Skip to content
DraconiticResearch
Search Sources API
201,683 studies31 sourcesUpdated just now
Peer-reviewedCC BY 4.0Life Science Alliance

EFhd2 regulates microtubule-dependent mitochondrial fitness at the B cell immune synapse

  • Leonie Weckwerth1,2
  • Benjamin Schmid3
  • Philipp Tripal3
  • Ann-Kathrin Himmelreich1,2
  • Jana Thomas1,2
  • Katharina Pracht1,2
  • Sophia Urbanczyk1,2
  • Hannah Allnach1,2
  • Anna Gottwald1,2
  • Georg Schett2,4,5
  • Ralph Palmisano3
  • Dirk Mielenz1,2,4
5 affiliations
  1. 1Department of Translational Immunology, Department of Medicine 3 - Rheumatology and Immunology, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Uniklinikum Erlangen
  2. 2Deutsches Zentrum Immuntherapie, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Uniklinikum Erlangen
  3. 3Optical Imaging Competence Centre Erlangen (FAU OICE), Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg
  4. 4FAU Profile Center Immunomedicine, FAU Erlangen-Nürnberg
  5. 5Department of Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Uniklinikum Erlangen
Read full textDOICite

Abstract

Immobilized antigen induces an immune synapse, which is supported by Swiprosin-1/EFhd2 (EFhd2) in B and T cells. Here, we find that EFhd2 regulates mitochondrial fitness in the B cell synapse. Whereas activated EFhd2-deficient (KO) B cells show higher mitochondrial mass than wildtype (WT) B cells, this potential advantage reverses on coated anti-IgM antibodies: activated WT B cells enhance basal and maximal respiration as well as proton leak, with large increments of mitochondrial spare capacity, but EFhd2KO B cells fail to do so. Actin destabilization, but much more so microtubule destabilization, impairs mitochondrial up-regulation in WT, but not in EFhd2KO B cells. Conversely, microtubule stabilization, and to a lesser extent actin stabilization, restore mitochondrial spare capacity in EFhd2KO B cells at the BCR synapse. EFhd2KO B cells fail to coordinate the microtubule organization center, mitochondria and IgM BCRs upon synapse formation. Hence, microtubule-dependent mitochondrial organization at the immune synapse coordinates mitochondrial fitness in B cells via EFhd2.

Related

  1. PACE4 Regulates Apoptosis in Human Prostate Cancer Cells via Endoplasmic Reticulum Stress and Mitochondrial Signaling Pathways [Retraction].
    Drug design, development and therapyPeer-reviewedCC BY-NCFull textMolecular biology & gene regulationEurope PMC
  2. TDP-43 regulates mitochondrial dsRNA accumulation and chromosome territory formation during prophase I of Drosophila male meiosis
    Victoria R. St. Amand, Geoff E. Stilwell, Stephen L. Helfand +1
    Communications BiologyPeer-reviewedCC BY-NC-ND 4.0Full textMolecular biology & gene regulationCrossref
  3. Sublethal chlorpyrifos exposure induces intergenerational fitness costs and mitochondrial alterations in Blattella germanica
    Xin Li, Jiang-Ling Chen, Zi-Han Xu +5
    Current Research in Insect SciencePeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationPMC
  4. Mitochondrial Fitness in Anti-Tumor T Cells: From Activation to Exhaustion and Memory Formation
    Dong-Keon Lee, Jae Ho Seo
    BiomoleculesPeer-reviewedCC BY 4.0Molecular biology & gene regulationCrossref
  5. Quiescence to proliferation transition regulates asynchronous mitochondrial DNA replication dynamics.
    Kiyoshi Miyagawa, Noriko Hosoya
    Proceedings of the National Academy of Sciences of the United States of AmericaPeer-reviewedCC BY-NC-NDFull textMolecular biology & gene regulationEurope PMC

Cite

BibTeXRIS
BibTeX
@article{weckwerth2026efhd2,
  title = {{EFhd2 regulates microtubule-dependent mitochondrial fitness at the B cell immune synapse}},
  author = {Leonie Weckwerth and Benjamin Schmid and Philipp Tripal and Ann-Kathrin Himmelreich and Jana Thomas and Katharina Pracht and Sophia Urbanczyk and Hannah Allnach and Anna Gottwald and Georg Schett and Ralph Palmisano and Dirk Mielenz},
  journal = {Life Science Alliance},
  year = {2026},
  month = nov,
  doi = {10.26508/lsa.202603876},
  url = {https://www.life-science-alliance.org/lookup/doi/10.26508/lsa.202603876},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - EFhd2 regulates microtubule-dependent mitochondrial fitness at the B cell immune synapse
AU  - Leonie Weckwerth
AU  - Benjamin Schmid
AU  - Philipp Tripal
AU  - Ann-Kathrin Himmelreich
AU  - Jana Thomas
AU  - Katharina Pracht
AU  - Sophia Urbanczyk
AU  - Hannah Allnach
AU  - Anna Gottwald
AU  - Georg Schett
AU  - Ralph Palmisano
AU  - Dirk Mielenz
PY  - 2026
DA  - 2026/11/04
JO  - Life Science Alliance
DO  - 10.26508/lsa.202603876
UR  - https://www.life-science-alliance.org/lookup/doi/10.26508/lsa.202603876
AB  - Immobilized antigen induces an immune synapse, which is supported by Swiprosin-1/EFhd2 (EFhd2) in B and T cells. Here, we find that EFhd2 regulates mitochondrial fitness in the B cell synapse. Whereas activated EFhd2-deficient (KO) B cells show higher mitochondrial mass than wildtype (WT) B cells, this potential advantage reverses on coated anti-IgM antibodies: activated WT B cells enhance basal and maximal respiration as well as proton leak, with large increments of mitochondrial spare capacity, but EFhd2KO B cells fail to do so. Actin destabilization, but much more so microtubule destabilization, impairs mitochondrial up-regulation in WT, but not in EFhd2KO B cells. Conversely, microtubule stabilization, and to a lesser extent actin stabilization, restore mitochondrial spare capacity in EFhd2KO B cells at the BCR synapse. EFhd2KO B cells fail to coordinate the microtubule organization center, mitochondria and IgM BCRs upon synapse formation. Hence, microtubule-dependent mitochondrial organization at the immune synapse coordinates mitochondrial fitness in B cells via EFhd2.
SN  - 2575-1077
ER  -