Brugnara, C. | bioRxiv Science

bioRxiv2026

High-light adaptation via ferredoxin-mediated tuning of the photosynthesis–photoprotection trade-off

O_LIPlants continuously adjust photosynthesis to balance growth and photoprotection under changing environmental conditions. Environmental fluctuations frequently impose a mismatch between energy production and CO2 assimilation. How photochemical reactions are regulated to maintain performance under these conditions remains a central question in plant biology. C_LIO_LIWe previously developed transplastomic tobacco (Fd1-OE plants) overexpressing ferredoxin (Fd) displaying enhanced photoprotection and growth penalties with a variegated leaf phenotype under greenhouse conditions. Here, we investigate how these plants respond to different growth irradiances using physiological, ultrastructural, and photosynthetic analyses, including PAM, gas exchange, and P700 absorbance measurements, and dynamic-light assays. C_LIO_LIFd1-OE plants progressively recovered growth, leaf phenotype and photosynthetic performance as growth irradiance increased, reaching near WT performance at 1400 mol m-{superscript 2} s-{superscript 1}. This enhanced adaptation to "high-light" was associated with a larger fraction of open PSII reaction centers and enhanced NPQ. Dynamic-light analyses further revealed faster plastoquinone (PQ) turnover, a more oxidized PQ pool and enhanced electron withdrawal downstream of PSI. C_LIO_LIOur results indicate that Fd overexpression redefines the balance between photochemistry and photoprotection. This adjustment shifts adaptation toward higher irradiance and enhances photosynthetic performance under changing light environments. Electron partitioning downstream of PSI emerges as a promising target to improve photosynthetic resilience. C_LI One sentence summaryOverexpression of Fd1 in tobacco plants adjusts photosynthesis/photoprotection trade off to enhance high-light adaptation

Plant Biology↗

bioRxiv2019

Causal role of L-glutamine in sickle cell disease painful crises: a Mendelian randomization analysis

In a recent clinical trial, the metabolite L-glutamine was shown to reduce painful crises in sickle cell disease (SCD) patients. To confirm this observation and identify other metabolites implicated in SCD clinical heterogeneity, we profiled 129 metabolites in the plasma of 705 SCD patients. We tested correlations between metabolite levels and six SCD-related complications (painful crises, cholecystectomy, retinopathy, leg ulcer, priapism, aseptic necrosis) or estimated glomerular filtration rate (eGFR), and used Mendelian randomization (MR) to assess causality. We found a causal relationship between L-glutamine levels and painful crises (N=1,278, odds ratio (OR) [95% confidence interval] = 0.68 [0.52 - 0.89], P=0.0048). In two smaller SCD cohorts (N=299 and 406), the protective effect of L-glutamine was observed (OR=0.82 [0.50-1.34]), although the MR result was not significant (P=0.44). We identified 66 significant correlations between the levels of other metabolites and SCD-related complications or eGFR. We tested these correlations for causality using MR analyses and found no significant causal relationship. The baseline levels of quinolinic acid was associated with prospectively ascertained survival in SCD patients, and this effect was dependent on eGFR. Metabolomics provide a promising approach to prioritize small molecules that may serve as biomarkers or drug targets in SCD.

genetics↗