RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes

Bennett, Alexis H; O’Donohue, Marie Francoise; Gundry, Stacey R.; CHAN, A; Widrick, J. J.; Draper, Isabelle; Chakraborty, Anirban; Zhou, Yi; Zon, Leonard I.; Gleizes, Pierre‐Emmanuel; Beggs, Alan H.; Gupta, Vandana

doi:10.1101/125484

Cited by 8 publications

(13 citation statements)

References 60 publications

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“…To test this hypothesis, the next work can be perform by construct a fusion protein of the DNA-RNA hybrid binding domain to further examine whether R-loop accumulated in ddx19 -/-, and to detect and compare the expression of DNA damage checkpoint protein kinases in wildtype and ddx19 -/-. Many members of the DEAD-box family are known to regulate development [42][43][44][45][46]. For example, Ddx27 deletion blocked proliferation and regeneration ability of skeletal muscle in zebrafish [42].…”

Section: Discussionmentioning

confidence: 99%

“…Many members of the DEAD-box family are known to regulate development [42][43][44][45][46]. For example, Ddx27 deletion blocked proliferation and regeneration ability of skeletal muscle in zebrafish [42]. Loss of Ddx18 results in G1 cell-cycle arrest, and specifically regulates the amount of primitive myeloid and erythroid cells [45].…”

Section: Discussionmentioning

confidence: 99%

“…Edu labeling was carried out as described [42]. We analyzed the proliferating cells in zebrafish embryos using Click-iT ® Plus Edu Imaging Kits (Invitrogen, C10639).…”

Section: Edu Labelingmentioning

confidence: 99%

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Zebrafish Ddx19 deficiency causes serious apoptosis and cell proliferation

Shi¹,

Bao²,

Zu³

et al. 2019

Preprint

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Background: DDX19 is known as for its role in mRNA transport. It is also involved in translation and innate immune responses. However, the function of Ddx19 during body development rarely reported. We know that ddx19 plays an important role in development of organisms, but we don't understand how it affects the process of cell development. Results: Here, we report ddx19-deleted mutation in zebrafish, obtained two types with base deletion of 46 bp and 7 bp using CRISPR/Cas9 gene knockout technology, show morphologic defects such as small head, small eyes, pericardial edema and trunk curvature in 24 hours post fertilization (hpf). The maximum survival time of ddx19 -/- was less than 5 day post fertilization (dpf). In comparison to the wildtype, the mutant embryos showed widespread up-regulation of cell apoptosis, and significant decrease in the number of cells. Conclusions: These data indicate loss of ddx19 is lethal, and is associated with cell apoptosis and proliferation abnormalities in the organism. Our results reveal that ddx19 is essential for the development of zebrafish embryos, which deepens the understanding of the developmental function of DEAD-box genes family.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Zebrafish Ddx19 deficiency causes serious apoptosis and cell proliferation

Shi¹,

Bao²,

Zu³

et al. 2019

Preprint

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“…Twenty-four hours after transfection, cells were fixed in 4% paraformaldehyde and immunofluorescence was performed as described previously 16 . M2 anti-FLAG antibody (Sigma, 1:250) and sodium potassium ATPase antibody (Abcam 76020,1:100).…”

Section: Immunofluorescence Analysismentioning

confidence: 99%

Homozygous TRPV4 mutation causes congenital distal spinal muscular atrophy and arthrogryposis

Velilla

Marchetti

Tóth-Petróczy

et al. 2018

Preprint

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ObjectiveThe objective of this study is to identify the genetic cause of disease in a congenital form of congenital spinal muscular atrophy and arthrogryposis (CSMAA). MethodsA 2-year-old boy was diagnosed with arthrogryposis multiplex congenita, severe skeletal abnormalities, torticollis, vocal cord paralysis and diminished lower limb movement. Whole exome sequencing was performed on the proband and family members. In silico modeling of protein structure and heterologous protein expression and cytotoxicity assays were performed to validate pathogenicity of the identified variant. 7 Appendix I NameLocation Role Contribution

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“…RNA helicases play a central role in the milieu of post-transcriptional gene regulation by modulating the secondary and tertiary structure of RNA, thereby regulating RNA\RNA and RNA\protein interaction (39,40). Further, multiple lines of investigation from vertebrates show that D-E-A-D Box RNA helicases are essential for maintaining skeletal muscle mass, architecture, and function as well as muscle repair and regeneration via regulating ribosome biogenesis (41)(42)(43). Here, we report the function of DDX24, a D-E-A-D Box RNA helicase, in planarian head regeneration.…”

Section: Introductionmentioning

confidence: 99%

DDX24, a D-E-A-D box RNA helicase, is required for muscle fiber organization and anterior pole specification essential for head regeneration in planarians

Palakodeti

Sarkar

Dubey

et al. 2021

Preprint

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Planarians have a remarkable ability to undergo whole-body regeneration. The timely establishment of polarity at the wound site followed by the specification of the organizing centers- the anterior pole and the posterior pole, are indispensable for successful regeneration. In planarians, polarity, pole, and positional-information determinants are predominantly expressed by muscles. The molecular toolkit that enables this functionality of planarian muscles however remains poorly understood. Here we report that SMED_DDX24, a D-E-A-D Box RNA helicase and the homolog of human DDX24, is critical for planarian head regeneration. DDX24 is enriched in muscles and its knockdown leads to defective muscle-fiber organization and failure to re-specify anterior pole/organizer. Overall, loss of DDX24 manifests into gross misregulation of many well-characterized positional-control genes and patterning-control genes, necessary for organogenesis and tissue positioning and tissue patterning. In addition, wound-induced Wnt signalling was also upregulated in ddx24 RNAi animals. Canonical WNT-βCATENIN signalling is known to suppress head identity throughout bilateria, including planarians. Modulating this Wnt activity by β-catenin-1 RNAi, the effector molecule of this pathway, partially rescues the ddx24 RNAi phenotype, implying that a high Wnt environment in ddx24 knockdown animals likely impedes their normal head regeneration. Furthermore, at a sub-cellular level, RNA helicases are known to regulate muscle mass and function by regulating their translational landscape. ddx24 knockdown leads to the downregulation of large subunit ribosomal RNA and the 80S ribosome peak, implying its role in ribosome biogenesis and thereby influencing the translational output. This aspect seems to be an evolutionarily conserved role of DDX24. In summary, our work demonstrates the role of a D-E-A-D box RNA helicase in whole-body regeneration through muscle fiber organization, and pole and positional-information re-specification, likely mediated through translation regulation.

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RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes

Cited by 8 publications

References 60 publications

Zebrafish Ddx19 deficiency causes serious apoptosis and cell proliferation

Zebrafish Ddx19 deficiency causes serious apoptosis and cell proliferation

Homozygous TRPV4 mutation causes congenital distal spinal muscular atrophy and arthrogryposis

DDX24, a D-E-A-D box RNA helicase, is required for muscle fiber organization and anterior pole specification essential for head regeneration in planarians

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