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Small GTP‐binding proteins in the brain‐corpus cardiacum‐corpus allatum complex of the silkworm, Bombyx mori: Involvement in the secretion of prothoracicotropic hormone
Author(s) -
Shirai Yasuhito,
Uno Tomohide,
Aizono Yasuo
Publication year - 1998
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/(sici)1520-6327(1998)38:4<177::aid-arch3>3.0.co;2-o
Subject(s) - corpus allatum , bombyx mori , biology , prothoracic gland , g protein , gtp' , gtp binding protein regulators , medicine , juvenile hormone , rab , endocrinology , bombyx , biochemistry , microbiology and biotechnology , gtpase , enzyme , hormone , receptor , ecdysone , gene
At least three GTP‐binding proteins (G‐proteins), 28, 25, and 21 kDa, were found in the brain‐corpus cardiacum‐corpus allatum complex (BR‐CC‐CA) of the silkworm, Bombyx mori. They bound to GTP and GDP specifically among nucleotides tested, indicating that these proteins are small G‐proteins. The 25 kDa G‐protein showed a cross‐reactivity to anti‐rab3A antibody, while it did not cross‐react with anti‐rhoA, rab3B, and anti‐ras antibodies. On the other hand, the 28 and 21 kDa G‐proteins showed no cross‐reactivity to any of those antibodies tested. Immunoblot analysis using the anti‐rab3A antibody demonstrated that the 25 kDa G‐protein was detected preferentially in the BR‐CC‐CA, and to some extent in the suboesophageal ganglion, but not in the salivary gland, fat body, prothoracic gland, and oesophagus. These results suggested that the 25 kDa G‐protein was a member of the rab family of G‐proteins. Furthermore, 1 mM GTPγS capable of activating G‐proteins induced BR‐CC‐CA to release PTTH under the conditions that stimulation of the PTTH release with hetero‐trimeric G‐protein was suppressed. These results indicated that the small G‐proteins may possibly contribute to PTTH release in Bombyx mori . Arch. Insect Biochem. Physiol. 38:177–184, 1998. © 1998 Wiley‐Liss, Inc.