Live imaging of hair bundle polarity acquisition demonstrates a critical timeline for transcription factor Emx2
Abstract
The asymmetric hair bundle on top of hair cells (HCs), comprises a kinocilium and stereocilia staircase, dictates HC's directional sensitivity. The mother centriole (MC) forms the base of the kinocilium, where stereocilia are subsequently built next to it. Previously we showed that transcription factor Emx2 reverses hair bundle orientation and its expression in the mouse vestibular utricle is restricted, resulting in two regions of opposite bundle orientation (Jiang et al, 2017). Here, we investigated establishment of opposite bundle orientation in embryonic utricles by live-imaging GFP-labeled centrioles in HCs. The daughter centriole invariably migrated ahead of the MC from the center to their respective peripheral locations in HCs. Comparing HCs between utricular regions, centriole trajectories were similar but they migrated towards opposite directions, suggesting that Emx2 pre-patterned HCs prior to centriole migration. Ectopic Emx2, however, reversed centriole trajectory within hours during a critical time-window when centriole trajectory was responsive to Emx2.
Data availability
The following figures contain the source data files. Figure 2 (source data 1), Figure 2 supplement 2 (source data 1-3), Figure 2 supplement 3 (source data 1-4), Figure 2 supplement 4 (source data 1-2), Figure 3 (source data 1-2), figure 3 supplement 2 (source data 1), Figure 4 (source data 1-2), Figure 5 (source data 1), Figure 6 (source data 1-2), Figure 7 (source data 1), Figure 7 supplement 1 (source data 1), Figure 8 (source data 1-2), Figure 9 (source data 1).
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Funding
National Institutes of Health (1ZIADC000021)
- Yosuke Tona
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Animal experimentation: All animal experiments were conducted according to NIH guidelines and under the approved Animal Care Protocol of NIDCD/NIH (#1212-17).
Copyright
This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
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