Journal of insect physiology最新文献

Environmental temperature and humidity fluctuations influence insect survival and adaptation, with relevance to both contemporary pest management and future climate scenarios. The cuticle, as the primary physical barrier against environmental stress, critically determines insect adaptive capacity. Here, we investigated the role of PxPCP, a pupal cuticular protein gene, in environmental adaptation of the diamondback moth Plutella xylostella, a globally distributed pest, using CRISPR/Cas9-mediated gene editing. PxPCP knockout significantly impaired developmental performance and reproductive capacity under high temperature while reducing tolerance to temperature extremes and desiccation stress. Mutants displayed increased cuticular permeability and, unexpectedly, elevated body water content under desiccation, indicating that PxPCP regulates active water homeostasis beyond forming passive physical barriers. Transcriptional analysis revealed that PxPCP deficiency triggered compensatory upregulation of cuticle-related genes, including chitin synthase and cuticular lipid metabolism enzymes; however, these transcriptional compensations failed to fully restore cuticular barrier function. Moreover, PxPCP deletion disrupted expression of water homeostasis-related genes, including downregulation of hygroreception sensors and diuretic hormone signaling components, coupled with dysregulated ion transport and osmoprotectant biosynthesis genes, providing molecular evidence for the observed systemic water balance dysfunction. Collectively, our findings demonstrate that PxPCP plays a pivotal role in environmental adaptation by regulating cuticle formation and water homeostasis, providing a molecular basis for understanding the persistent outbreak success of this pest under climate change. These findings offer novel insights into the molecular mechanisms underlying insect climate adaptation and identify a promising molecular target for developing climate-informed pest management strategies.

Diapause in many insects is a non-feeding state, yet energetic demands persist. This imbalance between energy in and energy out can be met by two main mechanisms: reduced metabolism, facilitated by decreasing temperatures, and storage of nutrients. In bivoltine insects, some individuals may continue direct development while others may enter diapause. Few studies have compared these two groups prior to the decision to diapause, even though biochemical differences are likely due to accumulation of nutrient stores and molecules involved in metabolic suppression. In Megachile rotundata, offspring oviposited in early summer develop directly to adults, while those oviposited later that summer enter diapause as prepupae. Here we test the hypothesis that prepupae between the two groups have distinct metabolomic signatures that will indicate key differences in energetic status. We collected 12 non-diapause and 15 diapause-destined nests. Two prepupae from each nest were flash frozen and kept in -80°C until extracted. Diapause state of frozen bees was verified by observing whether nestmates developed or underwent diapause. We used an untargeted GC-MS-based approach that identified 57 significant metabolites with the potential to differentiate between diapause-destined and non-diapause prepupae. Altered metabolites included sugars, polyols, intermediates of the tricarboxylic acid (TCA) cycle, and amino acids. Seventeen metabolites (60% carbohydrates) were more abundant in diapause destined prepupae. Forty metabolites (30% amino acids) were more abundant in non-diapausing prepupae. Several metabolites were previously implicated in diapausing insects. Some metabolites, e.g., putrescine, could be used as a biomarker to identify diapause status of nests, benefitting bee growers and farmers.

The fruit fly Drosophila melanogaster is a valuable model for studying cellular and metabolic processes conserved with mammals. Using its embryonic Schneider S2 cell line, a widely employed system for heterologous protein expression, we investigated how cell growth progression and short-term slight temperature changes affect mitochondrial physiology via high-resolution respirometry. We assessed five mitochondrial bioenergetic parameters and two coupling parameters at 2nd (early) and 7th (late) days of culture, and at two temperatures (26°C and 28°C). We observed that culture time is the overwhelming driver of cell density variation, while temperature effect is only modest. Importantly, a modest 2°C increase, combined with progression to the late growth phase, synergistically enhanced basal, OXPHOS, and leak respiration, while only marginally affecting coupling efficiency. Notably, spare and maximal respiratory capacities rose disproportionately with either cell growth or mild temperature increase, suggesting mitochondrial biogenesis and functional remodeling. These findings reveal that minor, short-term temperature shifts can elicit rapid mitochondrial acclimation that enhances bioenergetic capacity and metabolic flexibility without compromising efficiency. Such responses exemplify mitochondrial plasticity to environmental and developmental cues and may inform strategies to modulate mitochondrial physiology across biological and biomedical contexts.

Insect metamorphosis needs substantial energy mobilization, and lipid serves as a crucial energy resource during the non-feeding pupal stage. The Broad Complex (BR-C) acts as a critical mediator of ecdysone signaling, which is the key regulator of insect metamorphosis. While the functions of BR-C in developmental transitions have been extensively characterized, its potential role in regulating lipid metabolism remains largely unexplored. Here, we demonstrate that BR-C is essential for lipid synthesis in the fat body during the larval-pupal transition. BR-C knockdown in both Bombyx and Drosophila resulted in significantly reduced lipid contents in the fat body and downregulated transcription of critical lipid synthase genes, including long-chain acyl-CoA synthetase (Acsl) and phosphatidic acid phosphatase (Lipin). We further identified the nuclear receptor gene HR96 as a direct target of BR-C and showed that HR96 knockdown phenocopied the reduced lipid synthesis that caused by BR-C knockdown. Mechanistically, we revealed that HR96 protein directly binds to the promoter regions of Acsl and Lipin to activate their transcription. Together, our findings establish a novel BR-C-HR96-lipid synthesis cascade that is functionally conserved in insects.