Rab25a and Rab25b mutant embryos exhibit epithelial spreading delays during morphogenesis and are characterized by cytokinesis defects leading to cell fusions, heterogeneous epithelial cell sizes, and reduced cortical actomyosin contractility.
Theory explains how transport of gene expression vortices by cell advection may cause intermingled defective and normal segments along the body axis during resynchronization experiments in the zebrafish segmentation clock.
Systematic analysis of C. elegans zygotes manipulated to divide equally demonstrates that daughter cell size asymmetry is critical for proper cell cycle timing, positioning, and fates during subsequent embryogenesis.
The combined use of NAD+ with ribitol or ribose potentiates the rescue of α-dystroglycan functional glycosylation in FKRP-mutant patient-specific iPSC-derived myotubes, representing potential novel treatments for FKRP muscular dystrophies.
β-Catenin-mediated expansion of nephron progenitors is independent of direct β-catenin/chromatin engagement, while progenitor induction proceeds with a β-catenin-driven switch of repressive TCFL1/TCFL2 to activating TCF7/LEF1 factors on transcriptionally poised enhancers.
H3-G34R, V, and W oncohistonesin fission yeast cause differential K36 modification, DNA damage sensitivity and genome stability outcomes, highlighting the need for a thorough evaluation of distinct mutations.
Live quantitative monitoring of transcriptional bursting reveals that enhancers responding to different regulators use the same kinetic strategy to produce a complex composite pattern of developmental expression.