Seemingly contradictory findings of single-molecule and in vivo experiments on a major mechanism of chromosome organization are reconciled by computationally investigating mechanisms of loop extrusion that are consistent with both.
Disrupting extrusion, a process that drives epithelial cell death, leads to increased cell survival, poor barrier function, and enhanced cell invasion and, thereby, promotes tumor initiation and progression.
Expression of Pitx2c at the onset of gastrulation drives convergence and extension movements in the zebrafish embryo by promoting downstream pathways affecting chemokine signaling, integrin-ECM interactions, and planar cell polarity components.
Nodal signaling regulates gastrulation cell behaviors largely in parallel with planar cell polarity signaling and is sufficient for ex vivo extension of embryonic explants.
Models of chromosome compaction by condensins demonstrate that two-sided loop extrusion and long residence times are required for high compaction, suggesting a tight coupling between these two properties in vivo.
A rare example of direct transdifferentiation is discovered in zebrafish in which kidney epithelial cells change into an endocrine gland and undergo live-cell extrusion from the renal tubule.
Relying on RNA fragments derived from degradation or partial template copying, non-enzymatic primer extension with strand displacement offers a novel and prebiotically plausible approach to RNA self-replication.
Analysing Myosin II unipolar planar polarisation with high spatial and temporal resolution during Drosophila axis extension reveals how tissue boundaries drive polarized cell intercalation while limiting cell mixing.
