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Dev Biol 2018 May 15;4372:140-151. doi: 10.1016/j.ydbio.2018.03.015.
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Cdc42 controls primary mesenchyme cell morphogenesis in the sea urchin embryo.

Sepúlveda-Ramírez SP , Toledo-Jacobo L , Henson JH , Shuster CB .

In the sea urchin embryo, gastrulation is characterized by the ingression and directed cell migration of primary mesenchyme cells (PMCs), as well as the primary invagination and convergent extension of the endomesoderm. Like all cell shape changes, individual and collective cell motility is orchestrated by Rho family GTPases and their modulation of the actomyosin cytoskeleton. And while endomesoderm specification has been intensively studied in echinoids, much less is known about the proximate regulators driving cell motility. Toward these ends, we employed anti-sense morpholinos, mutant alleles and pharmacological inhibitors to assess the role of Cdc42 during sea urchin gastrulation. While inhibition of Cdc42 expression or activity had only mild effects on PMC ingression, PMC migration, alignment and skeletogenesis were disrupted in the absence of Cdc42, as well as elongation of the archenteron. PMC migration and patterning of the larval skeleton relies on the extension of filopodia, and Cdc42 was required for filopodia in vivo as well as in cultured PMCs. Lastly, filopodial extension required both Arp2/3 and formin actin-nucleating factors, supporting models of filopodial nucleation observed in other systems. Together, these results suggest that Cdc42 plays essential roles during PMC cell motility and organogenesis.

PubMed ID: 29555242
PMC ID: PMC5973877
Article link: Dev Biol
Grant support: [+]

Genes referenced: actr2 cdc42 LOC100887844 LOC100893746 LOC115919910 LOC590297
Antibodies: cdc42 Ab3 msp130 Ab6
Morpholinos: cdc42 MO1

Article Images: [+] show captions
References [+] :
Abraham, A Rac/Cdc42 exchange factor complex promotes formation of lateral filopodia and blood vessel lumen morphogenesis. 2015, Pubmed