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Perri, G.

Publications and source records attributed to Perri, G..

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Nutrition of honeybees is constrained by the ratios of essential amino acids in pollen protein

Bees pollinate most of the worlds flowering plants and collect and eat floral pollen as their sole source of dietary protein, yet we know relatively little about nutritional constraints imposed on them by pollinivory. Pollen protein provides bees with essential amino acid (EAA) profiles that vary as a function of plant species, but the extent of this variation and its impact on bee feeding behaviour and performance are unknown. Here, we measured the EAA profiles of pollen, bee bread, honeybees, and royal jelly to understand natural variation in protein quality and tested how mismatches in EAAs relative to bee tissues impacted protein-to-carbohydrate regulation in adult workers. Bees fed diets with an EAA profile that matched their own tissues consumed more food, gained more weight, and ate proportionally more protein relative to carbohydrate (1:72 EAA:C) while those fed with pollen sources including bee bread ate proportionally less protein and less food overall. Deficiencies found in pollen led us to discover that nutrient balancing for protein and carbohydrate in bees was driven by the inverse relationship between quantities of the branched-chain amino acids relative to histidine in dietary protein. We predict that the creation of bee bread, a mixture of bee-collected pollen, is a general adaptation to pollen feeding that reduces the impact of imbalances in the EAA profile of pollen protein.

ecology↗

Loss of TRIM21 drives UVB-induced systemic inflammation by regulating DNA-sensing pathways

BackgroundExposure of systemic lupus erythematosus (SLE) patients to ultraviolet light B (UVB) triggers local and systemic inflammation, with cytosolic DNA sensing and induction of type I interferons (IFNs) known to play a role. We previously identified TRIM21 as a negative regulator of DNA sensing and IFN expression. Here we explore the role of TRIM21 in regulating local and systemic responses following UVB exposure. MethodsWT (C57BL/6) and Trim21-/- mice were irradiated with UVB (100mJ/cm2) daily for 1 and 3 weeks, and UVB-induced inflammation in skin, blood, and spleen were analyzed by qPCR, histology, RNA sequencing and flow cytometry. Mechanistic studies were performed in bone marrow-derived macrophages (BMDMs) and mouse skin fibroblasts (MDF) from WT and Trim21-/- mice, and TRIM21-/-THP-1 cells. ResultsInfiltration of inflammatory cells and induction of type I IFN developed in UVB-exposed areas in both sets of mice, however Trim21-/-mice developed splenomegaly, enhanced total IgG levels and IFN-stimulated genes (ISG) in the blood and spleen. Enhanced basal and UVB-dependent Ifnb1 expression was observed in Trim21-/- BMDMs and MDFs, which was dependent on the cytosolic DNA sensing cGAS-STING pathway. Mechanistically, we found both degradation of DDX41 and STING levels were impaired in stimulated Trim21-/-BMDMs. ConclusionTaken together, our results indicate that TRIM21 protects against IFN induction at local and systemic levels through restricting STING signaling. Our finding that reduced levels of TRIM21 are observed in SLE patients with cutaneous involvement indicates a potential role for TRIM21 in guarding against systemic flare in SLE patients.

immunology↗