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Jishage, K. et al.

Jishage, Nezu, Kawase, Iwata, Watanabe, Miyoshi, Ose, Habu, Kake, Kamada, Ueda, Kinoshita, Jenne, Shimane, Suzuki,

Role of Lkb1, the causative gene of Peutz-Jegher's syndrome, in embryogenesis and polyposis.

Peutz-Jeghers syndrome (PJS) is a dominantly inherited human disorder characterized by gastrointestinal hamartomatous polyposis and mucocutaneous melanin pigmentation. LKB1 (STK11) serine/threonine kinase is the product of the causative gene of PJS, which has been mapped to chromosome 19p13. 3. However, several studies have produced results that are not consistent with a link between LKB1 gene mutation and PJS. We constructed a knockout gene mutation of Lkb1 to determine whether it is the causative gene of PJS and to examine the biological role of the Lkb1 gene. Lkb1(-/-) mice died in utero between 8.5 and 9.5 days postcoitum. At 9.0 days postcoitum, Lkb1(-/-) embryos were generally smaller than their age-matched littermates, showed developmental retardation, and did not undergo embryonic turning. Multiple gastric adenomatous polyps were observed in 10- to 14-month-old Lkb1(+/-) mice. Our results indicate that functional Lkb1 is required for normal embryogenesis and that it is related to tumor development. The Lkb1(+/-) mouse is suitable for studying molecular mechanism underlying the development of inherited gastric tumors in PJS.[1]

References

Role of Lkb1, the causative gene of Peutz-Jegher's syndrome, in embryogenesis and polyposis. Jishage, K., Nezu, J., Kawase, Y., Iwata, T., Watanabe, M., Miyoshi, A., Ose, A., Habu, K., Kake, T., Kamada, N., Ueda, O., Kinoshita, M., Jenne, D.E., Shimane, M., Suzuki, H. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]

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