Genetic analysis of molecular oscillators in mammalian somitogenesis: Clues for studies of human vertebral disorders

Sewell, William F.; Kusumi, Kenro

doi:10.1002/bdrc.20091

Cited by 14 publications

(5 citation statements)

References 105 publications

(103 reference statements)

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“…Somitogenesis is a complex and vital process in vertebrate development that involves many known genes distributed across several families of signaling proteins, and a vast amount of work has been done to characterize this process (see reviews: Stickney et al, 2000; Pourquié, 2001; Aulehla and Herrmann, 2004; Sewell and Kusumi, 2007; Geetha‐Loganathan et al, 2008; Dunwoodie, 2009). To our knowledge, there are currently no chromatin remodelers reported to play a role in somitogenesis.…”

Section: Discussionmentioning

confidence: 99%

Chd7 plays a critical role in controlling left–right symmetry during zebrafish somitogenesis

Jacobs-McDaniels¹,

Albertson²

2011

Developmental Dynamics

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Somitogenesis is a complex process during early vertebrate development involving interactions between many factors to form a bilateral somite series. A role for chromatin remodelers in somitogenesis has not yet been demonstrated. Here, we investigate the function of chromodomain helicase DNA binding protein 7 (chd7) during zebrafish somitogenesis. We show that Chd7 deficiency leads to asymmetric segmentation of the presomitic mesoderm (PSM), as revealed by expression of the somitogenesis genes, cdx1a, dlc, her7, mespa, and ripply1. Moreover, we show that abrogation of Chd7 results in the loss of asymmetric expression of spaw in the lateral plate mesoderm, which is consistent with more general laterality defects. Based on the observation that insufficient Chd7 leads to left-right asymmetry defects during PSM segmentation, and because CHD7 has been linked to human spinal deformities, we suggest that zebrafish chd7 morphants may be a good in vivo model to examine the pathophysiology of these diseases. Developmental Dynamics 240:2272-2280,

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Section: Discussionmentioning

confidence: 99%

Chd7 plays a critical role in controlling left–right symmetry during zebrafish somitogenesis

Jacobs-McDaniels¹,

Albertson²

2011

Developmental Dynamics

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“…A case-control study identified the association of variants of Raldh1A2, Cyp26A1, and CRABP1 retinoic genes and neural tube defects in humans ( 230 ). Experimental studies on mouse models have shown that overexpression of retinoic acid leads to neural tube defects ( 236 , 237 ). A recent study found that treatment of neural crest cells (NSCs) with all-trans-retinoic acid culminates in neural tube deformities ( 238 ).…”

Section: Signaling Pathways—neural Tube Defectsmentioning

confidence: 99%

A quest for genetic causes underlying signaling pathways associated with neural tube defects

Rai,

Leydier,

Sharma

et al. 2023

Front. Pediatr.

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Neural tube defects (NTDs) are serious congenital deformities of the nervous system that occur owing to the failure of normal neural tube closures. Genetic and non-genetic factors contribute to the etiology of neural tube defects in humans, indicating the role of gene-gene and gene-environment interaction in the occurrence and recurrence risk of neural tube defects. Several lines of genetic studies on humans and animals demonstrated the role of aberrant genes in the developmental risk of neural tube defects and also provided an understanding of the cellular and morphological programs that occur during embryonic development. Other studies observed the effects of folate and supplementation of folic acid on neural tube defects. Hence, here we review what is known to date regarding altered genes associated with specific signaling pathways resulting in NTDs, as well as highlight the role of various genetic, and non-genetic factors and their interactions that contribute to NTDs. Additionally, we also shine a light on the role of folate and cell adhesion molecules (CAMs) in neural tube defects.

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“…All-trans retinoic acid (atRA) is a normal metabolite of retinoic acid present in the body and is an important factor in embryonic development (11). Previous studies have reported that excess atRA leads to the occurrence of NTDs (12,13). However, its specific molecular mechanism remains to be elucidated.…”

Section: Effect Of Notch1 On Neural Tube Defects and Neural Stem Cell...mentioning

confidence: 99%

Effect of Notch1 on neural tube defects and neural stem cell differentiation induced by all‑trans retinoic acid

Chen

Zhang

et al. 2021

Mol Med Rep

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Neural tube defects (NTDs) are the most serious and common birth defects in the clinical setting. The Notch signaling pathway has been implicated in different processes of the embryonic neural stem cells (NSCs) during neural tube development. The aim of the present study was to investigate the expression pattern and function of Notch1 (N1) in all-trans retinoic acid (atRA)-induced NTDs and NSC differentiation. A mouse model of brain abnormality was established by administering 28 mg/kg atRA, and then brain development was examined using hematoxylin and eosin (H&E) staining. The N1 expression pattern was detected in the brain of mice embryos via immunohistochemistry and western blotting. NSCs were extracted from the fetal brain of C57 BL/6 embryos at 18.5 days of pregnancy. N1, Nestin, neurofilament (NF), glial fibrillary acidic protein (GFAP) and galactocerebroside (GALC) were identified using immunohistochemistry. Moreover, N1, presenilin 1 (PS1), Nestin, NF, GFAP and GALC were detected via western blotting at different time points in the NSCs with control media or atRA media. H&E staining identified that the embryonic brain treated with atRA was more developed compared with the control group. N1 was downregulated in the embryonic mouse brain between days 11 and 17 in the atRA-treated group compared with the untreated group. The distribution of N1, Nestin, NF, GFAP and GALC was positively detected using immunofluorescence staining. Western blotting results demonstrated that there were significantly, synchronous decreased expression levels of N1 and PS1, but increased expression levels of NF, GFAP and GALC in NSCs treated with atRA compared with those observed in the controls (P<0.05). The results suggested that the N1 signaling pathway inhibited brain development and NSC differentiation. Collectively, it was found that atRA promoted mouse embryo brain development and the differentiation of NSCs by inhibiting the N1 pathway.

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Genetic analysis of molecular oscillators in mammalian somitogenesis: Clues for studies of human vertebral disorders

Cited by 14 publications

References 105 publications

Chd7 plays a critical role in controlling left–right symmetry during zebrafish somitogenesis

Chd7 plays a critical role in controlling left–right symmetry during zebrafish somitogenesis

A quest for genetic causes underlying signaling pathways associated with neural tube defects

Effect of Notch1 on neural tube defects and neural stem cell differentiation induced by all‑trans retinoic acid

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