Germ cell ablation delays C. elegans aging, in part, because unconsumed fat triggers activation of the detoxification factor SKN-1/Nrf, which is regulated by lipid signals and maintains lipid homeostasis.
Environmental transmission is atypical of symbionts that have undergone genome degradation, yet genetically reduced deep-sea anglerfish symbionts likely persist in the deep sea biome in search of a new host.
The mechanism underlying Shprintzen–Goldberg syndrome is solved and reveals that missense mutations in the transcriptional repressor SKI abolish ligand-induced SKI degradation, which results in attenuation of TGF-β transcriptional responses.
Nup98-HoxA9 is recruited to Hox gene cluster regions together with the chromosomally pre-bound nuclear export factor Crm1, which induces aberrant expression of several Hox genes and affecting the differentiation of embryonic stem cells.
Eph receptor signaling commonly excludes migrating embryonic cells from regions of high ligand density; however, in sea urchin embryos pigmented immunocytes are attracted to regions expressing high levels of Ephrin.
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.
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.