ArticleResearch square2026
Polarity dependent Hippo-Yap regulation controls cortical development.
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.
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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.
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial polarity is established by partitioning the apical and basal domains within the cell. Antagonistic inhibitions between the apical and basal polarity complex proteins segregate them into their designated domains. Failure to achieve this causes developmental disorders and cancer. While the biochemical basis of this antagonism has been identified, the complexity of context-dependent cell-cell interactions obscures its cellular underpinnings. Here, through a series of genetic rescues in a murine model of brain malformation, the cellular mechanisms underlying this antagonism are uncovered. The expanded apical domain caused by the absence of the basal complex protein, Lethal Giant Larvae (Lgl)1 initiates subsequent cellular defects, including mislocalized adherens junctions and ectopic proliferation. Concurrent genetic removal of apical polarity complex, Crb1/2, abrogates cellular defects and heterotopia, evidence of their pivotal role. Gene expression, cell cycle, and rescue experiments revealed that antagonistic interactions converge onto Hippo-Yap signaling-dependent cell cycle kinetics. Our study highlights the fundamental antagonism of polarity proteins in preventing epithelial disruption and ectopic mitogenic activity.
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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 Socratic graph.