Abstract
The Forkhead box O (FoxO) transcription factors, including FoxO1, FoxO3a, and FoxO4, have been implicated in the regulation of several biological processes, including stress resistance, metabolism, and apoptosis. In the present study, FoxO1 and FoxO3a patterns and their role in the regulation of the insulin signalling and mitogen-activated protein kinase (MAPK) pathways were analyzed after starvation in the fat body cells of the silkworm, Bombyx mori. FoxO1 and FoxO3a are localized to the nuclei. It was found that the levels of the insulin receptor and phosphoryated kinase Akt (p-Akt) increased when the animals ceased feeding. Starvation conditions caused a decrease in extracellular-signal-regulated kinase (ERK) phosphorylation, and an increase in c-Jun N-terminal kinase (JNK) and p38 (MAP kinase) phosphorylation. This implies that the FoxO transcription factors are activated by starvation and that starvation leads to changes in the insulin signalling and MAPK pathways in B. mori. These results strongly suggest that the FoxO transcription factor may be involved in the regulation of the insulin signalling and MAPK pathways in B. mori. As such, the findings provide molecular entomologists with valuable information on the molecular mechanism of the signalling pathways in postembryonic development ofthe silkworm.
Highlights
Forkhead box O (FoxO) transcription factors play a critical role in regulating cell growth, survival, apoptosis, differentiation and proliferation, metabolism, cell cycle arrest, and protection from oxidative stress in a variety of cell types (Accili & Arden, 2004)
FoxO translocates into the nucleus and participates in the transcriptional activation of various genes involved in metabolism
Because FoxO proteins were partially regulated by control of nuclear localization, the nuclear and cytoplasmic distributions of FoxO1 and FoxO3a were measured after starvation
Summary
Forkhead box O (FoxO) transcription factors play a critical role in regulating cell growth, survival, apoptosis, differentiation and proliferation, metabolism, cell cycle arrest, and protection from oxidative stress in a variety of cell types (Accili & Arden, 2004). In conditions involving limited supply of these growth factors, the inhibition of FoxO activity by PI3K/Akt (phosphoinositide 3-kinase/serine threonine protein kinase) is relieved, and the FoxO transcription factors are activated and accumulate in the cell nucleus (Skurk et al, 2005). FoxO translocates into the nucleus and participates in the transcriptional activation of various genes involved in metabolism. Akt is an important effector molecule in the insulin-signalling pathway because it phosphorylates glucose transporters and glycogen synthase kinase to promote glucose absorption and glycogen synthesis (Taniguchi et al, 2006). This phosphorlyates and inhibits the activity of FoxO transcription factors (Barthel et al, 2005)
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