Integration of genomic and nongenomic pathways in juvenile hormone signaling inAedes aegypti

2016 ◽  
Author(s):  
Pengcheng Liu



2021 ◽  
Vol 118 (39) ◽  
pp. e2104461118
Author(s):  
Wei Luo ◽  
Suning Liu ◽  
Wenqiang Zhang ◽  
Liu Yang ◽  
Jianhua Huang ◽  
...  

It is well documented that the juvenile hormone (JH) can function as a gonadotropic hormone that stimulates vitellogenesis by activating the production and uptake of vitellogenin in insects. Here, we describe a phenotype associated with mutations in the Drosophila JH receptor genes, Met and Gce: the accumulation of mature eggs with reduced egg length in the ovary. JH signaling is mainly activated in ovarian muscle cells and induces laminin gene expression in these cells. Meanwhile, JH signaling induces collagen IV gene expression in the adult fat body, from which collagen IV is secreted and deposited onto the ovarian muscles. Laminin locally and collagen IV remotely contribute to the assembly of ovarian muscle extracellular matrix (ECM); moreover, the ECM components are indispensable for ovarian muscle contraction. Furthermore, ovarian muscle contraction externally generates a mechanical force to promote ovulation and maintain egg shape. This work reveals an important mechanism for JH-regulated insect reproduction.



PLoS Genetics ◽  
2014 ◽  
Vol 10 (1) ◽  
pp. e1004098 ◽  
Author(s):  
Hiroki Gotoh ◽  
Hitoshi Miyakawa ◽  
Asano Ishikawa ◽  
Yuki Ishikawa ◽  
Yasuhiro Sugime ◽  
...  


2015 ◽  
Vol 112 (12) ◽  
pp. 3740-3745 ◽  
Author(s):  
Jesus Lozano ◽  
Raúl Montañez ◽  
Xavier Belles

In 2009 we reported that depletion of Dicer-1, the enzyme that catalyzes the final step of miRNA biosynthesis, prevents metamorphosis inBlattella germanica. However, the precise regulatory roles of miRNAs in the process have remained elusive. In the present work, we have observed that Dicer-1 depletion results in an increase of mRNA levels of Krüppel homolog 1 (Kr-h1), a juvenile hormone-dependent transcription factor that represses metamorphosis, and that depletion of Kr-h1 expression in Dicer-1 knockdown individuals rescues metamorphosis. We have also found that the 3′UTR of Kr-h1 mRNA contains a functional binding site for miR-2 family miRNAs (for miR-2, miR-13a, and miR-13b). These data suggest that metamorphosis impairment caused by Dicer-1 and miRNA depletion is due to a deregulation of Kr-h1 expression and that this deregulation is derived from a deficiency of miR-2 miRNAs. We corroborated this by treating the last nymphal instar ofB. germanicawith an miR-2 inhibitor, which impaired metamorphosis, and by treating Dicer-1-depleted individuals with an miR-2 mimic to allow nymphal-to-adult metamorphosis to proceed. Taken together, the data indicate that miR-2 miRNAs scavenge Kr-h1 transcripts when the transition from nymph to adult should be taking place, thus crucially contributing to the correct culmination of metamorphosis.



2015 ◽  
Vol 11 ◽  
pp. 39-46 ◽  
Author(s):  
Marek Jindra ◽  
Xavier Bellés ◽  
Tetsuro Shinoda


FEBS Journal ◽  
2005 ◽  
Vol 272 (7) ◽  
pp. 1577-1589 ◽  
Author(s):  
Fang Fang ◽  
Yong Xu ◽  
Davy Jones ◽  
Grace Jones


Sign in / Sign up

Export Citation Format

Share Document