Prdm1a and olig4 act downstream of Notch signaling to regulate cell fate at the neural plate border

Laura Hernandez-Lagunas; Davalyn R. Powell; Jera Law; Kelly A. Grant; Kristin Bruk Artinger

doi:10.1016/j.ydbio.2011.06.005

Prdm1a and olig4 act downstream of Notch signaling to regulate cell fate at the neural plate border

Laura Hernandez-Lagunas, Davalyn R. Powell, Jera Law, Kelly A. Grant, Kristin Bruk Artinger

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

The zinc finger domain transcription factor prdm1a plays an integral role in the development of the neural plate border cell fates, including neural crest cells and Rohon-Beard (RB) sensory neurons. However, the mechanisms underlying prdm1a function in cell fate specification is unknown. Here, we test more directly how prdm1a functions in this cell fate decision. Rather than affecting cell death or proliferation at the neural plate border, prdm1a acts explicitly on cell fate specification by counteracting olig4 expression in the neighboring interneuron domain. olig4 expression is expanded in prdm1a mutants and olig4 knockdown can rescue the reduced or abrogated neural crest and RB neuron phenotype in prdm1a mutants, suggesting a permissive role for prdm1a in neural plate border-derived cell fates. In addition, prdm1a expression is upregulated in the absence of Notch function, and inhibiting Notch signaling fails to rescue prdm1a mutants. This suggests that prdm1a functions downstream of Notch in the regulation of cell fate at the neural plate border and that Notch regulates the total number of progenitor cells at the neural plate border.

Original language	English (US)
Pages (from-to)	496-505
Number of pages	10
Journal	Developmental Biology
Volume	356
Issue number	2
DOIs	https://doi.org/10.1016/j.ydbio.2011.06.005
State	Published - Aug 15 2011
Externally published	Yes

Bibliographical note

Funding Information:
We would like to thank ZIRC (P40 RR012546-NIH-NCRR) for reagents; Bruce Appel, Linda Barlow, Lee Niswander and Christy Rossi for helpful comments on the manuscript; Linda Barlow for help with imaging; Morgan Singleton for extraordinary fish care; Keith Anderson for discussion; David McKean for the initial observation of prdm1a expression in mindbomb mutants; Ajay Chitnis for mind bomb mutants and discussion. We gratefully acknowledge the support of NIH P30 NS04815 zebrafish and imaging core grant, and NIH HD050698 to K.B.A.

Keywords

Blimp1
Neural crest
Rohon-Beard sensory neurons

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10.1016/j.ydbio.2011.06.005

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title = "Prdm1a and olig4 act downstream of Notch signaling to regulate cell fate at the neural plate border",

abstract = "The zinc finger domain transcription factor prdm1a plays an integral role in the development of the neural plate border cell fates, including neural crest cells and Rohon-Beard (RB) sensory neurons. However, the mechanisms underlying prdm1a function in cell fate specification is unknown. Here, we test more directly how prdm1a functions in this cell fate decision. Rather than affecting cell death or proliferation at the neural plate border, prdm1a acts explicitly on cell fate specification by counteracting olig4 expression in the neighboring interneuron domain. olig4 expression is expanded in prdm1a mutants and olig4 knockdown can rescue the reduced or abrogated neural crest and RB neuron phenotype in prdm1a mutants, suggesting a permissive role for prdm1a in neural plate border-derived cell fates. In addition, prdm1a expression is upregulated in the absence of Notch function, and inhibiting Notch signaling fails to rescue prdm1a mutants. This suggests that prdm1a functions downstream of Notch in the regulation of cell fate at the neural plate border and that Notch regulates the total number of progenitor cells at the neural plate border.",

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note = "Funding Information: We would like to thank ZIRC (P40 RR012546-NIH-NCRR) for reagents; Bruce Appel, Linda Barlow, Lee Niswander and Christy Rossi for helpful comments on the manuscript; Linda Barlow for help with imaging; Morgan Singleton for extraordinary fish care; Keith Anderson for discussion; David McKean for the initial observation of prdm1a expression in mindbomb mutants; Ajay Chitnis for mind bomb mutants and discussion. We gratefully acknowledge the support of NIH P30 NS04815 zebrafish and imaging core grant, and NIH HD050698 to K.B.A.",

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N2 - The zinc finger domain transcription factor prdm1a plays an integral role in the development of the neural plate border cell fates, including neural crest cells and Rohon-Beard (RB) sensory neurons. However, the mechanisms underlying prdm1a function in cell fate specification is unknown. Here, we test more directly how prdm1a functions in this cell fate decision. Rather than affecting cell death or proliferation at the neural plate border, prdm1a acts explicitly on cell fate specification by counteracting olig4 expression in the neighboring interneuron domain. olig4 expression is expanded in prdm1a mutants and olig4 knockdown can rescue the reduced or abrogated neural crest and RB neuron phenotype in prdm1a mutants, suggesting a permissive role for prdm1a in neural plate border-derived cell fates. In addition, prdm1a expression is upregulated in the absence of Notch function, and inhibiting Notch signaling fails to rescue prdm1a mutants. This suggests that prdm1a functions downstream of Notch in the regulation of cell fate at the neural plate border and that Notch regulates the total number of progenitor cells at the neural plate border.

AB - The zinc finger domain transcription factor prdm1a plays an integral role in the development of the neural plate border cell fates, including neural crest cells and Rohon-Beard (RB) sensory neurons. However, the mechanisms underlying prdm1a function in cell fate specification is unknown. Here, we test more directly how prdm1a functions in this cell fate decision. Rather than affecting cell death or proliferation at the neural plate border, prdm1a acts explicitly on cell fate specification by counteracting olig4 expression in the neighboring interneuron domain. olig4 expression is expanded in prdm1a mutants and olig4 knockdown can rescue the reduced or abrogated neural crest and RB neuron phenotype in prdm1a mutants, suggesting a permissive role for prdm1a in neural plate border-derived cell fates. In addition, prdm1a expression is upregulated in the absence of Notch function, and inhibiting Notch signaling fails to rescue prdm1a mutants. This suggests that prdm1a functions downstream of Notch in the regulation of cell fate at the neural plate border and that Notch regulates the total number of progenitor cells at the neural plate border.

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Prdm1a and olig4 act downstream of Notch signaling to regulate cell fate at the neural plate border

Abstract

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Keywords

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