Dataset Information

Gut microbiome drives individual memory variation in bumblebees

ABSTRACT:

The potential of the gut microbiome as a driver of individual cognitive differences in natural populations of animals remains unexplored. Here, using metagenomic sequencing of individual bumblebee hindguts, we find a positive correlation between the abundance of Lactobacillus Firm-5 cluster and memory retention on a visual discrimination task. Supplementation with the Firm-5 species Lactobacillus apis (L. apis), but not other non-Firm-5 bacterial species, enhances bees’ memory. Untargeted metabolomics after L. apis supplementation show increased LPA (14:0) glycerophospholipid in the haemolymph. Oral administration of the LPA increases long-term memory significantly. Based on our findings and metagenomic/metabolomic analyses, we propose a molecular pathway for this gut-brain interaction. Our results provide insights into proximate and ultimate causes of cognitive differences in natural bumblebee populations.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS3637 | MetaboLights | 2021-11-16

REPOSITORIES: MetaboLights

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	HFX3_CN1_FZTM191633647-1A.raw	Raw
	HFX3_CN1_FZTM191633648-1A.raw	Raw
	HFX3_CN1_FZTM191633649-1A.raw	Raw
	HFX3_CN1_FZTM191633650-1A.raw	Raw
	HFX3_CN1_FZTM191633651-1A.raw	Raw

Items per page:

1 - 5 of 78

Similar Datasets

Project description:Targeted HIV cure strategies require definition of the mechanisms that maintain the virus. Here, we tracked HIV replication and the persistence of infected CD4 T cells in individuals with natural virologic control by sequencing viruses, T cell receptor genes, HIV integration sites and cellular transcriptomes. Our results revealed three mechanisms of HIV persistence operating within distinct anatomic and functional compartments. In lymph node, we detected viruses with genetic and transcriptional attributes of active replication in both T follicular helper (TFH) cells and non-TFH memory cells. In blood, we detected inducible proviruses of archival origin among highly differentiated, clonally expanded cells. Linking the lymph node and blood was a small population of circulating cells harboring inducible proviruses of recent origin. Thus, HIV replication in lymphoid tissue, clonal expansion of infected cells, and recirculation of recently infected cells act together to maintain the virus in HIV controllers despite effective antiviral immunity. Fluorescence-activated cell sorting (FACS) was used to sort subsets of CD4 T cells from blood (peripheral blood mononuclear cells; PBMC) and lymph node from a cohort of HIV-infected people with natural control of the virus (termed HIV controllers). Subsets of CD4 T cells that were sorted are as follows: from blood, (1) naÃ¯ve (N), (2) central memory (CM), (3) transitional memory (TM), and (4) effector memory (EM); from lymph node, (1) naÃ¯ve (N), (2) non-germinal center T-follicular helpers (nGC), (3) germinal center T-follicular helpers (Tfh), (4) effector memory (EM), and (5) other central memory-like subsets (CMPD1lo57lo, CMPD1lo57hi, and/or CMPD1lo). Total RNA and total DNA were extracted from these sorted subsets in separate fractions using RNAzol RT and DNAzol. Total cellular DNA was used for HIV quantification and sequence analysis as describe in the publication. Total RNA used for mRNA library construction by oligo-dT purification (Dynabeads), random fragmentation by heating in the presence of Magnesium (in form of 5x first-strand buffer, LifeTech), reverse transcription (SuperScript III), and then second-strand synthesis, end repair, a-tailing, and adaptor ligation using NEBNext enzyme master mixes and oligonucleotides. Libraries were sequenced on an Illumina HiSeq2000. Please note that each 'source name' value represent individual who havs HIV infection with natural control of the virus.

Project description:Individuals with Down syndrome (DS) exhibit neurological deficits throughout the lifespan culminating in Alzheimer’s disease (AD) pathology and cognitive impairment during early mid-life. At the cellular level, dysregulation in neuronal gene expression has been shown in the human brain and mouse models of DS. However, RNA- sequencing (RNA-Seq) analysis of genomic neuronal expression in the hippocampus have been limited, without separation of neuronal populations based on circuitry inputs. We postulate spatially characterized hippocampal excitatory neurons will present with unique gene expression patterns due in part to unique circuitry inputs in the DS mouse model. Here, we combined laser capture microdissection (LCM) to isolate individual neuron populations with low input RNA-seq analysis to determine gene expression analysis of three excitatory neuron populations from the rostral hippocampus. We utilized the Ts65Dn mouse model of DS at the start of degeneration (6MO) to query gene expression profiles of CA1 and CA3 pyramidal neurons, along with dentate gyrus (DG) granule cells. The hippocampal structure is critical for learning and memory, with significant impairments of both behavior and synaptic activity in the DS mouse model which undergo degeneration during aging. Each population of excitatory hippocampal neurons exhibited unique gene expression alterations in the DS mice. Bioinformatic queries revealed unique vulnerabilities and mechanistic differences which coincide with onset of degeneration in the Ts65Dn model of DS/AD. These unique vulnerabilities may underlie the degenerative phenotype in DS, suggesting precision medicine targeting individual populations of neurons may be required for therapeutic advancement. We further analyzed maternal choline supplementation in each neuronal population, treating the dams during gestation through weaning with choline normal diet (1.1g/kc choline chloride) or choline suppmentation (5.0g/kg choline chloride) in the normal (AIN-76A) mouse chow from Dyets. At weaning (postnatal day 21), pups were aged on a choline normal diet until 6 months old.

Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.

Dataset Information

Gut microbiome drives individual memory variation in bumblebees

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets