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The distribution of primary cilia in the mouse embyo

 

Primary cilia is formed by centrioles project from the surface of most vertebrate cells, and is involved in the response to specific developmental signals, including Hedgehog (Hh) ligands. Bangs et al. demonstrate the time and location that primary cilia appear in the mouse embryo. The article was published on Nature Cell Biology, recently.

 

Researchers established a transgenic mouse embryo cell line that express ARL13B fused to the red fluorescent protein mCherry in cilia, and Centrin 2 fused to GFP in centrosomes. At E6.0, primary cilia first appear in the epiblast on cells, following by the present on all derivatives of the epiblast. On the other hand, extraembryonic cell lines, such as visceral endoderm and trophectoderm lineages, are absent of cilia but have centrosomes. The results match with what they found in vivo. In addition, extraembryonic endoderm (XEN) stem cells, which lack cilia, can form cilia after inhibiting cilium disassembly pathway, AURKA-HDAC6. The absence of cilia on XEN stem cells indicates these cells are unable to respond to Hh ligands, which triggered the Hh signaling pathway to mediate embryo development. The findings suggest the ability of cells response to Hh ligands is regulated by the distribution of primary cilia in the placenta and yolk sac, therefore, influences embryo development. 

 

Reference:
Nat Cell Biol. 2015 Jan 19. doi: 10.1038/ncb3091.

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S1133 Alisertib (MLN8237) Alisertib (MLN8237) is a selective Aurora A inhibitor with IC50 of 1.2 nM in a cell-free assay. It has >200-fold higher selectivity for Aurora A than Aurora B. Alisertib induces cell cycle arrest, apoptosis and autophagy. Phase 3.
S1109 BI 2536 BI-2536 is a potent Plk1 inhibitor with IC50 of 0.83 nM in a cell-free assay. BI-2536 inhibits Bromodomain 4 (BRD4) with Kd of 37 nM and potently suppresses c-Myc expression. BI-2536 induces apoptosis and attenuates autophagy. Phase 2.

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Aurora Kinase PLK