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Fig. 5. The effects of b-adrenergic signaling on mesoderm-inde- pendent neural marker expressions. (A) The experimental proce- dure for B and C. Animal cap regions (ACs) were cut from embryos injected with/without mRNAs and/or Adrb2-MO, cul- tured with/without 1 lM of adrenaline solution until stage 26, and used for reverse transcription-polymerase chain reaction (RT- PCR) analyses. More than 0.01 mmol/L of adrenaline solution killed AC cells for unfathomable reasons. (B, C) Inhibition of anterior neural marker expression by up- or downregulation of b- adrenergic signaling. Anterior neural markers, Six3 and Rx2a, mid-hindbrain boundary marker, En2, posterior neural (spinal cord) marker, HoxB9, and pan-neural markers, NCAM and N- tubulin, were not affected in both cases. a-actin and ODC were respectively used for showing no contamination of mesoderm and loading control. (D) Downstream model of Adrb2. (E) Wes- tern blotting analysis of phospho-ERK in adrenaline treated embryos. Embryos were treated from 2-cell stage with 0.5 mmol/ L of adrenaline solution and fixed at stage 26.

Image published in: Mori S et al. (2013)

Copyright © 2013. Image reproduced with permission of the Publisher, John Wiley & Sons.

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