Key result
Replication forks linked to long nuclear actin filaments show increased mobility during stalling or breakage.
Why the study?
Nuclear actin filaments form during replication stress, but the function of short versus long filaments in the nuclear dynamics of replication sites was unclear.
Long nuclear actin filaments are associated with increased mobility of replication centers during mild replication stress, suggesting a role in relocalizing replication sites.
No immediate clinical implications; leaves open nuclear actin in replication stress responses for hypothesis-generating cardiovascular research.
Nuclear actin filaments (F-actin) form during S-phase and in response to replication stress to promote fork remodeling and repair. In mild replication stress conditions, nuclear actin polymerization is required to limit PrimPol recruitment to the fork while promoting fork reversal. Both short and long filaments form during this response, but their function in the nuclear dynamics of replication sites was unclear. Here, we show that replication centers associated with long nuclear actin filaments become more mobile than the rest of the forks, suggesting relocalization of replication sites as a response to prolonged fork stalling and/or fork breakage, even in response to mild replication stress.
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Merigliano et al. (2024) studied this question. Replication forks associated with long nuclear actin filaments under mild stress show increased mobility, indicating relocalization during fork stalling or breakage.
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