ArticleResearch square2026
Actomyosin contractility drives apical polarization and membrane transport during tubulogenesis.
Article in Research square, 2026. 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
Lumen formation during tubulogenesis requires the large-scale redistribution of cellular material, but the in vivo mechanisms remain unclear. Using the ascidian notochord as a tractable model, we show that actomyosin contractility orchestrates sequential, spatially distinct modes of cortical and cytoplasmic transport to promote lumen initiation and growth: lateral actomyosin centralizes apical determinants on cell contacts to position apical lumens; cyclic detachment and inward contraction of actomyosin bundles from a basal equatorial contractile ring drives internalization and transport of basal membranes toward the apical lumen surface to enable lumen growth. Basal membrane internalization/transport and lumen growth require both Ezrin/Radixin/Moesin (ERM) proteins and extracellular matrix (ECM). ERM promotes equatorial contractility and transmits inward contractile forces to basal membranes, while broad attachment to ECM resists inward forces to promote equatorial detachment. These findings reveal how cells integrate cortical and cytoplasmic modes of transport, driven by actomyosin contractility, to enable rapid lumen formation and likely other types of cellular remodeling.
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.