BMC Biology最新文献

Background: Recent trends towards lower washing temperatures and a reduction in the use of bleaching agents in laundry undoubtedly benefit our environment. However, these conditions impair microbial removal on clothes, leading to malodour generation and negative impacts on consumer well-being. Clothing undergoes cycles of wearing, washing and drying, with variable exposure to microorganisms and volatilomes originating from the skin, washing machine, water and laundry products. Laundry malodour is therefore a complex problem that reflects its dynamic ecosystem. To date, comprehensive investigations that encompass the evaluation of both microbial community and malodorous volatile organic compounds throughout all stages of the wash-wear-dry cycle are scarce. Furthermore, the microbial and malodour profiles associated with extended humid-drying conditions are poorly defined.

Results: Here we present olfaction-directed chemical and microbiological studies of synthetic T-shirts after wearing, washing and drying. Results show that although washing reduces the occurrence of known malodour volatile organic compounds, membrane-intact bacterial load on clothing is increased. Skin commensals are displaced by washing machine microbiomes, and for the first time, we show that this shift is accompanied by an altered pathogenomic profile, with many genes involved in biofilm build-up. We additionally highlight that humid-drying conditions are associated with characteristic malodours and favour the growth of specific Gram-negative bacteria.

Conclusions: These findings have important implications for the development of next-generation laundry products that enhance consumer well-being, while supporting environmentally friendly laundry practices.

Background: Glioblastoma is the most common and aggressive malignant brain tumour in the adult population and its prognosis is dismal. The heterogeneous nature of the tumour, to which epigenetic dysregulation significantly contributes, is among the main therapeutic challenges of the disease.

Results: We have leveraged SYNGN, an experimental pipeline enabling the syngeneic comparison of glioblastoma stem cells and expanded potential stem cell (EPSC)-derived neural stem cells to identify regulatory features driven by chromatin remodelling specifically in glioblastoma stem cells.

Conclusions: We show epigenetic regulation of the expression of genes and related signalling pathways contributing to glioblastoma development. We also identify novel epigenetically regulated druggable target genes on a patient-specific level, including SMOX and GABBR2.

Background: The marine crustacean Oratosquilla oratoria is economically significant in seafood and aquaculture industries. However, the lack of high-quality genome assembly has hindered our understanding of O. oratoria, particularly the mechanisms underlying its developed visual system.

Results: We generated a chromosome-level genome assembly for O. oratoria (2.97 Gb, 44 pseudo-chromosomes) using combination sequencing strategies. Our analysis revealed that more than half of the genome was covered by repeat sequences, and LINE elements showed significant expansion. Furthermore, phylogenetic analysis revealed a close relationship of O. oratoria with Dendrobranchiata and Pleocyemata. In addition, the evolutionary rate of O. oratoria was slightly faster than that of Dendrobranchiata and slower than that of Pleocyemata. Interestingly, we observed the significant expansion of middle-wavelength-sensitive (MWS) opsins in the O. oratoria genome by tandem duplication, partially contributing to their unique visual capabilities. Compared with other crustaceans, O. oratoria has evolved a thicker cornea that was possibly driven by visual adaptations and ecological requirements. Employing comparative transcriptome analysis, we identified a tandemly duplicated cuticle protein (CP) cluster that was specifically expanded and expressed in the ocular tissues of O. oratoria, potentially contributing to the thick cornea of O. oratoria.

Conclusions: Our study established the first chromosome-level genome for Stomatopoda species, providing a valuable genomic resource for studying the molecular mechanisms underlying the developed visual system of O. oratoria.

Background: During oocyte maturation, DNA double-strand breaks (DSBs) can decrease oocyte quality or cause mutations. How DSBs are repaired in dividing oocytes and which factors influence DSB repair are not well understood.

Results: By analyzing DSB repair pathways in oocytes at different stages, we found that break-induced replication (BIR) and RAD51-mediated homology-directed repair (HDR) were highly active in germinal vesicle breakdown (GVBD) oocytes but suppressed in metaphase II (MII) oocytes and the BIR in oocytes was promoted by CDK1 activity. By culturing oocytes in different media, we found that high-energy media, such as DMEM, decreased CDK1 protein levels and suppressed BIR or HDR in MII oocytes. In contrast, 53BP1-mediated nonhomologous end joining (NHEJ) repair was inhibited in germinal vesicle (GV) and GVBD oocytes but promoted in MII oocytes, and NHEJ was not affected by DMEM medium and CDK1 activity. In addition, in DSB MII oocytes, polymerase theta-mediated end joining (TMEJ) was found to be suppressed by CDK1 activity and promoted by high-energy media.

Conclusions: In summary, MII oocytes exhibit high heterogeneity in DSB repair, which is regulated by both metabolic factors and CDK1 activity. These results not only expand our understanding of oocyte DSB repair but also contribute to the modification of in vitro maturation medium for oocytes.

Background: RNA helicase MOV10 is highly expressed in postnatal brain and associates with FMRP and AGO2, suggesting a role in translation regulation in learning and memory.

Results: We generated a brain-specific knockout mouse (Mov10 Deletion) with greatly reduced MOV10 expression in cortex and hippocampus. Behavior testing revealed enhanced fear memory, similar to that observed in a mouse with reduced brain microRNA production, supporting MOV10's reported role as an AGO2 cofactor. Cultured hippocampal neurons have elongated distal dendrites, a reported feature of augmin/HAUS over-expression in Drosophila da sensory neurons. In mitotic spindle formation, HAUS is antagonized by the microtubule bundling protein NUMA1. Numa1 mRNA is a MOV10 CLIP target and is among the genes significantly decreased in Mov10 Deletion hippocampus. Restoration of NUMA1 expression and knockdown of HAUS rescued phenotypes of the Mov10 Deletion hippocampal neurons.

Conclusions: This is the first evidence of translation regulation of NUMA1 by MOV10 as a control point in dendritogenesis.

While psychologists have extensively discussed the notion of a "theory crisis" arising from vague and incorrect hypotheses, there has been no debate about such a crisis in biology. However, biologists have long discussed communication failures between theoreticians and empiricists. We argue such failure is one aspect of a theory crisis because misapplied and misunderstood theories lead to poor hypotheses and research waste. We review its solutions and compare them with methodology-focused solutions proposed for replication crises. We conclude by discussing how promoting inclusion, diversity, equity, and accessibility (IDEA) in theoretical biology could contribute to ameliorating breakdowns in the theory-empirical cycle.

Background: The compound eyes of insects exhibit extensive variation in ommatidia number and size, which affects how they see and underlies adaptations in their vision to different environments and lifestyles. However, very little is known about the genetic and developmental bases of differences in eye size. We previously showed that the larger eyes of Drosophila mauritiana compared to D. simulans are generally caused by differences in ommatidia size rather than number. Furthermore, we identified an X-linked chromosomal region in D. mauritiana that results in larger eyes when introgressed into D. simulans.

Results: Here, we used a combination of fine-scale mapping and gene expression analysis to further investigate positional candidate genes on the X chromosome. We found earlier expression of orthodenticle (otd) during ommatidial maturation in D. mauritiana than in D. simulans, and we show that this gene is required for the correct organisation and size of ommatidia in D. melanogaster. We discovered that the activity of an otd eye enhancer is consistent with the difference in the expression of this gene between species, with the D. mauritiana enhancer sequence driving earlier expression than that of D. simulans. When otd expression is driven prematurely during D. melanogaster eye development, the ommatidia grow larger, supporting a possible role for the timing of otd expression in regulating ommatidial size. We also identified potential direct targets of Otd that are differentially expressed between D. mauritiana and D. simulans during ommatidial maturation.

Conclusions: Taken together, our results suggest that differential timing of otd expression may contribute to natural variation in ommatidia size between D. mauritiana and D. simulans, which provides new insights into the mechanisms underlying the regulation and evolution of compound eye size in insects.

Background: Lung ischemia-reperfusion (I/R) injury is a common clinical pathology associated with high mortality. The pathophysiology of lung I/R injury involves ferroptosis and elevated protein O-GlcNAcylation levels, while the effect of O-GlcNAcylation on lung I/R injury remains unclear. This research aimed to explore the effect of O-GlcNAcylation on reducing ferroptosis in pulmonary epithelial cells caused by I/R.

Results: First, we identified O-GlcNAc transferase 1 (Ogt1) as a differentially expressed gene in lung epithelial cells of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) patients, using single-cell sequencing, and Gene Ontology analysis (GO analysis) revealed the enrichment of the ferroptosis process. We found a time-dependent dynamic alteration in lung O-GlcNAcylation during I/R injury. Proteomics analysis identified the differentially expressed proteins enriched in ferroptosis and multiple redox-related pathways based on KEGG annotation. Thus, we generated Ogt1-conditional knockout mice and found that Ogt1 deficiency aggravated ferroptosis, as evidenced by lipid reactive oxygen species (lipid ROS), malondialdehyde (MDA), Fe²⁺, as well as alterations in critical protein expression glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). Consistently, we found that elevated O-GlcNAcylation inhibited ferroptosis sensitivity in hypoxia/reoxygenation (H/R) injury-induced TC-1 cells via O-GlcNAcylated NF-E2-related factor-2 (Nrf2). Furthermore, both the chromatin immunoprecipitation (ChIP) assay and the dual-luciferase reporter assay indicated that Nrf2 could bind with translation start site (TSS) of glucose-6-phosphate dehydrogenase (G6PDH) and promote its transcriptional activity. As an important rate-limiting enzyme in the pentose phosphate pathway (PPP), elevated G6PDH provided a mass of nicotinamide adenine dinucleotide phosphate (NADPH) to improve the redox state of glutathione (GSH) and eventually led to ferroptosis resistance. Rescue experiments proved that Nrf2 knockdown or Nrf2-T334A (O-GlcNAcylation site) mutation abolished the protective effect of ferroptosis resistance.

Conclusions: In summary, we revealed that O-GlcNAcylation could protect against I/R lung injury by reducing ferroptosis sensitivity via the Nrf2/G6PDH pathway. Our work will provide a new basis for clinical therapeutic strategies for pulmonary ischemia-reperfusion-induced acute lung injury.

Background: The microbiome regulates the respiratory epithelium's immunomodulatory functions. To explore how the microbiome's biodiversity affects microbe-epithelial interactions, we screened 58 phylogenetically diverse microbes for their transcriptomic effect on human primary bronchial air-liquid interface (ALI) cell cultures.

Results: We found distinct species- and strain-level differences in host innate immunity and epithelial barrier response. Strikingly, we found that host interferon, an antiviral response, was one of the most variable host processes. This variability was not driven by microbial phylogenetic diversity, bioburden, nor by the microbe's ability to stimulate other innate immunity pathways.

Conclusions: Microbial colonization differentially stimulates host gene expression with variations observed across phylogenetically diverse microbes and across different strains of the same species. Our study provides a foundation for understanding how the respiratory microbiome's biodiversity affects epithelial, and particularly antiviral, innate immunity.