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doi: 10.1242/10.1242/jcs.00093

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Inactivation of G_z causes disassembly of the Golgi apparatus

Masami Nagahama, Shihomi Usui, Takashi Shinohara, Tomohiro Yamaguchi^*, Katsuko Tani and Mitsuo Tagaya

School of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo 192-0392, Japan
^* Present address: Department of Life Science, Graduate School and Faculty of Science, Himeji Institute of Technology, Ako-gun, Hyogo 678-1297, Japan

Author for correspondence (e-mail: tagaya{at}ls.toyaku.ac.jp)

Accepted 4 August 2002

We showed previously that overexpression of the subunit of G_z or G_i2 suppresses nordihydroguaiaretic acid-induced Golgi disassembly. To determine whether the active form of G is required to maintain the structure of the Golgi apparatus, we examined the effects of a series of G GAPs, regulators of G protein signaling (RGS) proteins, on the Golgi structure. Expression of RGSZ1 or RGSZ2, both of which exhibit high selectivity for G_z, markedly induced dispersal of the Golgi apparatus, whereas expression of RGS proteins that are rather selective for G_q or other G_i species did not. A mutated RGSZ1, which is deficient in the interaction with G_z, did not induce Golgi disassembly. These results suggest that the active form of G_z, but not G_i2, is crucial for maintenance of the structure of the Golgi apparatus. Consistent with this idea, Golgi disruption also took place in cells transfected with a dominant-negative G_z mutant. Although previous studies showed that the expression of G_z is confined to neuronal cells and platelets, immunofluorescence and mRNA expression analyses revealed that it is also expressed, albeit at low levels, in non-neuronal cells, and is located in the Golgi apparatus. These results taken together suggest a general regulatory role for G_z in the control of the Golgi structure.

Key words: Golgi apparatus, Heterotrimeric G protein, Regulator of G protein signaling

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