Pea aphid clonal resistance to the endophagous parasitoid Aphidius ervi

The physiological mechanism of resistance to the endophagous braconid Aphidius ervi Haliday (Hymenoptera, Braconidae) by a pink clone (PC) of Acyrthosiphon pisum (Harris) (Homoptera, Aphididae) has been investigated. Comparative data on parasitoid development and associated host biochemical changes in the resistant PC aphids and in a susceptible green clone (GC) of A. pisum are reported. When the PC aphids were attacked as early 4th instars, the developing parasitoid larvae showed a strongly reduced increase in size, compared to those synchronously developing in GC aphids, and were unable to produce a regular mummy. In contrast, parasitism of 2nd instar PC aphids, allowed completion of parasitoid development, but adults had a prolonged developmental time, due to a longer duration of parasitoid’s final (3rd) instar. In all cases, teratocytes, cells deriving from the A. ervi serosal membrane, and the proteins abundantly synthesised by them, were never found in the haemolymph of parasitised PC aphids. Host castration, as demonstrated by total protein incorporation into reproductive tissues, was total in the majority of early (2nd instar) parasitised host aphids, while it was limited when later instars (4th) of PC aphids were parasitised. This is partly due to the absence of the cytolytic activity of teratocytes on host embryos, which, through their persistence, may compete for nutritional resources with the developing parasitoid larvae. In parasitised PC aphids, this competitive effect is further aggravated for the parasitoid by the absence of the regulated amino acid titre increase in the host haemolymph, which is regularly observed in GC aphids. Failure of teratocyte development in the PC clone of the pea aphid is, then, the major functional constraint accounting for the reduction/inhibition of A. ervi larval growth. The reported results allow to assess in vivo the role of teratocytes in the host physiological redirection and nutritional exploitation by the parasitoid, and to integrate and validate the proposed physiological model of host-parasitoid interactions in the system A. pisum-A.ervi.