Injection of Dip-allatostatin or Dip-allatostatin pseudopeptides into mated female Diploptera punctata inhibits endogenous rates of JH biosynthesis and basal oocyte growth
Cs. Garside et al., Injection of Dip-allatostatin or Dip-allatostatin pseudopeptides into mated female Diploptera punctata inhibits endogenous rates of JH biosynthesis and basal oocyte growth, INSEC BIO M, 30(8-9), 2000, pp. 703-710
Studies on the catabolism of allatostatins (ASTs) provided the rationale fo
r the design of a series of Dip-allatostatin-derived pseudopeptide mimetic
analogues. In vitro, the Dip-ASTs and pseudopeptides show varying degrees o
f resistance to catabolism and all show significant inhibition of juvenile
hormone (JH) biosynthesis. This study was undertaken to determine whether p
otent Dip-ASTs and/or their pseudopeptide mimetic counterparts caused 'alla
tostatic' effects in vivo following injection into mated female Diploptera
punctata. Animals injected with aqueous solvent or Dip-AST 7(1-7) N-termina
l fragment, which excludes the active core region of the ASTs, were used as
controls. An in vitro radiochemical assay revealed that injection of Dip-A
ST 5, 7 or pseudopeptide analogues 397-2 or AST(b)phi 2 significantly inhib
ited the biosynthesis of JH (P<0.05). The results also indicate that basal
oocyte growth was significantly inhibited by injection of these same compou
nds, with the exception of Dip-AST 7 (P<0.05). Analogues 396-1 and 419 did
not significantly inhibit rates of JH biosynthesis but did significantly in
hibit the growth of basal oocytes. Analyses of feeding, excretion and food
absorption/utilization patterns of these same animals suggested that these
compounds are not toxic to the insect; rather they directly inhibit the bio
synthesis of JH by the corpora allata, and reduce the rate of growth of bas
al oocytes. Disruption of critical reproductive and/or developmental proces
ses by pseudopeptide analogues of the ASTs could provide novel and selectiv
e strategies for future insect pest management. (C) 2000 Elsevier Science L
td. All rights reserved.