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Montesinos, M.

Publications and source records attributed to Montesinos, M..

3 recordsLinked to original sources

Hidden biotic stress alters climate sensitivity in woody plants

Chronic infection by vascular pathogens is conventionally expected to severely constrain host biomass accumulation, yet empirical evidence from long-lived woody plants remains inconsistent. We investigated the long-term impacts of Xylella fastidiosa colonization on the radial growth and climate sensitivity of adult Mediterranean almond trees (Prunus dulcis), aiming to resolve how persistent vascular infections modulate tree performance and resilience under a changing climate. We coupled high-resolution dendrochronological analysis with a novel, ring-resolved molecular reconstruction of individual infection histories across 706 annual rings. This hindcasting approach allowed for the retrospective identification of precise colonization dates, bacterial loads (Ct values), and pathogen subspecies (subsp. fastidiosa vs. subsp. multiplex). Growth-climate relationships were modelled using standardized ring-width indices (RWI) against a crop-weighted water deficit index (CWDi). Intra-host colonization followed a steep radial gradient, with active bacterial abundance concentrated in newly formed, functional outer xylem. Surprisingly, chronic infection did not trigger a sustained reduction in baseline annual ring width. Instead, pathogens fundamentally reshaped climate-growth sensitivity. Hosts infected by subsp. fastidiosa maintained high plastic growth tracking during wet years, whereas this capacity was significantly attenuated in those harbouring subsp. multiplex. Despite the absence of a chronic signal in trunk radial growth, vascular impairment was tightly associated with severe retrograde canopy dieback. Our findings indicate that chronic infection by X. fastidiosa can act as a latent biotic stressor, altering host physiological sensitivity to environmental fluctuations without directly suppressing baseline stem growth. This pattern is consistent with the marked temporal decoupling between spring cambial activity and late-summer bacterial proliferation, together with progressive vascular dysfunction leading to severe canopy dieback. These results suggest that current abiotic-centred frameworks of drought-induced decline may underestimate the contribution of cryptic vascular pathogens to vegetation mortality under intensifying climate change.

plant biology↗

Global predictions for the risk of establishment of Pierce's disease of grapevines

The vector-borne bacterium Xylella fastidiosa is responsible for Pierces disease (PD), a lethal grapevine illness that originated in the Americas. The international plant trade is expanding the geographic range of this pathogen, posing a new threat to viticulture worldwide. To assess the potential incidence of PD, we have built a dynamic epidemiological model based on the response of 36-grapevine varieties to the pathogen in inoculation assays and on the vectors distribution when this information is available. Key temperature-driven epidemiological processes, such as PD symptom development and recovery, are mechanistically modelled. Integrating into the model highresolution spatiotemporal climatic data from 1981 onward and different infectivity (R0) scenarios, we show how the main wine-producing areas thrive mostly in non-risk, transient, or epidemic-risk zones with potentially low growth rates in PD incidence. Epidemic-risk zones with moderate to high growth rates are currently marginal outside the United States. However, a global expansion of epidemic-risk zones coupled with small increments in the disease growth rate is projected for 2050. Our study globally downscales the risk of PD establishment while highlighting the importance of considering climate variability, vector distribution and an invasive criterion in obtaining accurate risk maps to guide policy decision-making in plant health.

plant biology↗

Obesity-instructed TREM2high macrophages identified by comparative analysis of diabetic mouse and human kidney at single cell resolution

Mouse models are a tool for studying the mechanisms underlying complex diseases; however, differences between species pose a significant challenge for translating findings to patients. Here, we used single-cell transcriptomics and orthogonal validation approaches to provide cross-species taxonomies, identifying shared broad cell classes and unique granular cellular states, between mouse and human kidney. We generated cell atlases of the diabetic and obese kidney using two different mouse models, a high-fat diet (HFD) model and a genetic model (BTBR ob/ob), at multiple time points along disease progression. Importantly, we identified a previously unrecognized, expanding Trem2high macrophage population in kidneys of HFD mice that matched human TREM2high macrophages in obese patients. Taken together, our cross-species comparison highlights shared immune and metabolic cell-state changes.

genomics↗