ArticlebioRxiv : the preprint server for biology2025
Cell cycle-regulated tug-of-war between microtubule motors positions major trafficking organelles.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The morphology and integrity of the Golgi apparatus, which are critical for protein processing and sorting, undergo significant changes during interphase in proliferating mammalian cells. Initially compact during G1, the Golgi dissociates from the centrosomes in S-phase and transitions into an extended perinuclear ribbon in G2. The mechanisms underlying these changes remain unclear. Golgi positioning can be influenced by microtubule (MT)-dependent motors and membrane exchange with endoplasmic reticulum exit sites (ERES). We employ loss-of-function approaches and live-cell microscopy to demonstrate that CDK1-dependent signaling modulates the tug-of-war between plus- and minus-end-directed motors, resulting in differential positioning of the Golgi and ERES in G1 versus S/G2 phases. In G1, the Golgi and ERES are compacted by the minus-end-directed activity of dynein and KIFC3, respectively. In S/G2, organelle-specific combinations of kinesin-1 heavy and light chains overpower minus-end-directed motors. Our findings reveal a novel, cell cycle-regulated mechanism that coordinates organelle positioning via motor switching.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.