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Peer-reviewedCC BY 4.0Molecular Biology of the Cell

Excess p50 induces Arp1-dependent dynactin clusters containing the assembly factor VezA

  • Jun Zhang1
  • Rongde Qiu1
  • Xin Xiang1
  1. 1Department of Biochemistry and Molecular Biology, The Uniformed Services University of the Health Sciences- F. Edward Hébert School of Medicine, Bethesda, Maryland 20814
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Abstract

Dynactin, a complex essential for cytoplasmic dynein function, contains an Arp1 mini-filament with a pointed-end sub-complex including Arp11 and a shoulder sub-complex including p50 and p150. We recently identified in Aspergillus nidulans a vezatin homologue, VezA, that enhances dynactin assembly, but VezA does not co-localize with dynactin, suggesting a transient interaction. It was found that overexpression of p50 separates the shoulder from the mini-filament and causes late-onset neurodegeneration in mice, but its cellular effects in the context of VezA need to be studied. Here, we surprisingly found that p50 overexpression in A. nidulans causes Arp11, p50 (but not p150), and VezA to form co-localized clusters whose presence depends on Arp1. Formation of the VezA cluster also depends on Arp11, and VezA significantly enhances the intensity of Arp11-GFP clusters but not that of p50-GFP clusters. Moreover, an evolutionarily conserved region of p50 (aa17-25) forming a beta-sheet structure with Arp1, as revealed in previous cryo-EM studies, is critical for the formation of Arp11, p50, and VezA clusters. These results suggest that excess p50 induces cluster formation driven by p50-Arp1 interactions, and that this assembly intermediate lacking the intact shoulder traps VezA, which participates in the Arp11-Arp1-p50 interactions.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026excess,
  title = {{Excess p50 induces Arp1-dependent dynactin clusters containing the assembly factor VezA}},
  author = {Jun Zhang and Rongde Qiu and Xin Xiang},
  journal = {Molecular Biology of the Cell},
  year = {2026},
  month = oct,
  doi = {10.1091/mbc.e26-06-0275},
  url = {https://doi.org/10.1091/mbc.e26-06-0275},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Excess p50 induces Arp1-dependent dynactin clusters containing the assembly factor VezA
AU  - Jun Zhang
AU  - Rongde Qiu
AU  - Xin Xiang
PY  - 2026
DA  - 2026/10/26
JO  - Molecular Biology of the Cell
DO  - 10.1091/mbc.e26-06-0275
UR  - https://doi.org/10.1091/mbc.e26-06-0275
AB  - Dynactin, a complex essential for cytoplasmic dynein function, contains an Arp1 mini-filament with a pointed-end sub-complex including Arp11 and a shoulder sub-complex including p50 and p150. We recently identified in Aspergillus nidulans a vezatin homologue, VezA, that enhances dynactin assembly, but VezA does not co-localize with dynactin, suggesting a transient interaction. It was found that overexpression of p50 separates the shoulder from the mini-filament and causes late-onset neurodegeneration in mice, but its cellular effects in the context of VezA need to be studied. Here, we surprisingly found that p50 overexpression in A. nidulans causes Arp11, p50 (but not p150), and VezA to form co-localized clusters whose presence depends on Arp1. Formation of the VezA cluster also depends on Arp11, and VezA significantly enhances the intensity of Arp11-GFP clusters but not that of p50-GFP clusters. Moreover, an evolutionarily conserved region of p50 (aa17-25) forming a beta-sheet structure with Arp1, as revealed in previous cryo-EM studies, is critical for the formation of Arp11, p50, and VezA clusters. These results suggest that excess p50 induces cluster formation driven by p50-Arp1 interactions, and that this assembly intermediate lacking the intact shoulder traps VezA, which participates in the Arp11-Arp1-p50 interactions.
SN  - 1059-1524
SN  - 1939-4586
ER  -