Grapevine is one of the most economically important fruit crops due to the high value of its fruit and its importance in winemaking. The current decrease in grape berry quality and production can be seen as the consequence of various abiotic constraints imposed by climate changes. Specifically, produced wines have become too sweet, with a stronger impression of alcohol and fewer aromatic qualities. Potassium is known to play a major role in grapevine growth, as well as grape composition and wine quality. Importantly, potassium ions (K⁺) are involved in the initiation and maintenance of the berry loading process during ripening. Moreover, K⁺ has also been implicated in various defense mechanisms against abiotic stress. The first part of this review discusses the main negative consequences of the current climate, how they disturb the quality of grape berries at harvest and thus ultimately compromise the potential to obtain a great wine. In the second part, the essential electrical and osmotic functions of K⁺, which are intimately dependent on K⁺ transport systems, membrane energization, and cell K⁺ homeostasis, are presented. This knowledge will help to select crops that are better adapted to adverse environmental conditions.

Distinct ligand-receptor interaction (LRI) inference tools often produce markedly different results, and their performance can vary considerably across datasets. Indeed, performance is influenced by differences in experimental designs and dataset-specific features, making it difficult to establish a universal LRI tool. To address this challenge, we expanded our SingleCellSignalR Bioconductor package to provide an integrated framework that incorporates alternative scoring strategies and adjustable analytical depth. We motivate this choice through the analysis of two single-cell transcriptomics datasets that exemplify contrasting experimental designs. Leveraging the new framework flexibility, we present a detailed analysis of paired single-cell proteomics and transcriptomics data, providing, to our knowledge, the first direct comparison of LRI inference across these complementary modalities at single-cell resolution. Finally, we demonstrate how the same framework seamlessly accommodates additional underexplored data types from the LRI perspective, including patient-derived mouse xenografts and bulk RNA sequencing of upstream-sorted cell populations.

Src-family kinases (SFKs) regulate proliferation in colonic epithelial cells (CECs), but the mechanisms that restrain their activity remain poorly defined. We identify Src-like adaptor protein (SLAP), a negative regulator of receptor tyrosine kinase signaling, as a key suppressor of SFK activity in the colon. Constitutive and inducible epithelial-specific Slap deletion using a villin-CreERT2 model increases CEC proliferation and accelerates tumorigenesis in the azoxymethane/dextran sodium sulfate model. Slap deficiency also enhances SFK-dependent expansion of normal and tumor-derived colonic organoids. Mechanistically, we identify the receptor tyrosine kinase EPHB2 as a critical upstream activator of SFKs and a direct target of SLAP-mediated regulation. Loss of Slap increased EphB2 protein abundance and tyrosine phosphorylation, and enhanced its association with active SRC. Pharmacological inhibition of EPHB2 suppressed SRC activation and reversed the hyperproliferative phenotype induced by Slap deficiency. Together, these findings uncover a non-genetic mechanism driving SFK activation during colonic transformation and establish SLAP as a tumor suppressor that constrains oncogenic EPHB2–SFK signaling in the colonic epithelium.