Barmpoutis, P. | bioRxiv Science

bioRxiv2025

Polli-markers: spectral and chemical biomarkers for detecting cryptic early plant pollination responses

O_LIPollination is essential for plant reproduction, ecosystem resilience and human health. Yet, our capability to map pollination service delivery in real-time across large areas remains poor. Determining where and when flowers are pollinated is vital to mitigate widespread pollination deficits, increase plant health and yield, and support pollinator management. Hence, innovative approaches are urgently needed for establishing scalable predictive bioindicators of plant pollination status with the goal of achieving real-time landscape-scale monitoring. C_LIO_LIHere we present two parallel controlled pollination assays in which we characterise the post-pollination petal physiology of a world leading flowering crop, Brassica napus, using in-situ close-range hyperspectral reflectance and semi-untargeted metabolomics. C_LIO_LIThis multiomics approach coupled with supervised machine learning and biomarker detection reveals cryptic changes in the UV petal reflectance spectrum which are predictive of pollination status, representing a novel set of candidate pollination bioindicators ( polli-markers), and our high-resolution time series enables prediction of when this pollination event occurred. It also reveals an associated set of candidate metabolites, including flavonoids and senescence markers, shedding light on the functional pathways related to our polli-markers. C_LIO_LIThis study provides key insights into floral development, enabling a transformative step towards predicting, mapping and quantifying pollination service delivery at the landscape scale. C_LI

ecology↗

bioRxiv2022

Mutation Rate Evolution Drives Immune Escape In Mismatch Repair-Deficient Cancer

Mutation rate optimisation drives evolution and immune evasion of bacteria and lentiviral strains, including HIV. Whether evolving cancer lineages similarly adapt mutation rates to increase tumour cell fitness is unknown. Here, by mapping the clonal topography of mismatch repair-deficient (MMRd) colorectal cancer, we show that genomic MMRd mutability co-evolves with neoantigen selection to drive intratumour diversification and immune escape. Mechanistically, we find that microsatellite instability modulates subclonal DNA repair by toggling two hypermutable mononucleotide homopolymer runs in the mismatch repair genes MSH6 and MSH3 (C8 and A8, respectively) through stochastic frameshift switching. Spontaneous mutation and reversion at these evolvability switches modulates subclonal mutation rate, mutation bias, and clonal HLA diversity during MMRd cancer evolution. Combined experimental and simulation studies demonstrate that subclonal immune selection favours incremental MMR mutations. MMRd cancers thus fuel intratumour heterogeneity by adapting subclonal mutation rate and mutation bias to immune selection, revealing a conserved co-evolutionary arms race between neoantigen selection and adaptive genomic mutability. Our work reveals layers of mutational complexity and microsatellite biology in MMRd cancer evolution previously hidden in bulk analyses.

cancer biology↗