The gut microbiome promotes locomotion of Drosophila larvae via octopamine signaling.

The gut microbiome is a key partner of animals, influencing various aspects of their physiology and behaviors. Among the diverse behaviors regulated by the gut microbiome, locomotion is vital for survival and reproduction, although the underlying mechanisms remain unclear. Here, we reveal that the gut microbiome modulates the locomotor behavior of Drosophila larvae via a specific neuronal type in the brain. The crawling speed of germ-free (GF) larvae was significantly reduced compared to the conventionally reared larvae, while feeding and excretion behaviors were unaffected. Recolonization with Acetobacter and Lactobacillus can fully and partially rescue the locomotor defects in GF larvae, respectively, probably due to the highest abundance of Acetobacter as a symbiotic bacterium in the larval gut, followed by Lactobacillus. Moreover, the gut microbiome promoted larval locomotion, not by nutrition, but rather by enhancing the brain levels of tyrosine decarboxylase 2 (Tdc2), which is an enzyme that synthesizes octopamine (OA). Overexpression of Tdc2 rescued locomotion ability in GF larvae. These findings together demonstrate that the gut microbiome specifically modulates larval locomotor behavior through the OA signaling pathway, revealing a new mechanism underlying larval locomotion regulated by the gut microbiome.

Portable ratiometric fluorescence detection of Cu2+and thiram.

Food contaminants pose a danger to human health, but rapid, sensitive and reliable food safety detection methods can offer a solution to this problem. In this study, an optical fiber ratiometric fluorescence sensing system based on carbon dots (CDs) and o-phenylenediamine (OPD) was constructed. The ratiometric fluorescence response of Cu2+and thiram was carried out by the fluorescence resonance energy transfer (FRET) between CDs and 2,3-diaminophenazine (ox-OPD, oxidized state o-phenylenediamine). The oxidation of OPD by Cu2+resulted in the formation of ox-OPD, which quenched the fluorescence of CDs and exhibited a new emission peak at 573 nm. The formation of a [dithiocarbamate-Cu2+] (DTC-Cu2+) complex by reacting thiram with Cu2+, inhibits the OPD oxidation reaction triggered by Cu2+, thus turning off the fluorescence signal of OPD-Cu2+. The as-established detection system presented excellent sensitivity and selectivity for the detection of Cu2+and thiram in the ranges of 1 ∼ 100µM and 5 ∼ 50µM, respectively. The lowest detection limits were 0.392µM for Cu2+and 0.522µM for thiram. Furthermore, actual sample analysis indicated that the sensor had the potential for Cu2+and thiram assays in real sample analysis.

Gut microbiome modulates Drosophila aggression through octopamine signaling.

Gut microbiome profoundly affects many aspects of host physiology and behaviors. Here we report that gut microbiome modulates aggressive behaviors in Drosophila. We found that germ-free males showed substantial decrease in inter-male aggression, which could be rescued by microbial re-colonization. These germ-free males are not as competitive as wild-type males for mating with females, although they displayed regular levels of locomotor and courtship behaviors. We further found that Drosophila microbiome interacted with diet during a critical developmental period for the proper expression of octopamine and manifestation of aggression in adult males. These findings provide insights into how gut microbiome modulates specific host behaviors through interaction with diet during development.

A genetic risk factor for thrombophilia in a Han Chinese family.

Thrombophilia is a multifactorial disorder involving environmental and genetic factors. Well­known factors that result in predisposition to congenital disorders associated with thrombophilia include antithrombin deficiency, protein C and S deficiency, Factor V Leiden mutation, abnormal prothrombin and antiphospholipid syndrome. The present study revealed an association between a mutation of the F2 gene, which codes for coagulation factor II, thrombin, and the risk of thrombophilia in a Han Chinese family, of which four members (I­2, II­2, II­3 and III­1) had a history of deep venous thromboembolism. The disease was measured in this family using laboratory measurements and computed tomography angiography. To identify the abnormality underlying the increased thrombophilia risk, whole­exome sequencing technology was used to analyze two affected individuals (II­2 and III­1). An exonic missense F2 mutation, T165M (NM_000506:c.C494T:p.T165M;rs5896), was identified from a total of 2,222 and 2,203 genetic variations observed in the two affected individuals, respectively, which were subsequently filtered and confirmed using Sanger sequencing. I­2, II­3 and III­1 shared this mutation with the proband (II­2), and II­6 had a heterozygous form of the mutation. This deleterious mutation was not identified in normal controls. The present study may improve understanding of the function of the F2 gene.