Dicer is required for survival of differentiating neural crest cells

Zehir, Ahmet; Hua, Lisa L.; Maska, Emily; Morikawa, Yuka; Cserjesi, Peter

doi:10.1016/j.ydbio.2010.01.039

Cited by 124 publications

(120 citation statements)

References 46 publications

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“…The loss of the microRNA-processing enzyme dicer has been shown to severely reduce the survival of sympathetic neuron precursors (Huang et al 2010;Zehir et al 2010) and also partially to affect the establishment of their typical neuronal gene expression pattern (Stubbusch et al 2013). Notably, sympathetic neurons of dicer-deficient mouse embryos exhibit reduced expression levels of synaptic marker genes and thus become more reminiscent of wildtype chromaffin cells in this respect.…”

Section: Discussionsupporting

confidence: 85%

MiR-124 is differentially expressed in derivatives of the sympathoadrenal cell lineage and promotes neurite elongation in chromaffin cells

Shtukmaster¹,

Narasimhan²,

Faitwri³

et al. 2016

Cell Tissue Res

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The neural-crest-derived sympathoadrenal cell lineage gives rise to sympathetic neurons and to endocrine chromaffin cells of the adrenal medulla. Both cell types express a largely overlapping set of genes, including those coding for the molecular machinery related to the synthesis and exocytotic release of catecholamines. During their early development, sympathetic neurons and chromaffin cells rely on a shared transcription factor network that controls the establishment of these common features. Despite many similarities, mature sympathetic neurons and chromaffin cells significantly differ regarding their morphology and function. Most prominently, sympathetic neurons possess axons that are absent in mammalian adrenal chromaffin cells. The molecular mechanism underlying the divergent development of sympathoadrenal cells into neuronal and endocrine cells remains elusive. Mutational inactivation of the ribonuclease dicer hints at the importance of microRNAs in this diversification. We show here that miR-124 is detectable in developing sympathetic neurons but absent in chromaffin cell precursors. We further demonstrate that miR-124 promotes neurite elongation when transfected into cultured chromaffin cells indicating its capability to support the establishment of a neuronal morphology in non-neuronal sympathoadrenal cells. Our results also show that treatment of PC12 cells with the neurotrophin nerve growth factor leads to an upregulation of miR-124 expression and that inhibition of miR-124 reduces nerve-growthfactor-induced neurite outgrowth in PC12 cells. Thus, our data indicate that miR-124 contributes to the establishment of specific neuronal features in developing sympathoadrenal cells.

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Section: Discussionsupporting

confidence: 85%

MiR-124 is differentially expressed in derivatives of the sympathoadrenal cell lineage and promotes neurite elongation in chromaffin cells

Shtukmaster¹,

Narasimhan²,

Faitwri³

et al. 2016

Cell Tissue Res

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“…Using a mouse with loss of neural crest-derived tissue, we have shown that the neural crest cartilage is needed for the formation of the mesodermally derived stapedial footplate, and in the absence of neural crest cartilage the oval window does not form correctly. In the Wnt1cre-Dicer mice, neural crest cells are able to migrate and are found within the same locations as in control littermates at E11 (Zehir et al, 2010), but cells do not differentiate into cartilage but undergo apoptosis (Huang et al, 2010;Zehir et al, 2010). It is possible, therefore, that the migrating neural crest cells at E11 are able to signal to the otic capsule, positioning the oval window before stapes differentiation.…”

Section: Neural Crest Part Of the Stapes Is Needed For Formation Of Tmentioning

confidence: 99%

“…For this, we took advantage of the Wnt1cre/Dicer mouse, which has been shown to lack cartilages of neural crest origin, including the stapes (Huang et al, 2010). In these mutants, migration of crest into the head appears normal, but the cells do not differentiate into cartilage and high apoptosis is observed in the mandible mesenchyme at E12.5 (Huang et al, 2010;Zehir et al, 2010). At E18.5, in the wild-type mouse the middle ear ossicles can be seen strongly stained with Alcian blue (Fig.…”

Section: Developmental Dynamicsmentioning

confidence: 99%

The origin of the stapes and relationship to the otic capsule and oval window

Thompson

Ohazama

Sharpe

et al. 2012

Developmental Dynamics

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Background: The stapes, an ossicle found within the middle ear, is involved in transmitting sound waves to the inner ear by means of the oval window. There are several developmental problems associated with this ossicle and the oval window, which cause hearing loss. The developmental origin of these tissues has not been fully elucidated. Results: Using transgenic reporter mice, we have shown that the stapes is of dual origin with the stapedial footplate being composed of cells of both neural crest and mesodermal origin. Wnt1cre/Dicer mice fail to develop neural crest-derived cartilages, therefore, have no middle ear ossicles. We have shown in these mice the mesodermal stapedial footplate fails to form and the oval window is induced but underdeveloped. Conclusions: If the neural crest part of the stapes fails to form the mesodermal part does not develop, indicating that the two parts are interdependent. The stapes develops tightly associated with the otic capsule, however, it is not essential for the positioning of the oval window, suggesting that other tissues, perhaps within the inner ear are needed for oval window placement. Developmental Dynamics 241:1396-1404, 2012. V C 2012 Wiley Periodicals, Inc.Key words: stapes; oval window; neural crest; lineage labeling; mesoderm Key Findings:The stapedial footplate is of neural crest and mesoderm origin. The otic capsule contributes to the stapedial footplate. The neural crest component of the stapedial footplate is needed for development of the mesodermal component and for proper formation of the oval window. The position of the oval window appears independent of the stapes.

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“…[26] that both the dicer and miRNAs are required for the survival of neural crest-derived tissues by preventing apoptosis during differentiation because the dicer was essential for the differentiation process related to the neural crest cells survival, while neuronal crest needs specific hdac1 function during its development as shown in a series of zebrafish experiment [27]. In the trunk region, the ventrally migrating neural crest cells move through the somitic mesenchyme in a segmented pattern, presumably setting the basis for the sensory and sympathetic ganglia metameric organization along the anterior-posterior axis later in development [28].…”

Section: Genetics and Clinical Characteristicsmentioning

confidence: 99%

Anatomic Origin and Molecular Genetics in Neuroblastoma

Tosun¹,

Karabekir²,

Durmaz³

et al. 2017

Neuroblastoma - Current State and Recent Updates

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Neuroblastoma is considered as the most common extracranial solid tumor occurring during childhood, but takes place rarely after the age of 10 years. The tumors are considered as embryonal tumors that result from the fetal or early postnatal life development and are formed from neural crest-derived cells, and their origination is from the early nerve cells which are called as neuroblasts of sympathetic nervous system. Being heterogeneous in their biological, genetic, and morphological characteristics, tumors which are distinct from other solid tumors due to their biological heterogeneity result in the clinical pattern changes from spontaneous regression to a highly aggressive metastatic disease. Neuroblastoma tumorigenesis is regulated by Myc oncogene, leading to aggressive tumor subset. Many epigenetic factors play crucial role in the disease induction and development, while regulatory effect and outcome result in epigenetic patterns distinguishing neuroectoderm, neural crest, and more mature neural states. Neuroblastoma patients' clinical management is based on prognostic categories subtracted from studies correlating outcome and clinico-biological variables. Neuroblastoma anatomic boundaries include primarily autonomic nervous system besides other rare locations. Neuroblastoma molecular pathogenesis classifies the tumor according to the different clinical behaviors that are important for the improvement of the patients outcome and overall survival according to the different therapy modalities applied.

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Dicer is required for survival of differentiating neural crest cells

Cited by 124 publications

References 46 publications

MiR-124 is differentially expressed in derivatives of the sympathoadrenal cell lineage and promotes neurite elongation in chromaffin cells

MiR-124 is differentially expressed in derivatives of the sympathoadrenal cell lineage and promotes neurite elongation in chromaffin cells

The origin of the stapes and relationship to the otic capsule and oval window

Anatomic Origin and Molecular Genetics in Neuroblastoma

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