Ecm29-Dependent Proteasome Localization Regulates Cytoskeleton Remodeling at the Immune Synapse

Jorge Ibañez-Vega, Felipe Del Valle, Juan José Sáez, Fanny Guzman, Jheimmy Diaz, Andrea Soza*, María Isabel Yuseff*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

The formation of an immune synapse (IS) enables B cells to capture membrane-tethered antigens, where cortical actin cytoskeleton remodeling regulates cell spreading and depletion of F-actin at the centrosome promotes the recruitment of lysosomes to facilitate antigen extraction. How B cells regulate both pools of actin, remains poorly understood. We report here that decreased F-actin at the centrosome and IS relies on the distribution of the proteasome, regulated by Ecm29. Silencing Ecm29 decreases the proteasome pool associated to the centrosome of B cells and shifts its accumulation to the cell cortex and IS. Accordingly, Ecm29-silenced B cells display increased F-actin at the centrosome, impaired centrosome and lysosome repositioning to the IS and defective antigen extraction and presentation. Ecm29-silenced B cells, which accumulate higher levels of proteasome at the cell cortex, display decreased actin retrograde flow in lamellipodia and enhanced spreading responses. Our findings support a model where B the asymmetric distribution of the proteasome, mediated by Ecm29, coordinates actin dynamics at the centrosome and the IS, promoting lysosome recruitment and cell spreading.

Original languageEnglish
Article number650817
JournalFrontiers in Cell and Developmental Biology
Volume9
DOIs
StatePublished - 2021

Bibliographical note

Publisher Copyright:
© Copyright © 2021 Ibañez-Vega, Del Valle, Sáez, Guzman, Diaz, Soza and Yuseff.

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology

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