Expression patterns of Rbm24 in lens, nasal epithelium, and inner ear during mouse embryonic development

Grifone, Raphaëlle; Saquet, Audrey; Xu, Zhigang; Shi, De-Li

doi:10.1002/dvdy.24666

Cited by 33 publications

(50 citation statements)

References 37 publications

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“…Therefore, we unveil a critical role of vertebrate Rbm24 in cytoplasmic polyadenylation. This unprecedented function of Rbm24 may be not limited to lens differentiation; it may also operate in other tissues or cells where Rbm24 is localized in the cytoplasm, such as the inner ear, nasal epithelium, and myoblasts (23,32).…”

Section: Discussionmentioning

confidence: 99%

“…Our recent work shows that the mouse Rbm24 protein is first localized in the cytoplasm of lens fiber cells at the posterior region of the lens vesicle and then in the equatorial epithelial cells, which will give rise to the secondary lens fibers (32). As these cells differentiate, they terminally leave the cell cycle, start to elongate, and express numerous genes that help to establish lens transparency (51,52).…”

Section: Discussionmentioning

confidence: 99%

“…It plays an important role in skeletal and cardiac muscle development (21)(22)(23)(24) by regulating mRNA stability (25,26), pre-mRNA splicing (24,(27)(28)(29)(30), and mRNA translation (31). Moreover, its expression in head sensory organs, particularly in the lens, is also conserved in vertebrates (23,32). Recent studies have associated the rbm24 gene with microphthalmia and anophthalmia (33,34), highlighting its implication in vertebrate eye development.…”

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confidence: 99%

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Rbm24 controls poly(A) tail length and translation efficiency of crystallin mRNAs in the lens via cytoplasmic polyadenylation

Shao

Lü

Zhang

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Lens transparency is established by abundant accumulation of crystallin proteins and loss of organelles in the fiber cells. It requires an efficient translation of lens messenger RNAs (mRNAs) to overcome the progressively reduced transcriptional activity that results from denucleation. Inappropriate regulation of this process impairs lens differentiation and causes cataract formation. However, the regulatory mechanism promoting protein synthesis from lens-expressed mRNAs remains unclear. Here we show that in zebrafish, the RNAbinding protein Rbm24 is critically required for the accumulation of crystallin proteins and terminal differentiation of lens fiber cells. In the developing lens, Rbm24 binds to a wide spectrum of lens-specific mRNAs through the RNA recognition motif and interacts with cytoplasmic polyadenylation element-binding protein (Cpeb1b) and cytoplasmic poly(A)-binding protein (Pabpc1l) through the C-terminal region. Loss of Rbm24 reduces the stability of a subset of lens mRNAs encoding heat shock proteins and shortens the poly(A) tail length of crystallin mRNAs encoding lens structural components, thereby preventing their translation into functional proteins. This severely impairs lens transparency and results in blindness. Consistent with its highly conserved expression in differentiating lens fiber cells, the findings suggest that vertebrate Rbm24 represents a key regulator of cytoplasmic polyadenylation and plays an essential role in the posttranscriptional control of lens development.Rbm24 | lens | cataract | cytoplasmic polyadenylation | zebrafish

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Rbm24 controls poly(A) tail length and translation efficiency of crystallin mRNAs in the lens via cytoplasmic polyadenylation

Shao

Lü

Zhang

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…Beside its expression and implication in skeletal and cardiac muscle development (Li et al 2010;Poon et al 2012;Grifone et al 2014;Maragh et al 2014;Yang et al 2014), it is also expressed in a subset of cells within the differentiating head sensory organs. Particularly, Rbm24 protein colocalizes in the cytoplasm with Myo7A in inner and outer cells of the cochlea, as well as in the saccular and utricular maculae, and in semicircular canals of the mouse early embryo (Grifone et al 2018). This implies that Rbm24 may posttranscriptionally regulate hair cell development and function, but no functional evidence has been reported in vertebrates.…”

Section: Loss Of Rbm24 Causes Defective Hair Cell Development In the mentioning

confidence: 95%

“…RNA-binding proteins (RBPs) are implicated in posttranscriptional regulation of gene expression in development and disease (Brinegar and Cooper, 2016). Rbm24 exhibits strongly localized and highly conserved expression pattern in all vertebrate embryos (Grifone et al 2014(Grifone et al , 2018. Beside its expression and implication in skeletal and cardiac muscle development (Li et al 2010;Poon et al 2012;Grifone et al 2014;Maragh et al 2014;Yang et al 2014), it is also expressed in a subset of cells within the differentiating head sensory organs.…”

Section: Loss Of Rbm24 Causes Defective Hair Cell Development In the mentioning

confidence: 99%

Loss of Rbm24a causes defective hair cell development in the zebrafish inner ear and neuromasts

Cheng

Zhang

Shi

2020

Journal of Genetics and Genomics

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RBM24 is required for mouse hair cell development through regulating pre‐mRNA alternative splicing and mRNA stability

Wang

Zhang

Peng

et al. 2023

Journal Cellular Physiology

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As the sensory receptor cells in vertebrate inner ear and lateral lines, hair cells are characterized by the hair bundle that consists of one tubulin‐based kinocilium and dozens of actin‐based stereocilia on the apical surface of each hair cell. Hair cell development is tightly regulated, and deficits in this process usually lead to hearing loss and/or balance dysfunctions. RNA‐binding motif protein 24 (RBM24) is an RNA‐binding protein that is specifically expressed in the hair cells in the inner ear. Previously, we showed that RBM24 affects hair cell development in zebrafish by regulating messenger RNA (mRNA) stability. In the present work, we further investigate the role of RBM24 in hearing and balance using conditional knockout mice. Our results show that Rbm24 knockout results in severe hearing and balance deficits. Hair cell development is significantly affected in Rbm24 knockout cochlea, as the hair bundles are poorly developed and eventually degenerated. Hair bundle disorganization is also observed in Rbm24 knockout vestibular hair cells, although to a lesser extent. Consistently, significant hair cell loss is observed in the cochlea but not vestibule. RNAseq analysis identified several genes whose mRNA stability or pre‐mRNA alternative splicing is affected by Rbm24 knockout. Among them are Cdh23, Pcdh15, and Myo7a, which have been shown to play important roles in stereocilia development as well as mechano‐electrical transduction. Taken together, our present work suggests that RBM24 is required for mouse hair cell development through regulating pre‐mRNA alternative splicing as well as mRNA stability.

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Expression patterns of Rbm24 in lens, nasal epithelium, and inner ear during mouse embryonic development

Abstract: Altogether, these results highlight that Rbm24 may potentially function as a novel key regulator for the development of the eye, nasal epithelium, and inner ear in vertebrates. Developmental Dynamics 247:1160-1169, 2018. © 2018 Wiley Periodicals, Inc.

Cited by 33 publications

References 37 publications

Rbm24 controls poly(A) tail length and translation efficiency of crystallin mRNAs in the lens via cytoplasmic polyadenylation

Rbm24 controls poly(A) tail length and translation efficiency of crystallin mRNAs in the lens via cytoplasmic polyadenylation

Loss of Rbm24a causes defective hair cell development in the zebrafish inner ear and neuromasts

RBM24 is required for mouse hair cell development through regulating pre‐mRNA alternative splicing and mRNA stability

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