Regulation of root hair cell differentiation by R3 MYB transcription factors in tomato and Arabidopsis

Hair cell fate determination in the inner ear has been shown to be controlled by specific genes. Recent loss-of-function and gain-of-function experiments have demonstrated that Math1, a mouse homolog of the Drosophila gene atonal, is essential for the production of hair cells. To identify genes that may interact with Math1 and inhibit hair cell differentiation, we have focused on Hes1, a mammalian hairy and enhancer of split homolog, which is a negative regulator of neurogenesis. We report here that targeted deletion of Hes1 leads to formation of supernumerary hair cells in the cochlea and utricle of the inner ear. RT-PCR analysis shows that Hes1 is expressed in inner ear during hair cell differentiation and its expression is maintained in adulthood. In situ hybridization with late embryonic inner ear tissue reveals that Hes1 is expressed in supporting cells, but not hair cells, of the vestibular sensory epithelium. In the cochlea, Hes1 is selectively expressed in the greater epithelial ridge and lesser epithelial ridge regions which are adjacent to inner and outer hair cells. Co-transfection experiments in postnatal rat explant cultures show that overexpression of Hes1 prevents hair cell differentiation induced by Math1. Therefore Hes1 can negatively regulate hair cell differentiation by antagonizing Math1. These results suggest that a balance between Math1 and negative regulators such as Hes1 is crucial for the production of an appropriate number of inner ear hair cells.

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CLE14 peptide signaling in Arabidopsis root hair cell fate determination

Plant Biotechnology ◽

10.5511/plantbiotechnology.18.0122a ◽

2018 ◽

Vol 35 (1) ◽

pp. 17-22 ◽

Cited By ~ 5

Author(s):

Naoto Hayashi ◽

Takuya Tetsumura ◽

Shinichiro Sawa ◽

Takuji Wada ◽

Rumi Tominaga-Wada

Keyword(s):

Hair Cell ◽

Cell Fate ◽

Root Hair ◽

Cell Fate Determination ◽

Arabidopsis Root ◽

Fate Determination ◽

Peptide Signaling ◽

Root Hair Cell

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Distinct relationships between GLABRA2 and single-repeat R3 MYB transcription factors in the regulation of trichome and root hair patterning in Arabidopsis

New Phytologist ◽

10.1111/j.1469-8137.2009.03067.x ◽

2009 ◽

Vol 185 (2) ◽

pp. 387-400 ◽

Cited By ~ 30

Author(s):

Shucai Wang ◽

Christa Barron ◽

John Schiefelbein ◽

Jin-Gui Chen

Keyword(s):

Transcription Factors ◽

Root Hair ◽

Myb Transcription Factors

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A counter gradient of Activin A and follistatin instructs the timing of hair cell differentiation in the murine cochlea

eLife ◽

10.7554/elife.47613 ◽

2019 ◽

Vol 8 ◽

Cited By ~ 3

Author(s):

Meenakshi Prajapati-DiNubila ◽

Ana Benito-Gonzalez ◽

Erin Jennifer Golden ◽

Shuran Zhang ◽

Angelika Doetzlhofer

Keyword(s):

Cell Differentiation ◽

Hair Cell ◽

Hair Cells ◽

Activin A ◽

Sensory Epithelium ◽

Outer Hair Cells ◽

Longitudinal Gradient ◽

Hair Cell Differentiation ◽

Local Gradient ◽

Molecular Signals

The mammalian auditory sensory epithelium has one of the most stereotyped cellular patterns known in vertebrates. Mechano-sensory hair cells are arranged in precise rows, with one row of inner and three rows of outer hair cells spanning the length of the spiral-shaped sensory epithelium. Aiding such precise cellular patterning, differentiation of the auditory sensory epithelium is precisely timed and follows a steep longitudinal gradient. The molecular signals that promote auditory sensory differentiation and instruct its graded pattern are largely unknown. Here, we identify Activin A and its antagonist follistatin as key regulators of hair cell differentiation and show, using mouse genetic approaches, that a local gradient of Activin A signaling within the auditory sensory epithelium times the longitudinal gradient of hair cell differentiation. Furthermore, we provide evidence that Activin-type signaling regulates a radial gradient of terminal mitosis within the auditory sensory epithelium, which constitutes a novel mechanism for limiting the number of inner hair cells being produced.

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A Critical E-box in Barhl1 3′ Enhancer Is Essential for Auditory Hair Cell Differentiation

Cells ◽

10.3390/cells8050458 ◽

2019 ◽

Vol 8 (5) ◽

pp. 458 ◽

Cited By ~ 2

Author(s):

Kun Hou ◽

Hui Jiang ◽

Md. Rezaul Karim ◽

Chao Zhong ◽

Zhouwen Xu ◽

...

Keyword(s):

Cell Differentiation ◽

Hair Cell ◽

Hair Cells ◽

Embryonic Stem ◽

Cell Development ◽

Homologous Gene ◽

Auditory Hair Cells ◽

E Box ◽

Hair Cell Differentiation

Barhl1, a mouse homologous gene of Drosophila BarH class homeobox genes, is highly expressed within the inner ear and crucial for the long-term maintenance of auditory hair cells that mediate hearing and balance, yet little is known about the molecular events underlying Barhl1 regulation and function in hair cells. In this study, through data mining and in vitro report assay, we firstly identified Barhl1 as a direct target gene of Atoh1 and one E-box (E3) in Barhl1 3’ enhancer is crucial for Atoh1-mediated Barhl1 activation. Then we generated a mouse embryonic stem cell (mESC) line carrying disruptions on this E3 site E-box (CAGCTG) using CRISPR/Cas9 technology and this E3 mutated mESC line is further subjected to an efficient stepwise hair cell differentiation strategy in vitro. Disruptions on this E3 site caused dramatic loss of Barhl1 expression and significantly reduced the number of induced hair cell-like cells, while no affections on the differentiation toward early primitive ectoderm-like cells and otic progenitors. Finally, through RNA-seq profiling and gene ontology (GO) enrichment analysis, we found that this E3 box was indispensable for Barhl1 expression to maintain hair cell development and normal functions. We also compared the transcriptional profiles of induced cells from CDS mutated and E3 mutated mESCs, respectively, and got very consistent results except the Barhl1 transcript itself. These observations indicated that Atoh1-mediated Barhl1 expression could have important roles during auditory hair cell development. In brief, our findings delineate the detail molecular mechanism of Barhl1 expression regulation in auditory hair cell differentiation.

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