading and maintenance of X-inactivation.
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