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Skn-1a/Pou2f3 is required for the generation of Trpm5-expressing microvillous cells in the mouse main olfactory epithelium

Tatsuya Yamaguchi1, Junpei Yamashita1, Makoto Ohmoto2, Imad Aoudé3, Tatsuya Ogura3, Wangmei Luo3, Alexander A Bachmanov2, Weihong Lin3, Ichiro Matsumoto2* and Junji Hirota14*

Author Affiliations

1 Department of Bioengineering, Graduate School of Bioscience and Bioengineering, Tokyo Institute of Technology, Yokohama 226-8501, Japan

2 Monell Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104, USA

3 Department of Biological Sciences, University of Maryland, Baltimore County, Baltimore, MD 21250, USA

4 Center for Biological Resources and Informatics, Tokyo Institute of Technology, 4259-B63 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan

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BMC Neuroscience 2014, 15:13  doi:10.1186/1471-2202-15-13

Published: 16 January 2014

Additional files

Additional file 1: Table S1:

Summary of the quantification of Skn-1a-, Trpm5-, and Mash1-expressing cells in the MOE. The populations of Skn-1a-, Trpm5-, and Mash1-expressing cells in the MOE were quantified by in situ hybridization. This table summarizes the total numbers of cells counted in individual mice to calculate the populations in Figure 2D and E.

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Additional file 2: Figure S1:

IP3R3 -positive microvillous cells remained in the Skn-1a-/- MOE. Effects of Skn-1a deficiency on IP3R3 -positive microvillous cells were examined by immunostaining with an anti-Trpm5 (green) and an anti-IP3R3 (red) antibodies using coronal sections of the wild-type and Skn-1a-/- MOE of adult mice. Trpm5-positive cells did not overlap with IP3R3-positive cells in the wild-type MOE. In the Skn-1a-/- MOE, IP3R3-positive cells were observed, whereas no immunoreactive signal for Trpm5 was detected, suggesting that one of remaining superficial microvillous cells in the Skn-1a-/- MOE would be IP3R3-microvillous cells, and Skn-1a is not essential to generate them. Scale bars, 10 μm.

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