Two insulin receptors coordinate oogenesis and oviposition via two pathways in the green lacewing, Chrysopa pallens

Abstract

Insulin signalling in insects, as in mammals, regulates various physiological functions, such as reproduction. However, the molecular mechanism by which insulin signals orchestrate ovarian stem cell proliferation, vitellogenesis, and oviposition remains elusive. Here, we investigate the functions of the phosphoinositide 3-kinase (PI3K)-serine/threonine kinase (Akt) pathway, GTPase Ras/mitogen-activated protein kinase (MAPK) pathway, and their downstream messengers in a natural predator, Chrysopa pallens, by the RNAi method. When C. pallens vitellogenin gene 1 (CpVg1) expression was knocked down, the follicle maturation was arrested and total fecundity was reduced. Silencing C. pallens insulin receptor 1 (CpInR1) suppressed Vg transcription and reduced egg mass and hatching rate. Depletion of C. pallens insulin receptor 2 (CpInR2) transcripts lowered Vg transcript level, hampered ovarian development and decreased reproductive output. Knockdown of C. pallens Akt (CpAkt) and C. pallens extracellular-signal-regulated kinase (Cperk) caused phenotypes similar to those caused by knockdown of CpInR2. Disruption of C. pallens transcription factor forkhead box O (CpFoxO) expression caused no significant effects on ovarian development, but sharply impaired total fecundity. Interference with the expression of C. pallens target of rapamycin (CpTor) gene and C. pallens cAMP-response element binding protein (CpCreb) gene led to a down-regulation of Vg transcription, blocking of ovariole growth, and decrease in egg quality. These results suggested the two CpInRs orchestrate oogenesis and oviposition via two signalling pathways to guarantee natural reproduction in the green lacewing, C. pallens.