Chemical detoxification vs mechanical removal of host plant toxins in Eucalyptus feeding sawfly larvae (Hymenoptera: Pergidae).

The essential oils that characterize the eucalypts and related Myrtaceae pose a challenge for herbivores. Phytophagous insects that feed on oil-rich Myrtaceae have developed specific mechanisms to deal with these oils, some of which are notoriously toxic (e.g. 1,8-cineole). Some of the eight Australian subfamilies in the sawfly family Pergidae are associated exclusively with Eucalyptus and Melaleuca species that often have high concentrations of essential oils. Unexpectedly, the Perginae and Pterygophorinae use different mechanisms to deal with the same toxic components in their respective host plants. Larvae of the Perginae have the inner surface of their mandibles equipped with soft brush-like structures that are unique among phytophagous insects in general. The proposed role of these ancillary mandibular structures in separating leaf oils from nutritive plant matter could be confirmed in experiments with larvae of two pergine species. The oil sequestration is, however, incomplete and chemical gut content analyses by gas-chromatography (GC) revealed that 1,8-cineole does enter the midgut and is metabolised to hydroxycineole. Although the related Pterygophorinae also feed mainly on oil-rich Myrtaceae, they do not sequester the oil and lack morphological structures on their mandibles. Chemical analysis of the gut content of two pterygophorine species showed that they rely solely on chemical detoxification of the relevant plant compounds, with GC demonstrating that the 1,8-cineole is removed far more rapidly and completely than in the pergine species.

Mating activity of Bactrocera cacuminata (Hering) (Diptera: Tephritidae) on its larval host plant Solanum mauritianum Scopoli in southeast Queensland.

A detailed study was conducted on the mating behaviour of Bactrocera cacuminata (Hering) (Diptera: Tephritidae) in nature. Plant tissues from Solanum mauritianum Scopoli, the primary larval host for B. cacuminata, were also analysed for methyl eugenol content. In the field, over a 15 month period, 44,171 observations of adult B. cacuminata individuals were made including 1109 mating pairs on S. mauritianum. Calling behaviour consisting of wing fanning and anus beating by males was also consistently observed on the underside of leaves of S. mauritianum after sunset. Female flies that arrived into these groups of 10-15 calling males were mated and often remained coupled until dawn. No methyl eugenol was detected from the analysis of leaves, flowers and fruits of S. mauritianum. Thus, B. cacuminata does not need to aggregate at sites where methyl eugenol is present and the hypothesis that this chemical plays a role in the selection of mating sites by B. cacuminata is not supported by the current study. It is concluded that S. mauritianum is the primary site of mating for B. cacuminata in nature and that the concept that the larval host plant is the centre of activity for dacine fruit flies remains robust, being fully supported by the results of this study.

Determination of free choline in plasma and erythrocyte samples and choline derived from membrane phosphatidylcholine by a chemiluminescence method.

A sensitive chemiluminescence method for assay of choline which has been developed for analysis of erythrocyte and plasma levels of choline is reported here. This method includes a charcoal purification step which yields consistent results with plasma and erythrocyte extracts. Further, choline derived from membrane phosphatidylcholine may also be measured by an extension of this method following digestion with phospholipase D. This method has been used to study abnormal levels of erythrocyte choline that occur in cluster headache patients compared to control subjects and migraine patients. In addition, the time course of changes in plasma and erythrocyte choline following a fatty meal have been monitored. Plasma choline levels rise to a maximum between 1 and 3 h after the meal and this is followed by a rise in erythrocyte choline levels which are maximal 3 h after the meal.