In this investigation the NlVg relative transcript level was

In this investigation, the NlVg relative transcript level was also prompted by 1.3-fold compared to the untreated control in the TZP treatment, while there was a slight increase of 13.6% for NlVgR (Fig. 7A and B). One underlying molecular mechanism for the TZP-induced fecundity is the significant up-regulation of Vg expression and Vg protein level (Bao et al., 2010; Ge et al., 2011b). The protein accumulation of fat bodies and ovaries was largely reduced after dsHex-1 diet (Fig. 4). Vg is a female-specific protein that is mainly synthesized in the fat body and transferred by vitellogenin receptor (VgR) into growing oocytes (Lu et al., 2015; Tufail and Takeda, 2009), generally regarded as a key molecular marker for insect fecundity (Qiu et al., 2016). Reduced fecundity has been recorded when VgR expression is suppressed by a mutation in Bombyx mori (Ying et al., 2013) or by RNAi in N. lugens (), which was clearly exhibited in TZP + dsHex-1-treated female adults with substantially decreased NlVg and NlVgR mRNA transcript (Fig. 7A and B). The western blot analysis (Fig. 7C) strongly supported this point of view. In terms of T. castaneum, after the TcHexA1 dsRNA injection, oviposition is almost completely abolished (Fraga et al., 2013). We observed that TZP + dsHex-1 treatment led to reduced the number of eggs laid (Fig. 6). Upon dissection of the ovaries, few fully developed oocytes were observed in TZP + dsHex-1 group; however, ovarioles of the TZP and TZP + dsGFP groups displayed three or more ripe banana-shaped oocytes (Fig. 8). This underdeveloped ovary morphology is probably related to oviposition reduction after Hex-1 suppression (Fig. 6). To sum up, we inferred that RNAi-Hex-1 might result in down-regulation of NlVg and NlVgR expression, affect Vg synthesis in female fat body, and hamper the ovary development, which can be the root cause for the reduced egg-laying. In conclusion, glycolysis as the primary approach to AR-13324 production, was disrupted in the initial step by Hex-1 silencing, resulting in substantially decreased contents of protein, soluble sugar, glucose as well as reduced Vg protein level and eggs laid, which corroborates our hypothesis that Hex-1 serves as an energy switch in modulating insect fecundity and glycometabolic homeostasis. This report together with our previous work (Ge et al., 2017) systematically elucidates the molecular mechanisms whereby the glycolytic pathway implicate insect fecundity physiology, which may assist in novel management of insect pest.
Conflict of interest
Acknowledgement This work was co-financed by grants in aid from the National Key R & D Program of China (2017YFD0200400), the  Natural Science Foundation of Jiangsu Province (BK20171283), the National Natural Science Foundation of China (31872283).
Introduction Leaf senescence is a part of normal plant life cycle, which is associated with degradation and recycling of macromolecules. It is well characterized by a decline in chlorophyll content and in photosynthetic activity (Van Doorn and Woltering, 2004, Lim et al., 2007). Leaf senescence is regulated by various external and internal factors, such as shortening of the light period in autumn, drought stress, nitrogen deficiency, natural shading or induced darkness. Internal factors, such as the lack of nutrients, changes in sink–source relations or in intracellular sugar levels participate also in the induction of senescence (Van Doorn, 2008, Zhang and Zhou, 2013). Starvation or accumulation of sugars can also induce senescence, which strongly depends on the experimental setup thus there are controversial hypotheses and results in this field (Van Doorn, 2008). It can be concluded that sugars, especially hexoses are not only one, but very important factors in the initiation of senescence. Other senescence-inducing components can also be found in mitochondria, thus they connect sugar metabolism to the initiation of senescence (Bolouri-Moghaddam et al., 2010). Both the mitochondrial and chloroplastic electron transport chains may generate reactive oxygen species (ROS) in plant cells. The imbalance between ROS production and antioxidant defence leads to oxidative stress, which contributes to the initiation of cell death. These processes can be different in light or dark environments (Poór et al., 2017).