Protein kinase C modulates ecdysteroidogenesis in the prothoracic gland of the tobacco hornworm, Manduca sexta

The prothoracic gland is the primary source of ecdysteroid hormones in the immature insect. Ecdysteroids coordinate gene expression necessary for growth, molting and metamorphosis. Prothoracicotropic hormone (PTTH), a brain neuropeptide, regulates ecdysteroid synthesis in the prothoracic gland. PTTH...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2006-06, Vol.251 (1), p.78-87
Main Authors: Rybczynski, Robert, Gilbert, Lawrence I.
Format: Article
Language:English
Subjects:
Animals
Calcium Signaling
Ecdysteroids - metabolism
Extracellular signal-regulated kinase (ERK)
Extracellular Signal-Regulated MAP Kinases - metabolism
Insect Hormones - metabolism
Insect molting
Insect steroids
Isoenzymes - metabolism
Manduca - metabolism
Manduca - physiology
Mitogen-Activated Protein Kinases - metabolism
Molting - physiology
Neuropeptides - metabolism
Phospholipase C
Phospholipase C beta
Phosphorylation
Protein Kinase C - metabolism
Protein Kinase C - physiology
Receptors, G-Protein-Coupled - metabolism
Signal Transduction
Type C Phospholipases - metabolism
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Summary:The prothoracic gland is the primary source of ecdysteroid hormones in the immature insect. Ecdysteroids coordinate gene expression necessary for growth, molting and metamorphosis. Prothoracicotropic hormone (PTTH), a brain neuropeptide, regulates ecdysteroid synthesis in the prothoracic gland. PTTH stimulates ecdysteroid synthesis through a signal transduction cascade that involves at least four protein kinases: protein kinase A (PKA), p70 S6 kinase, an unidentified tyrosine kinase, and the extracellular signal-regulated kinase (ERK). In this report, the participation of protein kinase C (PKC) in PTTH signalling is demonstrated and characterized. PTTH stimulates PKC activity through a PLC and Ca 2+-dependent pathway that is not cAMP regulated. Inhibition of PKC inhibits PTTH-stimulated ecdysteroidogenesis as well as PTTH-stimulated phosphorylation of ERK and its upstream regulator, MAP/ERK kinase (MEK). These observations reveal that the acute regulation of prothoracic gland steroidogenesis is dependent on a web of interacting kinase pathways, which probably converge on factors that regulate translation.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2006.02.015