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Cyanobacteria cope with both predictable day/night changes and natural fluctuations in light during the day by adjusting the expression dynamics of circadian-clock-controlled genes via a network of transcriptional regulators.

A gene regulatory network model provides a simplified explanation of the molecular interactions that orchestrate muscle development in the sea urchin embryo.

The theory of Buffered Qualitative Stability uses the importance of biological robustness to explain many features of gene regulatory networks in a wide range of organisms, and has implications for diverse biological phenomena including the ability of bacteria and cancer cells to ‘loosen’ their robustness and hence evade treatment.

The gene regulatory network controlling directed cell migration in a sea urchin is strikingly similar to a sub-circuit for eye development in Drosophila, suggesting that ancient systems-level controls may be adapted for diverse functions in different animals.

Pervasive ‘futile cycling’ by chromatin-modifying factors suggests a mechanism for creating new links in gene regulatory networks.

Greater phenotypic variation is exposed by mutations in a gene regulatory system compared to mutations in its constitutive components, namely the transcription factor and the promoter, alone.

Coordinated microRNAs activity induced by VEGF represses cell proliferation and favors cell migration at the onset of sprouting angiogenesis in endothelial cells.

ATAC-seq, transcriptomics, and transcription factor motif searches collaborate to build a network that regulates gene expression in different cortical layers.

During early embryogenesis of the sea urchin, asymmetrical positioning of the dorsal/ventral organizer relies upon the suppression of organizer activities in dorsal blastomeres by the Hbox12 homeodomain-containing repressor.

miR-142 is instrumental for actin homeostasis, and its loss disrupts the cytoskeleton organization and thrombopoiesis of megakaryocytes.