Biology subjects

Cano, F.

Publications and source records attributed to Cano, F..

2 recordsLinked to original sources

bioRxiv2025

Attributing the temperature response of tree seedling growth to underlying mechanisms

Studies of plant responses to temperature often focus on rates photosynthesis and respiration. However, within-plant utilisation and allocation of carbon are also strongly affected. It is unclear how much each of these processes contribute to determining the overall temperature response of growth. We applied a data assimilation framework to a glasshouse experiment with detailed physiological and growth measurements to investigate the relative contribution of different physiological processes to the overall temperature response of tree seedling growth. We found that both short-term effects of temperature and acclimatory responses of photosynthesis and respiration had a significant impact on the temperature response of growth. However, the effect of temperature on biomass allocation patterns to different tissues, non-structural carbohydrate utilisation and C losses to other unmeasured losses were also substantial in determining the temperature response of growth, particularly at sub-optimal temperatures. Our work demonstrates that the growth response to warming cannot be predicted using only the direct effect of temperature on photosynthesis and respiration and emphasizes the importance of temperature acclimation of photosynthesis, respiration and other C balance processes. Our results provide new guidance for process-based models to correctly describe the temperature effects on tree growth.

plant biology↗

bioRxiv2025

CISH, a novel intracellular immune checkpoint, in comparison and combination to existing and emerging cancer immune checkpoints

Over the past decade, Immuno-Oncology has largely focused on blocking inhibitory surface receptors like PD-1 to enhance T cell anti-tumor activity. However, intracellular immune checkpoints such as CISH, which function independently of tumor-expressed ligands, offer powerful and previously untapped therapeutic potential. As a downstream regulator of TCR signaling, CISH controls T cell activation, expansion, and neoantigen reactivity. Though historically considered undruggable, recent advances in CRISPR engineering have enabled functional interrogation of these targets. We demonstrate that CISH deletion enhances T cell activation and anti-cancer functions more effectively than other emerging intracellular checkpoints. In CAR-T cells, CISH inactivation significantly increased sensitivity to tumor antigen, enabling robust recognition and killing even at low antigen levels, conditions that often lead to treatment failure with conventional T cell therapies, mirroring antigen escape scenarios seen in solid tumors. Our findings further validate CISH as a potent and druggable intracellular checkpoint capable of boosting anti-tumor T cell responses across diverse cancer types, independent of PD-L1 status. The underlying mechanisms of CISH inhibition may help explain the positive outcomes reported in recent clinical studies of this approach in solid tumor immunotherapy.

cancer biology↗