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Yuseff, M.-I.

Publications and source records attributed to Yuseff, M.-I..

3 recordsLinked to original sources

Spatiotemporal control of microtubule acetylation by mechanical cues regulates lysosome dynamics at the immune synapse of B cells to promote antigen presentation

The capacity of B cells to extract immobilized antigens through the formation of an immune synapse can be tuned by the physical characteristics of the surface where antigens are encountered. However, the underlying mechanisms that couple mechanosensing by B cells to antigen extraction and processing remain poorly understood. We show that B cells activated by antigens associated with stiffer substrates exhibit enhanced spreading responses and higher tubulin acetylation at the center of the immune synapse, where less motile lysosomes preferentially localize. This process is coupled to the translocation of the microtubule acetylase, ATAT1 to the cytoplasm of B cells, which occurs as a mechano-response during BCR stimulation. Accordingly, B cells silenced for ATAT1 are unable to stabilize lysosomes at the synaptic interface and display a lower capacity to extract and present immobilized antigens to T cells. Overall, these findings highlight how BCR-dependent mechano-responses trigger microtubule network modifications to precisely orchestrate lysosome positioning to promote antigen extraction and presentation in B cells.

cell biology↗

B cells adapt their nuclear morphology to organize the immune synapse and help antigen extraction

Upon interaction with immobilized antigens B cells form an immune synapse, where actin remodeling and re-positioning of the microtubule-organizing center (MTOC) together with lysosomes can facilitate antigen extraction. B cells have restricted cytoplasmic space, mainly occupied by a large nucleus, yet the role of nuclear morphology in the formation of the immune synapse has not been addressed. Here we show that, upon activation, B cells re-orientate and adapt the size of their nuclear groove facing the immune synapse, where the MTOC sits and lysosomes accumulate. Silencing nuclear envelope proteins, Nesprin-1 and Sun-1, impairs nuclear reorientation towards the synapse and leads to defects in actin organization at this level. Consequently, B cells are unable to internalize the BCR after antigen activation. Nesprin-1 and Sun-1-silenced B cells also fail to accumulate the tethering factor Exo70 at the center of the synaptic membrane and display defective lysosome positioning, impairing efficient antigen extraction at the immune synapse. Thus, changes in nuclear morphology and positioning emerge as critical regulatory steps to coordinate B cell activation.

cell biology↗

Ecm29-dependent proteasome localization regulates cytoskeleton remodeling at the immune synapse

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.

cell biology↗