Chemical components that attract males in the laboratory were extracted from the female elytra of the white-spotted longicorn beetle, Anoplophora malasiaca (Thomson) (Coleoptera: Cerambycidae), and found to be comprised of several sesquiterpene hydrocarbons. Males located females that had fed on the bark of the host plant Citrus unshiu more frequently than those fed on an artificial diet in the laboratory. Male attraction was also confirmed in the corresponding sesquiterpene fractions of the host plant. The sesquiterpene fractions of female elytra and C. unshiu leaves showed quite similar GC profiles. In the field, the beetles were found on C. unshiu trees baited with intact females or males as frequently as those baited with the leaf extracts containing the sesquiterpenes at different purification levels. The beetles were found on those baited trees significantly more frequently than on unbaited control trees. Males, as well as females attracted both sexes, and the male elytra also contained the sesquiterpenes that were identical with those in female and C. unshiu. This indicated that active components in the elytra are acquired from C. unshiu by feeding, contact and/or adsorption. These sesquiterpenes may serve for intraspecific communication in A. malasiaca. The major sesquiterpenes from the C. unshiu leaves were isolated and elucidated by NMR analyses of four sesquiterpene hydrocarbons, b-elemene, b-caryophyllene, a-humulene, and a-farnesene.

Interspecific and latitudinal variation in diapause characteristics were examined in 12 strains of Orius species (Heteroptera: Anthocoridae) including O. sauteri (Poppius), O. nagaii Yasunaga, O. minutus (L.), O. strigicollis (Poppius), and O. tantillus (Motschulsky) from Japan. A latitudinal cline was found in the photoperiodic response controlling reproductive diapause: the lower the latitude, the lower the diapause incidence and the shorter the critical daylength. To examine the overwintering success, eight strains including four species derived from different latitudes (26-43 • N) were reared outdoors in Tsukuba (36 • N), central Japan from the autumn of 1998 to the summer of 1999, and their winter survival and spring fecundity were recorded. Most females of the northern strains entered diapause in the autumn when the temperature was still high, and died before winter without oviposition. In the southern strains including a nondiapause Okinawa (26 • N) strain of O. strigicollis, females overwintered as well as native strains in a state of quiescence. In all strains, the winter survival was significantly lower in males than in females, and eggs and nymphs failed to overwinter.

No abstract

During mammalian neocortical development, neural precursor cells generate neurons first and astrocytes later. The cell fate switch from neurons to astrocytes is a key process generating proper numbers of neurons and astrocytes. Although the intracellular mechanisms regulating this cell fate switch have been well characterized, extracellular regulators are still largely unknown. Here, we uncovered that fibroblast growth factor (FGF) regulates the cell fate switch from neurons to astrocytes in the developing cerebral cortex using mice of both sexes. We found that the FGF signaling pathway is activated in radial glial cells of the ventricular zone at time points corresponding to the switch in cell fate. Our loss-and gain-of-function studies using in utero electroporation indicate that activation of FGF signaling is necessary and sufficient to change cell fates from neurons to astrocytes. We further found that the FGF-induced neuron-astrocyte cell fate switch is mediated by the MAPK pathway. These results indicate that FGF is a critical extracellular regulator of the cell fate switch from neurons to astrocytes in the mammalian cerebral cortex.Although the intracellular mechanisms regulating the neuron-astrocyte cell fate switch in the mammalian cerebral cortex during development have been well studied, their upstream extracellular regulators remain unknown. By using in utero electroporation, our study provides in vivo data showing that activation of FGF signaling is necessary and sufficient for changing cell fates from neurons to astrocytes. Manipulation of FGF signaling activity led to drastic changes in the numbers of neurons and astrocytes. These results indicate that FGF is a key extracellular regulator determining the numbers of neurons and astrocytes in the mammalian cerebral cortex, and is indispensable for the establishment of appropriate neural circuitry.