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A directional electrode separator improves anodic biofilm current density in a well-mixed single-chamber bioelectrochemical system
In this study, a directional electrode separator (DES) was designed and incorporated into a single-chamber bioelectrochemical system (BES) to reduce migration and reoxidation of hydrogen. This issue arises when H 2 , generated at the cathode, travels to the anode where anodic biofilms use H 2 . To test the feasibility of our design, a 3D-printed BES reactor equipped with a DES was inoculated with anaerobic digestor granules and operated under fed-batch conditions using fermented corn stover effluent. The DES equipped reactor achieved significantly higher current densities (~53 A/m²) compared to a conventional single-chamber BES without a separator (~16 A/m²), showing a 3.3 times improvement. Further, control abiotic electrochemical experiments revealed that the DES exhibited significantly higher proton conductivity (456±127 µS/mm) compared to a proton exchange membrane (67±21 µS/mm) with a statistical significance of P=0.03. The DES also effectively reduced H 2 migration to the anode by 21-fold relative to the control. Overall, incorporating a DES in a single-chamber BES enhanced anodic current density by reducing H 2 migration to the anode.
Enhanced production of taxadiene in Saccharomyces cerevisiae
Cost-effective production of the highly effective anti-cancer drug, paclitaxel (Taxol ® ), remains limited despite growing global demands. Low yields of the critical taxadiene precursor remains a key bottleneck in microbial production. In this study, the key challenge of poor taxadiene synthase (TASY) solubility in S. cerevisiae was revealed, and the strains were strategically engineered to relieve this bottleneck. Multi-copy chromosomal integration of TASY harbouring a selection of fusion solubility tags improved taxadiene titres 22-fold, up to 57 ± 3 mg/L at 30 °C at microscale, compared to expressing a single episomal copy of TASY. The scalability of the process was highlighted through achieving similar titres during scale up to 25 mL and 250 mL in shake flask and bioreactor cultivations, respectively at 20 and 30 °C. Maximum taxadiene titres of 129 ± 15 mg/L and 127 mg/L were achieved through shake flask and bioreactor cultivations, respectively, of the optimal strain at a reduced temperature of 20 °C. The results of this study highlight the benefit of employing a combination of molecular biology and bioprocess tools during synthetic pathway development, with which TASY activity was successfully improved by 6.5-fold compared to the highest literature titre in S. cerevisiae cell factories.
SPOP mutation induces replication over-firing by impairing Geminin ubiquitination and triggers replication catastrophe upon ATR inhibition
Geminin and its binding partner Cdt1 are essential for the regulation of DNA replication. Here we show that the CULLIN3 E3 ubiquitin ligase adaptor protein SPOP binds Geminin at endogenous level and regulates DNA replication. SPOP promotes K27-linked non-degradative poly-ubiquitination of Geminin at lysine residues 100 and 127. This poly-ubiquitination of Geminin prevents DNA replication over-firing by indirectly blocking the association of Cdt1 with the MCM protein complex, an interaction required for DNA unwinding and replication. SPOP is frequently mutated in certain human cancer types and implicated in tumorigenesis. We show that cancer-associated SPOP mutations impair Geminin K27-linked poly-ubiquitination and induce replication origin over-firing and re-replication. The replication stress caused by SPOP mutations triggers replication catastrophe and cell death upon ATR inhibition. Our results reveal a tumor suppressor role of SPOP in preventing DNA replication over-firing and genome instability and suggest that SPOP-mutated tumors may be susceptible to ATR inhibitor therapy.
Life-cycle analysis of microalgae-based polyurethane foams
Polyurethane plastics are essential in many consumer and commercial products such as insulation, furniture, automotive interiors, and clothing. Pathways for producing polyurethane from microalgae offer an opportunity to reduce greenhouse gas emissions and other environmental impacts and can incorporate processes that avoid the use of toxic isocyanates typically used in conventional polyurethane production processes. In this study, the greenhouse gas emissions, fossil energy, and water consumption of biobased polyurethane and biobased non-isocyanate polyurethane were evaluated via life-cycle analysis using the R&D Greenhouse Gases, Regulated Emissions, and Energy Use in Technologies model. Microalgae-based polyurethane foam was found to achieve greenhouse gas emission reductions of up to 79% compared with conventional polyurethane foam production. The greenhouse gas reductions for the non-isocyanate microalgae polyurethane pathway are slightly lower at 58% compared with conventional polyurethane foam. However, it offers additional benefits by reducing toxicity potential compared to the isocyanate polyurethane pathway. The analysis also included a biorefinery-level analysis to evaluate the impact of incorporating polyurethane production into fuel-processing microalgae biorefineries. The sensitivity analyses conducted in this study reveal that improved algae cultivation strategies can lead to decreases of up to 127% and 80% in GHG emissions from the baseline process of Bio-PU and Bio-NIPU, respectively. Likewise, implementation of renewable electricity can result in up to 128% and 74% lower GHG emissions compared to the baseline production of Bio-PU and Bio-NIPU, respectively. Finally, the analysis evaluated different coproduct handling methods including displacement and allocation (based on mass, energy, and market-value). The results suggest that it is important to consider both the displacement and allocation methods as these led to significant differences in the environmental impacts.
The inheritance of anthracnose (Colletotrichum sublineola) resistance in sorghum differential lines QL3 and IS18760
Anthracnose caused by the fungal pathogen C. sublineola is an economically important constraint on worldwide sorghum production. The most effective strategy to safeguard yield is through the introgression of resistance alleles. This requires elucidation of the genetic basis of the different resistance sources that have been identified. In this study, 223 recombinant inbred lines (RILs) derived from crossing anthracnose-differentials QL3 (96 RILs) and IS18760 (127 RILs) with the common susceptible parent PI609251 were evaluated at four field locations in the United States (Florida, Georgia, Texas, and Puerto Rico) for their anthracnose resistance response. Both RIL populations were highly susceptible to anthracnose in Florida and Georgia, while in Puerto Rico and Texas they were segregating for anthracnose resistance response. A genome scan using a composite linkage map of 982 single nucleotide polymorphisms (SNPs) detected two genomic regions of 4.31 and 0.85 Mb on chromosomes 4 and 8, respectively, that explained 10–27% of the phenotypic variation in Texas and Puerto Rico. In parallel, a subset of 43 RILs that contained 67% of the recombination events were evaluated against anthracnose pathotypes from Arkansas (2), Puerto Rico (2) and Texas (4) in the greenhouse. A genome scan showed that the 7.57 Mb region at the distal end of the short arm of chromosome 5 is associated with the resistance response against the pathotype AMP-048 from Arkansas. Comparative analysis identified the genomic region on chromosome 4 overlaps with an anthracnose resistance locus identified in another anthracnose-differential line, SC414-12E, indicating this genomic region is of interest for introgression in susceptible sorghum germplasm. Candidate gene analysis for the resistance locus on chromosome 5 identified an R -gene cluster that has high similarity to another R -gene cluster associated with anthracnose resistance on chromosome 9.
Variants in the MS4A cluster interact with soluble TREM2 expression on biomarkers of neuropathology
Recent evidence suggests that Alzheimer’s disease (AD) genetic risk variants (rs1582763 and rs6591561) of the MS4A locus are genome-wide significant regulators of soluble TREM2 levels such that the minor allele of the protective variant (rs1582763) is associated with higher sTREM2 and lower AD risk while the minor allele of (rs6591561) relates to lower sTREM2 and higher AD risk. Our group previously found that higher sTREM2 relates to higher Aβ 40 , worse blood–brain barrier (BBB) integrity (measured with the CSF/plasma albumin ratio), and higher CSF tau, suggesting strong associations with amyloid abundance and both BBB and neurodegeneration complicate interpretation. We expand on this work by leveraging these common variants as genetic tools to tune the interpretation of high CSF sTREM2, and by exploring the potential modifying role of these variants on the well-established associations between CSF sTREM2 as well as TREM2 transcript levels in the brain with AD neuropathology. Biomarker analyses leveraged data from the Vanderbilt Memory & Aging Project (n = 127, age = 72 ± 6.43) and were replicated in the Alzheimer’s Disease Neuroimaging Initiative (n = 399, age = 73 ± 7.39). Autopsy analyses were performed leveraging data from the Religious Orders Study and Rush Memory and Aging Project (n= 577, age = 89 ± 6.46). We found that the protective variant rs1582763 attenuated the association between CSF sTREM2 and Aβ 40 (β= -0.44, p-value= 0.017) and replicated this interaction in ADNI (β = -0.27, p = 0.017). We did not observe this same interaction effect between TREM2 mRNA levels and Aβ peptides in brain (Aβ total β = -0.14, p = 0.629; Aβ 1-38 , β = 0.11, p = 0.200). In contrast to the effects on Aβ, the minor allele of this same variant seemed to enhance the association with blood–brain barrier dysfunction (β = 7.0e-4, p = 0.009), suggesting that elevated sTREM2 may carry a much different interpretation in carriers vs. non-carriers of this allele. When evaluating the risk variant (rs6591561) across datasets, we did not observe a statistically significant interaction against any outcome in VMAP and observed opposing directions of associations in ADNI and ROS/MAP on Aβ levels. Together, our results suggest that the protective effect of rs1582763 may act by decoupling the associations between sTREM2 and amyloid abundance, providing important mechanistic insight into sTREM2 changes and highlighting the need to incorporate genetic context into the analysis of sTREM2 levels, particularly if leveraged as a clinical biomarker of disease in the future.