ECB-ART-42404Dev Biol 2012 Apr 15;3642:259-67. doi: 10.1016/j.ydbio.2012.02.003.
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Cis-regulatory logic driving glial cells missing: self-sustaining circuitry in later embryogenesis.
The glial cells missing (gcm) regulatory gene of the sea urchin Strongylocentrotus purpuratus is first expressed in veg2 daughter cells as the genomic target of late cleavage stage Delta-Notch signaling from the skeletogenic mesoderm precursors. Gcm is required in veg2 progeny during late cleavages for the early phase of pigment cell precursor specification. Here we report on a later acting cis-regulatory module that assumes control of gcm expression by the early mesenchyme blastula stage and maintains it through pigment cell differentiation and dispersal. Cis-perturbation analyses reveal that the two critical elements within this late module are consensus matches to Gcm and Six1 binding sites. Significantly, six1 mRNA localizes to gcm+cells from the mesenchyme blastula stage onwards. Trans-perturbations with anti-sense morpholinos reveal a co-dependency between six1 and gcm. Six1 mRNA levels fall sharply after Gcm is depleted, while depleting Six1 leads to significant reductions in output of endogenous gcm or modular-reporters. These results support the conclusion gcm and six1 comprise a positive intergenic feedback loop in the mesodermal GRN. This often employed cross regulatory GRN feature here ensures self-sustaining gcm output in a cohort of fully specified pigment cell precursors at a relatively early developmental stage.
PubMed ID: 22509525
PMC ID: PMC3561781
Article link: Dev Biol
Genes referenced: gcml LOC100887844 LOC115919910 LOC115921237 LOC575170 six1
Morpholinos: LOC575231 MO1 gcml MO1 six1 MO2
References [+] :
Brown, Paircomp, FamilyRelationsII and Cartwheel: tools for interspecific sequence comparison. 2006, Pubmed