The Golgi feels and responds to mechanical forces from outside the cell

Cells are not fixed objects; they are constantly spreading, stretching, and physically adapting to external conditions. The surface and the nucleus have been largely believed to be the main structures responsible for sensing and responding to these mechanical cues, but researchers at ICFO Dr. Javier Vera Lillo, Dr. Eugènia Almacellas, Dr. Nicolás Mateos, Dr. Jessica Angulo Capel, Adam Wolowczyk, ICREA Prof. María F. García Parajo, and Prof. Dr. Fèlix Campelo have now broadened this picture. In collaboration with CNRS, IBEC, Tokyo University of Pharmacy and Life Sciences, UB and UPF, the team has shown that the Golgi apparatus, an internal organelle, can also actively sense and respond to mechanical forces, and that its own activity, in turn, can affect how the cell physically behaves.  

The study, published in the Journal of Cell Biology and recently highlighted by the same journal, therefore introduces a new role for the Golgi complex, whose main function is to collect the proteins made in the endoplasmic reticulum, process them, sort them, and pack them into small vesicles that will finally fuse with the cell’s membrane to release their contents. By applying different mechanical stimuli to cells, the team observed that Golgi export changed; and by chemically and genetically blocking such export, the team found that the cell lost its ability to properly spread and adapt mechanically to its surroundings.  

Thus, the cell’s mechanical properties modify the activity in the Golgi, which in turn affects the mechanical properties of the cell. “That feedback loop is the novel conceptual contribution,” explains Dr. Javier Vera Lillo, first co-author of the article. “It positions the Golgi as an active player in mechanoadaptation, not just a downstream factory.” For instance, the researchers observed that physically stretching the cell increased the number of secretory carriers leaving the Golgi, and that when the cell was spreading on stiffer substrates, the Golgi’s membrane tension increased.  

The team notes that this newly discovered mechanical sensitivity of the Golgi could have implications for contexts in which cells experience altered mechanics, such as cancer invasion and fibrosis. “Identifying molecular nodes in this pathway could eventually offer new angles for therapeutic intervention, targeting aberrant secretion in these disease states,” says Dr. Fèlix Campelo, senior author of the article. “We hope that using more localized, quantitative tools to dissect how mechanical forces are spatially and temporally translated into the Golgi will help us further elucidate this potential connection.” 

Reference: 

Chandini Bhaskar Naidu, et. al.; Mechanical forces stimulate Golgi export. J Cell Biol 5 October 2026; 225 (10): e202510026.  

DOI: https://doi.org/10.1083/jcb.202510026 

Acknowledgements: 

We acknowledge support from the Government of Spain (RYC- 2017-22227, PID2020-113068RB-I00/10.13039/501100011033, and PID2023-147711NB-100; PID2022-138282NB-I00 project funded by the Ministerio de Ciencia e Innovación (MCIN)/Agencia Estatal de Investigación (AEI)/10.13039/501100011033/FEDER, UE; PID2022-142672NB-I00; “Unidad de Excelencia María de Maeztu” CEX2024-001431-M, funded by MICIU/AEI/10.13039/ 501100011033 to MELIS-UPF, and Severo Ochoa CEX2019- 000910-S toICFO and CEX2023-001282-S to Institute for Bioengineering of Catalonia, Fundació Privada Cellex, Fundació Privada Mir-Puig, and Generalitat de Catalunya (CERCA, AGAUR), ERC Advanced Grants NANO-MEMEC (GA 788546) and MechanoSynth (GA 101097753), as well as LaserLab 4 Europe (GA 654148). E. Almacellas acknowledges the support of the Beatriu de Pinós postdoctoral fellowship program of the Department of Research and Universities of the Generalitat de Catalunya (2023 BP 00210). N. Mateos acknowledges funding from the European Union H2020 under Marie Sklodowska- Curie grant 754558-PREBIST. J. Angulo-Capel acknowledges funding from the European Union H2020 under the Marie Sklodowska-Curie grant agreement No 847517. A. Wolowczyk was supported by joint funding from an ICFO Student Research Fellowship (Fall 2024) and a grant from Homerton College, Cambridge, UK. Y. Wakana acknowledges support from Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (grant number 25K09568); and AMED Multidisciplinary Frontier Brain and Neuroscience Discoveries (Brain/MINDS 2.0) (grant number JP24wm0625506). P. Roca-Cusachs acknowledges support from the prize “ICREA Academia” for excellence in research. This work was supported by Centre National de la Recherche Scientifique, the Labex Cell(n)Scale - grants ANR-11-LABX-0038, ANR-10-IDEX-0001-02, the French Agence Nationale de la Recherche (ANR), grant number ANR- 22-CE13-0044 “MECHANGOLGI” project. C. Bhaskar Naidu was supported by the international EuReCa PhD program of Institut Curie, H2020-MSCA-COFUND-2018-EuReCa-Grant Agreement number: 847718. The authors greatly acknowledge the Cell and Tissue Imaging (PICT-IBiSA), Institut Curie, member of the national infrastructure France-BioImaging (https://ror. org/01y7vt929) supported by the French National Research Agency (ANR-24-INBS-0005 FBI BIOGEN). The authors also thank the recombinant antibody platform of the Institut Curie. Open Access funding provided by the Universitat Pompeu Fabra.