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Phosphoinositide 3-kinase is involved in Xenopus and Labrus melanophore aggregation

Artikel i vetenskaplig tidskrift
Författare T. P. M. Andersson
Helen Nilsson Sköld
S. P. S. Svensson
Publicerad i Cellular Signalling
Volym 15
Nummer/häfte 12
Sidor 1119-1127
ISSN 0898-6568
Publiceringsår 2003
Publicerad vid Institutionen för marin ekologi
Sidor 1119-1127
Språk en
Länkar <Go to ISI>://000186443400006
Ämnesord melanophore, pigment cell, aggregation, xenopus laevis, labrus bimaculatus, pi3-k, phosphodiesterase, nucleotide phosphodiesterase isozymes, activated protein-kinase, vascular smooth-muscle, melanosome movement, pigment granules, cyclic-amp, selective inhibitors, laevis melanophores, signaling pathways, organelle movement
Ämneskategorier Biologiska vetenskaper, Ekologi

Sammanfattning

Melanophores are pigmented cells capable of quick colour changes through coordinated transport of their intracellular pigment granules. We demonstrate the involvement of phosphoinositide 3-kinase (PI3-K) in Xenopus and Labrus aggregation by the use of the PI3-K inhibitor, LY-294002. In Xenopus, wortmannin-insensitive PI3-K was found to be essential for the aggregation, mitogen-activated protein kinase (MAPK) activation and tyrosine phosphorylation of a 280-kDa protein, and for the maintenance of low cyclic adenosine 3':5'-monophosphate (cAMP) during the aggregated state. Pre-aggregated cells disperse completely to LY-294002 at 50-100 muM, involving a transient elevation in cAMP due to adenylate cyclase (AC) stimulation or to inhibition of cyclic nucleotide phosphodiesterase (PDE). The inactive analogue LY-303511 did not induce dispersion at the same concentrations. PDE4 and/or PDE2 was found to be involved in melanosome aggregation. The similar kinetics of LY-294002 and various PDE inhibitors indicates that the elevation of cAMP might be due to inhibition of PDE. In Labrus melanophores, LY-294002 had a less dramatic effect, probably due to less dependence on PDE in regulation of cAMP levels. In Xenopus aggregation, we suggest that melatonin stimulation of the Mel1c receptor via G(betagamma) activates PI3-K that, directly or indirectly via MAPK, activates PDE. (C) 2003 Elsevier Inc. All rights reserved.

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