RNA helicase Mov10 is essential for gastrulation and central nervous system development

Skariah, Geena; Perry, Kimberly J.; Drnevich, Jenny; Henry, Jonathan J.; Ceman, Stephanie

doi:10.1002/dvdy.24615

Cited by 8 publications

(8 citation statements)

References 48 publications

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“…Through Cross-Linking ImmunoPrecipitation (CLIP) experiments, it has been established that FMRP and MOV10 share a common RNA interactome. Unlike FMRP, the Mov10 knockout (KO) is embryonic lethal [ 15 , 16 ]; however the Mov10 heterozygous (Het) mouse has increased anxiety and hyperactivity, which are features shared with Fragile X syndrome [ 17 ] and suggest impaired neuronal function [ 15 ]. We were thus interested in investigating the consequences of Mov10 and Fmr1 reduction on dendritic development.…”

Section: Introductionmentioning

confidence: 99%

FMRP and MOV10 regulate Dicer1 expression and dendrite development

et al. 2021

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Fragile X syndrome results from the loss of expression of the Fragile X Mental Retardation Protein (FMRP). FMRP and RNA helicase Moloney Leukemia virus 10 (MOV10) are important Argonaute (AGO) cofactors for miRNA-mediated translation regulation. We previously showed that MOV10 functionally associates with FMRP. Here we quantify the effect of reduced MOV10 and FMRP expression on dendritic morphology. Murine neurons with reduced MOV10 and FMRP phenocopied Dicer1 KO neurons which exhibit impaired dendritic maturation Hong J (2013), leading us to hypothesize that MOV10 and FMRP regulate DICER expression. In cells and tissues expressing reduced MOV10 or no FMRP, DICER expression was significantly reduced. Moreover, the Dicer1 mRNA is a Cross-Linking Immunoprecipitation (CLIP) target of FMRP Darnell JC (2011), MOV10 Skariah G (2017) and AGO2 Kenny PJ (2020). MOV10 and FMRP modulate expression of DICER1 mRNA through its 3’untranslated region (UTR) and introduction of a DICER1 transgene restores normal neurite outgrowth in the Mov10 KO neuroblastoma Neuro2A cell line and branching in MOV10 heterozygote neurons. Moreover, we observe a global reduction in AGO2-associated microRNAs isolated from Fmr1 KO brain. We conclude that the MOV10-FMRP-AGO2 complex regulates DICER expression, revealing a novel mechanism for regulation of miRNA production required for normal neuronal morphology.

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Section: Introductionmentioning

confidence: 99%

FMRP and MOV10 regulate Dicer1 expression and dendrite development

et al. 2021

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“…Interestingly, the Mov10 heterozygous knockout mice showed increased genomic L1 content, decreased hippocampal dendritic arborization as well as behavioral deficits suggesting an important role for MOV10 in the formation of normal brain circuitry. The importance of MOV10 in the development of CNS was also demonstrated in X. laevis (Skariah et al, 2018). MOV10's absence in tadpoles led to shorter body length and smaller eyes.…”

Section: Mov10's Role In Organisms and During Developmentmentioning

confidence: 79%

“…A critical role for MOV10 in development was first discovered by the embryonic lethality of a full body Mov10 knockout mouse (Skariah et al, 2017). To identity the developmental step where MOV10 was required, the authors turned to Xenopus laevis (Skariah et al, 2018). They used morpholinos to block the maternal Mov10 mRNA in X. laevis embryos and found that they failed to complete gastrulation.…”

Section: Mov10's Role In Organisms and During Developmentmentioning

confidence: 99%

Unwinding the roles ofRNAhelicaseMOV10

et al. 2021

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MOV10 is an RNA helicase that associates with the RNA-induced silencing complex component Argonaute (AGO), likely resolving RNA secondary structures. MOV10 also binds the Fragile X mental retardation protein to block AGO2 binding at some sites and associates with UPF1, a principal component of the nonsense-mediated RNA decay pathway. MOV10 is widely expressed and has a key role in the cellular response to viral infection and in suppressing retrotransposition. Posttranslational modifications of MOV10 include ubiquitination, which leads to stimulation-dependent degradation, and phosphorylation, which has an unknown function. MOV10 localizes to the nucleus and/or cytoplasm in a cell type-specific and developmental stage-specific manner. Knockout of Mov10 leads to embryonic lethality, underscoring an important role in development where it is required for the completion of gastrulation. MOV10 is expressed throughout the organism; however, most studies have focused on germline cells and neurons. In the testes, the knockdown of Mov10 disrupts proliferation of spermatogonial progenitor cells. In brain, MOV10 is significantly elevated postnatally and binds mRNAs encoding cytoskeleton and neuron projection proteins, suggesting an important role in neuronal architecture. Heterozygous Mov10 mutant mice are hyperactive and anxious and their cultured hippocampal neurons have reduced dendritic arborization. Zygotic knockdown of Mov10 in Xenopus laevis causes abnormal head and eye development and mislocalization of neuronal precursors in the brain. Thus, MOV10 plays a vital role during development, defense against viral infection and in neuronal development and function: its many roles and regulation are only beginning to be unraveled.

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“…To date, a lot of the identified RNA helicases belong to the SF2, only a dozen of SF1 RNA helicases have been identified. Among them, MOV10 and MOV10L1 both encode SF1 RNA helicases, which involved in various kinds of biological contexts, such as defense of RNA virus invasion, early development, neuron system, germ cell [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…Knockdown of maternal mov10 in xenopus embryos led to gastrulation defects, likely resulting from the large scales changes in mRNA expression due to Mov10’s role in miRNA mediated regulation of maternal-zygotic transition. In addition, zygotic Mov10 is necessary for development of the central nervous system [ 9 ]. In mouse, the Mov10 knockout one led to embryonic lethality, suggesting MOV10 is critical for early development.…”

Section: Introductionmentioning

confidence: 99%

Evolutionary and Expression Analysis of MOV10 and MOV10L1 Reveals Their Origin, Duplication and Divergence

Yang

Zhang

et al. 2022

IJMS

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MOV10 and MOV10L1 both encode ATP-dependent RNA helicases. In mammals, MOV10 and MOV10L1 participate in various kinds of biological contexts, such as defense of RNA virus invasion, neuron system, germ cell and early development. However, mov10 and mov10l1 in zebrafish are obscure and the evolutionary relationships of mov10 among different species remain unclear. In this study, we found MOV10 and MOV10L1 had some variations despite they possessed the conserved feature of RNA helicase, however, they may originate from a single ancestor although they shared limited homology. A single MOV10L1 gene existed among all species, while MOV10 gene experienced lineage-specific intra-chromosomal gene duplication in several species. Interestingly, the mov10 gene expanded to three in zebrafish, which originating from a duplication by whole genome specific duplication of teleost lineage followed by a specific intra-chromosome tandem duplication. The mov10 and mov10l1 showed distinct expression profiles in early stages, however, in adult zebrafish, three mov10 genes exhibited similar diverse expression patterns in almost all tissues. We also demonstrated mov10 genes were upregulated upon virus challenge, highlighting they had redundant conserved roles in virus infection. These results provide valuable data for the evolution of MOV10 and MOV10L1 and they are important to the further functional exploration.

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RNA helicase Mov10 is essential for gastrulation and central nervous system development

Abstract: Mov10 is essential for gastrulation and normal CNS development. Developmental Dynamics 247:660-671, 2018. © 2017 Wiley Periodicals, Inc.

Cited by 8 publications

References 48 publications

FMRP and MOV10 regulate Dicer1 expression and dendrite development

FMRP and MOV10 regulate Dicer1 expression and dendrite development

Unwinding the roles ofRNAhelicaseMOV10

Evolutionary and Expression Analysis of MOV10 and MOV10L1 Reveals Their Origin, Duplication and Divergence

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