Juvenile Hormone Activates the Transcription of Cell-division-cycle 6 (Cdc6) for Polyploidy-dependent Insect Vitellogenesis and Oogenesis

Abstract

Although juvenile hormone (JH) is known to prevent insect larval metamorphosis and stimulate adult reproduction, the molecular mechanisms of JH action in insect reproduction remain largely unknown. Earlier, we reported that the JH-receptor complex, composed of methoprene-tolerant and steroid receptor co-activator, acts on mini-chromosome maintenance (Mcm) genes Mcm4 and Mcm7 to promote DNA replication and polyploidy for the massive vitellogenin (Vg) synthesis required for egg production in the migratory locust (Guo, W., Wu, Z., Song, J., Jiang, F., Wang, Z., Deng, S., Walker, V. K., and Zhou, S. (2014) PLoS Genet. 10, e1004702). In this study we have investigated the involvement of cell-division-cycle 6 (Cdc6) in JH-dependent vitellogenesis and oogenesis, as Cdc6 is essential for the formation of prereplication complex. We demonstrate here that Cdc6 is expressed in response to JH and methoprene-tolerant, and Cdc6 transcription is directly regulated by the JH-receptor complex. Knockdown of Cdc6 inhibits polyploidization of fat body and follicle cells, resulting in the substantial reduction of Vg expression in the fat body as well as severely impaired oocyte maturation and ovarian growth. Our data indicate the involvement of Cdc6 in JH pathway and a pivotal role of Cdc6 in JHmediated polyploidization, vitellogenesis, and oogenesis.

Azadirachtin effects on mating success, gametic abnormalities and progeny survival in Drosophila melanogaster (Diptera)

“…Furthemore, azadirachtin interferes with ecdysteroid synthesis and vitellogenin synthesis (and/or its uptake), affecting oocyte development via JH as noted in D. melanogaster . The impact of azadirachtin on D. melanogaster adult females, as highlighted here, thus may be related to the fact that JH stimulates vitellogenesis for the developing oocytes and, together with 20E and insulin‐signalling pathways, controls the nutrient‐sensitive checkpoint in oogenesis . Reduction in the cyst number and the abnomalities observed can be explained by the impact of azadirachtin on the meiotic process responsible for sperm production and on histological and cellular structures .…”

Juvenile hormone signaling – a mini review

“…In L . migratoria , JH signaling promotes endoreplication of adult fat body cells to prepare the female for vitellogenesis (Guo et al ., ; Song et al ., ; Wu et al ., ) and is indispensable for basal oocyte development (Marchal et al ., ). In P .…”

“…Different from the status quo action, the roles of JH in regulating female reproduction vary greatly from species to species. In L. migratoria, JH signaling promotes endoreplication of adult fat body cells to prepare the female for vitellogenesis (Guo et al, 2014;Song et al, 2014;Wu et al, 2016) and is indispensable for basal oocyte development (Marchal et al, 2014). In P. apterus, reduction of expression of Met or Tai, but not Kr-h1, blocked ovarian development and suppressed vitellogenin gene expression (Smykal et al, 2014a).…”

Protein kinase C mediates juvenile hormone–dependent phosphorylation of Na+/K+-ATPase to induce ovarian follicular patency for yolk protein uptake

“…By in vivo Vg uptake assays, we documented that knocking down Na ϩ /K ϩ -ATPase ␣-subunit precluded methoprene-induced ovarian Vg uptake. As locust ovaries are panoistic, Vg is synthesized in the fat body, released into hemolymph, and transported to maturing oocytes through patency in the follicular epithelium (1,63,64). The reduced Vg uptake from Na ϩ /K ϩ -ATPase ␣-subunitdepleted adult female locusts might consequently result in impaired oocyte maturation and ovarian growth.…”