Diapause hormone directly stimulates the prothoracic glands of diapause larvae under juvenile hormone regulation in the bamboo borer, Omphisa fuscidentalis Hampson.

Larval diapause in many lepidopteran insects is induced and maintained by high juvenile hormone (JH). In the case of the bamboo borer, Omphisa fuscidentalis, the effect of JH is the opposite: The application of juvenile hormone analog (JHA: S-methoprene) terminates larval diapause, unlike in other insect species. Here, we analyzed the expression of JH-receptor Met, DH-PBAN, and Kr-h1 in the subesophageal ganglion (SG) from October to April using semi-quantitative polymerase chain reaction (PCR).

Larval diapause termination in the bamboo borer, Omphisa fuscidentalis.

In insects, juvenile hormone (JH) and 20-hydroxyecdysone (20E) regulate larval growth and molting. However, little is known about how this cooperative control is terminating larval diapause especially in the bamboo borer, Omphisa fuscidentalis. In both in vivo and in vitro experiments, we here measured the expression levels of genes which were affected by juvenile hormone analogue (JHA: S-methoprene) and 20-hydroxyecdysone (20E) in diapausing O.

Molecular characterization and gene expression of juvenile hormone binding protein in the bamboo borer, Omphisa fuscidentalis.

Juvenile hormone (JH) plays an important role in many physiological processes in insect development, diapause and reproduction. An appropriate JH titer in hemolymph is essential for normal development in insects. Information concerning its carrier partner protein, juvenile hormone binding protein (JHBP), provides an alternative approach to understanding how JH regulates metamorphosis.

Programmed cell death of larval tissues induced by juvenile hormone in the bamboo borer, Omphisa fuscidentalis.

Programmed cell death (PCD) plays a critical role during animal development through the destruction of unneeded cells and tissues. In some insects, the prothoracic glands (PGs) and anterior silk glands (ASGs) are larval-specific tissues that are normally eliminated by PCD after pupation. Previous studies report that juvenile hormone analog (JHA) terminates the larval diapause of Omphisa fuscidentalis by increasing the hemolymph ecdysteroids that trigger PCD.

Ca2+-PKC-caspase 3-like protease pathway mediates DNA and nuclear fragmentation in ecdysteroid-induced programmed cell death.

20-Hydroxyecdysone (20E) induces programmed cell death in the anterior silk gland of the silkworm. Here, we report the direct interaction between Ca(2+) and protein kinase C (PKC)-caspase 3-like protease pathway in the 20E-induced cell death. The calcium ionophore can mimic 20E effects in inducing DNA and nuclear fragmentation, but such mimicry is only possible in the glands precultured for 18 h with 20E.

Intracellular mobilization of Ca2+ by the insect steroid hormone 20-hydroxyecdysone during programmed cell death in silkworm anterior silk glands.

20-Hydroxyecdysone (20E) triggers programmed cell death (PCD) and regulates de novo gene expression in the anterior silk glands (ASGs) of the silkworm Bombyx mori. PCD is mediated via a nongenomic pathway that includes Ca2+ as a second messenger and the activation of protein kinase C/caspase-3-like protease; however, the steps leading to a concomitant buildup of intracellular Ca2+ are unknown. We employed pharmacological tools to identify the components of this pathway.

Hormonal mechanisms underlying termination of larval diapause by juvenile hormone in the bamboo borer, Omphisa fuscidentalis.

Topical application of methoprene, a juvenile hormone analogue (JHA), induces pupation by activating the prothoracic glands (PGs) in diapausing larvae of the bamboo borer, Omphisa fuscidentalis. To determine the minimum stimulation period for PG activation, we transplanted PGs of JHA-treated larvae (donors) into non-treated larvae (recipients) on successive days after JHA treatment and observed the recipients for pupation. JHA stimulation for 1 day was sufficient to induce pupation.