Artemia is a genus of halophilic zooplanktons comprising bisexual and parthenogenetic forms, which is an important model for investigating adaption to hypersaline ecosystems. The genus Artemia in China comprises four species: A. sinica, A. tibetiana, A. franciscana and A. parthenogenetica. To investigate the evolutionary relationship of bisexual and parthenogenetic Artemia in China, we analyzed the morphometrics and phylogenetics among twenty-two geographical populations in China. We found significant morphological differentiation across different species and strains of Artemia in China, which exhibited a high level of intra-population variation. We also found overlaps in morphological characteristics between populations, which may raise challenges for the classification of Artemia species using traditional morphological methods. A. franciscana, which originated from various regions in America, was generally distributed along the Chinese coastlines through multiple human introductions. Additionally, native Asian clades split into Western and Eastern Lineages during the late Miocene due to the Himalayan orogeny. Within the Western Lineage, A. tibetiana can be grouped into three taxon units: A. tibeitiana, A. sorgeloosi and A. urmiana. We also found that the distribution and genetic structure of A. sinica were influenced by climate oscillations during the Pleistocene, which might play a pivotal role in driving the formation of parthenogenetic strains in the Eastern Lineage. Overall, our study provides new insight into invertebrate evolution under geographical and climatic impacts in hypersaline environments.

Energy metabolism is essential for insect development, reproduction and detoxification. Insects often reallocate energy and resources to manage external stress, balancing the demands of detoxification and reproduction. Glucose transport 4 (Glut4), a glucose transporter, is involved in glucose and lipid metabolism. However, the specific molecular mechanism of Glut4 in insect reproduction, and its role in the response to insecticide-induced oxidative stress remain unclear. In this study, LmGlut4 was identified and analyzed in Locusta migratoria. Silencing of LmGlut4 significantly reduced vitellogenin (Vg) biosynthesis in the fat body and Vg absorption by oocytes, ultimately hindering ovarian development and oocyte maturation. Knockdown of LmGlut4 also inhibited the biosynthesis of key insect hormones, such as juvenile hormone (JH), 20-hydroxyecdysone (20E) and insulin. Furthermore, LmGlut4 knockdown led to reduced triglyceride (TG) and glycogen content in the fat body and ovary, as well as decreased capacity for trehalose biosynthesis in adipocytes. Additionally, dsLmGlut4-treated locusts showed heightened sensitivity to deltamethrin, leading to increased triglyceride depletion during detoxification. This study sheds light on the biological function of LmGlut4 in the ovary and provides potential target genes for exploring biological pest management strategies.

The TRP channel superfamily was widely found in multiple species. They were involved in many extrasensory perceptions and were important for adapting to the environment. The migratory locust was one of the worldwide agricultural pests due to huge damage. In this study, we identified 13 TRP superfamily genes in the locust genome. The number of LmTRP superfamily genes was consistent with most insects. The phylogenetic tree showed that LmTRP superfamily genes could be divided into seven subfamilies. The conserved motifs and domains analysis documented that LmTRP superfamily genes contained unique characteristics of the TRP superfamily. The expression profiles in different organs identified LmTRP superfamily genes in the head and antennae, which were involved in sensory function. The expression pattern of different life phases also demonstrated that LmTRP superfamily genes were mainly expressed in third-instar nymphs and male adults. Our findings could contribute to a better understanding of the TRP channel superfamily gene and provide potential targets for insect control.