@article{21490,
  abstract     = {Auxin canalization is a self-organizing process that governs the flexible formation of vasculature by reinforcing the formation of auxin transport channels. A key prerequisite is the feedback between auxin signaling and directional auxin transport, mediated by PIN transporters. Despite the developmental importance of canalization, the molecular components linking auxin perception to the regulation of PIN auxin transporters remain poorly understood. Here, we identify TOW, a novel and essential component of auxin canalization that links intracellular auxin signaling with cell surface auxin perception. TOW is regulated downstream of TIR1/AFB-Aux/IAA-WRKY23 transcriptional auxin signaling. tow mutants exhibit defects in regeneration and de novo vasculature formation, along with impaired formation of polarized, PIN-expressing auxin channels. At the subcellular level, these mutants display disrupted auxin-induced PIN polarization and altered PIN endocytic trafficking dynamics. TOW localizes predominantly to the plasma membrane, where it interacts with receptor-like kinases involved in auxin canalization, including the TMK1 auxin co-receptor and the CAMEL-CANAR complex. TOW promotes PIN interaction with these kinases and stabilizes PINs at the cell surface. Together, our findings identify TOW as a molecular link between intracellular and cell surface auxin signaling mechanisms that converge on PIN trafficking and polarity, providing new insights into how auxin signaling regulates directional auxin transport for the self-organizing formation of vasculature during flexible plant development.},
  author       = {Li, Mingyue and Rydza, Nikola and Mazur, Ewa and Molnar, Gergely and Nodzyński, Tomasz and Friml, Jiří},
  issn         = {0960-9822},
  journal      = {Current Biology},
  number       = {6},
  pages        = {1468--1480.e6},
  publisher    = {Elsevier},
  title        = {{Receptor-like-kinase-interacting protein TOW stabilizes PIN transporters for auxin canalization}},
  doi          = {10.1016/j.cub.2026.02.023},
  volume       = {36},
  year         = {2026},
}

@article{21776,
  abstract     = {Pyridyl motifs equipped with N-substituents can be powerful ligands for catalysis, yet their broader adoption is limited by the lack of a practical method to prepare these scaffolds. We report a modular, robust, and versatile Buchwald–Hartwig amination protocol that enables the rapid synthesis of bipyridine, phenanthroline, terpyridine, and pybox ligands bearing dialkylamine, diarylamine, and heteroaromatic N-substituents. These conditions streamline ligand library synthesis and will facilitate systematic studies in catalysis and related applications.},
  author       = {Petrik, Adam and Bena, Aleksander and Baunis, Haralds and Kelch, Riley M. and Yoon, Tehshik P. and Pieber, Bartholomäus},
  issn         = {1615-4169},
  journal      = {Advanced Synthesis & Catalysis},
  number       = {9},
  publisher    = {Wiley},
  title        = {{Facile access to N-substituted pyridyl ligands}},
  doi          = {10.1002/adsc.70417},
  volume       = {368},
  year         = {2026},
}

@article{21914,
  abstract     = {Cyclic adenosine monophosphate (cAMP) is a fundamental second messenger involved in diverse signaling pathways across both animals and plants. While the role of 3′,5′-cAMP has been extensively characterized, the biological significance of its structural isomer, 2′,3′-cAMP, remains largely unexplored, particularly in plants. Here, we show that 2′,3′-cAMP and 3′,5′-cAMP represent parallel signaling systems in Arabidopsis thaliana, with different enzymatic origins and largely distinct downstream effects. In vitro enzymatic assays show that plant adenylate cyclases (ACs), including AFB5 and HpAC1, produce specifically 3′,5′-cAMP from ATP, whereas the TIR domain of protein L7 also catalyzes the formation of 2′,3′-cAMP from RNA. Comprehensive multiomics analyses reveal that two isomers elicit distinct yet partially overlapping metabolic, proteomic, and transcriptional response: 2′,3′-cAMP activates broad, stress-adaptive gene expression reprogramming, while 3′,5′-cAMP fine-tunes responses related to nutrient status and cellular homeostasis. Our findings establish the existence of dual cAMP signaling systems in plants, each with specialized functions and provide insights into the complex regulatory networks governing plant physiology.},
  author       = {Li, Mingyue and Chodasiewicz, Monika and Muraleedharan, Malavika and Lopez, Israel M. and Gorka, Michal and Kerber, Olga and Alotaibi, Saqer S. and Nelson, Andrew D.L. and Lenobel, Rene and Friedecká, Jaroslava and Skirycz, Aleksandra and Friml, Jiří},
  issn         = {2375-2548},
  journal      = {Science Advances},
  number       = {19},
  publisher    = {AAAS},
  title        = {{Biogenesis and downstream effects of 3',5' and 2',3' cAMP isomers in plants}},
  doi          = {10.1126/sciadv.aea7828},
  volume       = {12},
  year         = {2026},
}

@unpublished{21962,
  abstract     = {The generation of faithful cell-type diversity and correct projection neuron numbers is essential for cerebral cortex development. Corticogenesis is however susceptible to genetic interference of critical signaling pathways, including mutations in Mtor/Rptor that lead to microcephaly. How the loss of Rptor/mTORC1 function affects cortical developmental programs, at single cell level, is still unknown. Here, we utilized Mosaic Analysis with Double Markers (MADM) technology to probe Rptor gene function upon sparse single cell- or global tissue-wide ablation. We found that tissue-wide effects drive the etiology of cortical microcephaly upon loss of Rptor, rather than deficits in projection neuron genesis. Conversely, Rptor function is cell-autonomously required for postnatal projection neuron survival in a highly cell-type-specific manner. Collectively, our results suggest that the fine balance of precise cell-type-specific cell-autonomous Rptor/mTORC1 function in concert with non-cell-autonomous tissue-wide effects is essential for the development of a properly-sized cerebral cortex with accurate projection neuron diversity.},
  author       = {Villalba Requena, Ana and Beattie, Robert J and Pauler, Florian and Streicher, Carmen and Miranda, Osvaldo and Krausgruber, Thomas and Senekowitsch, Martin and Farlik, Matthias and Bock, Christoph and Rülicke, Thomas and Hippenmeyer, Simon},
  booktitle    = {bioRxiv},
  title        = {{Mtor/Rptor function globally prevents cortical microcephaly and cell-autonomously promotes postnatal neuron survival in cell type specific manner}},
  doi          = {10.64898/2026.05.01.722172},
  year         = {2026},
}

@article{18892,
  abstract     = {Sick individuals often conceal their disease status to group members, thereby preventing social exclusion or aggression. Here we show by behavioural, chemical, immunological and infection load analyses that sick ant pupae instead actively emit a chemical signal that in itself is sufficient to trigger their own destruction by colony members. In our experiments, this altruistic disease-signalling was performed only by worker but not queen pupae. The lack of signalling by queen pupae did not constitute cheating behaviour, but reflected their superior immune capabilities. Worker pupae suffered from extensive pathogen replication whereas queen pupae were able to restrain their infection. Our data suggest the evolution of a finely-tuned signalling system in which it is not the induction of an individual’s immune response, but rather its failure to overcome the infection, that triggers pupal signalling for sacrifice. This demonstrates a balanced interplay between individual and social immunity that efficiently achieves whole-colony health.},
  author       = {Dawson, Erika and Hönigsberger, Michaela and Kampleitner, Niklas and Grasse, Anna V and Lindorfer, Lukas and Robb, Jennifer and Beikzadeh Abbasi, Farnaz and Strahodinsky, Florian and Leitner, Hanna and Rajendran, Harikrishnan and Schmitt, Thomas and Cremer, Sylvia},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  publisher    = {Springer Nature},
  title        = {{Altruistic disease signalling in ant colonies}},
  doi          = {10.1038/s41467-025-66175-z},
  volume       = {16},
  year         = {2025},
}