Back

Viral rewiring of APC/C-CDC20 drives Aurora B hyperubiquitination, mitotic regression and polyploidy

Srivastava, S.; Sengupta, D.; Jasiqi, Y.; Povolo, V. R.; Bauer, M.; Hubert, M.; Haselmann, U.; Schneider, M.; Helm, D.; Greber, U. F.; Prasad, V.

2026-02-15 cell biology
10.64898/2026.02.13.705602 bioRxiv
Show abstract

Cytokinesis requires elaborate processes in the midbody, including the timely inactivation of Aurora B kinase (AurB) and membrane fission to separate the daughter cells. Here, we show that human adenovirus (AdV) perturbs midbody function, prevents daughter separation and induces cytoplasmic regression of both cancer cells and primary diploid human airway basal cells resulting in polyploidy. Infected cells undergo cleavage furrow regression after midbody formation driven by the viral protein E4orf4 independently of E4orf4 interaction with protein phosphatase 2A. The co-activator of the anaphase-promoting complex/cyclosome (APC/C), CDC20 is upregulated in AdV infection and required for regression. E4orf4 directly interacts with CDC20 and redirects the E3-ubiquitin ligase APC/C-CDC20 towards AurB, promoting hyperubiquitination and premature extraction of AurB from the midbody. Loss of midbody-associated AurB coincides with midbody collapse and furrow regression. Our findings reveal a previously unrecognized APC/C-CDC20-dependent pathway controlling late cytokinesis through AurB extraction from the midbody.

Matching journals

The top 4 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.