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Covariation of plant functional traits, that is, phenotypic integration, might constrain their variability. This was observed for inter- and intraspecific variation, but there is no evidence of a relationship between phenotypic integration and the functional variation within single plants (within-individual trait variation; WTV), which could be key to understand the extent of WTV in contexts like plant-plant interactions. We studied the relationship between WTV and phenotypic integration in c. 500 trees of 21 species in planted forest patches varying in species richness in subtropical China. Using visible and near-infrared spectroscopy (Vis-NIRS), we measured nine leaf morphological and chemical traits. For each tree, we assessed metrics of single and multitrait variation to assess WTV, and we used plant trait network properties based on trait correlations to quantify phenotypic integration. Against expectations, strong phenotypic integration within a tree led to greater variation across leaves. Not only this was true for single traits, but also the dispersion in a tree's multitrait hypervolume was positively associated with tree's phenotypic integration. Surprisingly, we only detected weak influence of the surrounding tree-species diversity on these relationships. Our study suggests that integrated phenotypes allow the variability of leaf phenotypes within the organism and supports that phenotypic integration prevents maladaptive variation.
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http://dx.doi.org/10.1111/nph.19250 | DOI Listing |
J Clin Invest
September 2025
Department of Cellular and Molecular Medicine, UCSD, La Jolla, United States of America.
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Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, United States of America.
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División de Ciencias Naturales y Exactas, Departamento de Biología, Universidad de Guanajuato, Zip Code 36050, Guanajuato, Mexico.
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Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR), and HER2, and remains one of the most aggressive and therapeutically challenging breast cancer subtypes, marked by early relapse, metastasis, and limited targeted treatment options. In a recent study published in The Journal of Pathology, Kuo et al provide compelling evidence that nicotine exposure, whether from tobacco smoke or e-cigarette vapor, drives TNBC progression by promoting stem-like and metastatic phenotypes. Integrating clinical datasets, patient tissues, cell lines, and in vivo models, the authors demonstrate that nicotine enhances tumor aggressiveness via coordinated upregulation of CHRNA9 and IGF1R.
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