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Journal of Biochemistry Advance Access originally published online on September 23, 2006
Journal of Biochemistry 2006 140(5):619-625; doi:10.1093/jb/mvj194
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© 2006 The Japanese Biochemical Society.

ARTICLE

Disruption of Phospholipase C{delta}4 Gene Modulates the Liver Regeneration in Cooperation with Nuclear Protein Kinase C

Atsushi Akutagawa1,2, Kiyoko Fukami3, Yoshiko Banno4, Tadaomi Takenawa5, Reiji Kannagi2, Yukihiro Yokoyama1, Koji Oda1, Masato Nagino1, Yuji Nimura1, Shonen Yoshida6 and Keiko Tamiya-Koizumi2,7,*

1 Division of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65, Tsurumai-cho, Showa-ku, Nagoya 466-8550; 2 Department of Molecular Pathology, Aichi Cancer Center Institute, 1-1, Kanokoden, Chikusa-ku, Nagoya 464-8681; 3 Laboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouchi, Hachioji-shi, Tokyo 192-0392; 4 Department of Cell Signaling, Gifu University, Graduate School of Medicine, 1-1, Yanagido, Gifu 501-1194; 5 Division of Biochemistry, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, 4-6-1, Shiroganedai, Minato-ku, Tokyo 108-8639; 6 Nagoya Kyoritsu Hospital, 1-172, Hokke, Nakagawa-ku, Nagoya 454-8525; and 7 Nagoya University School of Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20, Daiko-minami, Higashi-ku, Nagoya 461-8673

* To whom correspondence should be addressed. Tel/Fax: +81 52 719 1186, E-mail: kkoizumi{at}met.nagoya-u.ac.jp

Phospholipase C{delta}4 (PLC {delta}4) gene has been cloned from the cDNA library of regenerating rat liver. Using PLC {delta}4 gene–disrupted mice (PLC {delta}4–/–), we studied a role of PLC {delta}4 during liver regeneration after partial hepatectomy (PH). In PLC {delta}4–/–, liver regeneration occurred in an apparently normal way. However, BrdU-indices indicated that PLC {delta}4 gene disruption delayed the onset of DNA synthesis by 2 h. Noticeably, the BrdU-indices in PLC {delta}4+/+ remained rather constant throughout S phase, 25–35%, whereas in PLC {delta}4–/–, it fluctuated drastically from 25% at 34 h to 65% at late S, 42 h after PH. This fact showed that PLC {delta}4 gene disruption caused a higher synchronization of cell proliferation. The mRNA for PLC {delta}4 in PLC {delta}4+/+ appeared at late G1, and the expression continued throughout S phase. PLC activity increased transiently in chromatin at the late G1 and S phases in only PLC {delta}4+/+, but not in PLC {delta}4–/–. The specific increases in PLC activity well correlated with the transient increases of protein kinase C (PKC) {alpha} in chromatin of PLC {delta}4+/+. PKC {varepsilon} also increased transiently in chromatin from PLC {delta}4+/+ at late S. It is concluded that PLC {delta}4 regulates the liver regeneration in cooperation with nuclear PKC {alpha} and {varepsilon}.


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