Folate receptor 1 is necessary for neural plate cell apical constriction during <i>Xenopus</i> neural tube formation

Balashova, Olga A; Visina, Olesya; Borodinsky, Laura N.

doi:10.1242/dev.137315

Cited by 24 publications

(43 citation statements)

References 76 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, in other vertebrates like Xenopus laevis , the necessity for cell divisions during neural tube formation has been ruled out by demonstrating that blocking DNA synthesis does not interfere with neurulation (Harris and Hartenstein, ). Nevertheless, folate action is necessary during Xenopus laevis neural tube formation, as recently demonstrated by our study (Balashova et al, ), suggesting that folate might play additional functions during neural tube formation besides its role as a vitamin for DNA synthesis. Moreover, many knockout mice for enzymes directly involved in folate metabolism did not exhibit increases in NTD incidence (Watanabe et al, ; Chen et al, ; Swanson et al, ).…”

Section: Introductionsupporting

confidence: 77%

Folate action in nervous system development and disease

Balashova

Visina²,

Borodinsky³

2018

Developmental Neurobiology

Self Cite

View full text Add to dashboard Cite

The vitamin folic acid has been recognized as a crucial environmental factor for nervous system development. From the early fetal stages of the formation of the presumptive spinal cord and brain to the maturation and maintenance of the nervous system during infancy and childhood, folate levels and its supplementation have been considered influential in the clinical outcome of infants and children affected by neurological diseases. Despite the vast epidemiological information recorded on folate function and neural tube defects, neural development and neurodegenerative diseases, the mechanisms of folate action in the developing neural tissue have remained elusive. Here we compiled studies that argue for a unique role for folate in nervous system development and function and its consequences to neural disease and repair. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 391-402, 2018.

show abstract

Section: Introductionsupporting

confidence: 77%

Folate action in nervous system development and disease

Balashova

Visina²,

Borodinsky³

2018

Developmental Neurobiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In this light, it is notable that there is evidence that Folr1 can also function as a transcription factor in mammalian cells, with a large number of developmentally important genes as its target [ 213 ]. Furthermore, recent observations in Xenopus have pointed to a novel mechanism for the role of Folr1 and folate in neural tube closure [ 214 ]. Knockdown of Folr1 during neurulation in Xenopus causes failure to develop a neural tube.…”

Section: Folate and Ntdmentioning

confidence: 99%

Insights into the Etiology of Mammalian Neural Tube Closure Defects from Developmental, Genetic and Evolutionary Studies

Juriloff

Harris

2018

JDB

View full text Add to dashboard Cite

The human neural tube defects (NTD), anencephaly, spina bifida and craniorachischisis, originate from a failure of the embryonic neural tube to close. Human NTD are relatively common and both complex and heterogeneous in genetic origin, but the genetic variants and developmental mechanisms are largely unknown. Here we review the numerous studies, mainly in mice, of normal neural tube closure, the mechanisms of failure caused by specific gene mutations, and the evolution of the vertebrate cranial neural tube and its genetic processes, seeking insights into the etiology of human NTD. We find evidence of many regions along the anterior–posterior axis each differing in some aspect of neural tube closure—morphology, cell behavior, specific genes required—and conclude that the etiology of NTD is likely to be partly specific to the anterior–posterior location of the defect and also genetically heterogeneous. We revisit the hypotheses explaining the excess of females among cranial NTD cases in mice and humans and new developments in understanding the role of the folate pathway in NTD. Finally, we demonstrate that evidence from mouse mutants strongly supports the search for digenic or oligogenic etiology in human NTD of all types.

show abstract

“…Molecular mechanisms underlying this seemingly bi-directional interaction are a matter for future work, but our ndings reveal a dynamic interplay between PCP, microtubules and actomyosin in the mammalian neuroepithelium. It has been suggested that promotion of apical constriction is one of the bene cial consequences of folate which may contribute to its ability to prevent a proportion of human NT defects 92,93 . These interactions may therefore be speci cally disrupted in patients with mosaic PCP mutations and may identify more widely-applicable therapeutic targets.…”

Section: Resulting Apical Constriction Of Neuroepithelial Cells Requimentioning

confidence: 99%

Cell non-autonomy amplifies disruption of neurulation by mosaic Vangl2 deletion

Galea

Maniou

Marshall

et al. 2020

Preprint

View full text Add to dashboard Cite

Post-zygotic mutations that generate tissue mosaicism are increasingly associated with severe congenital defects, including those arising from failed neural tube closure. We observed that elevation of the neural folds during mouse spinal neurulation is vulnerable to deletion of the planar cell polarity core component Van Gogh-like (Vangl)2 in as few as 16% of neuroepithelial cells. Vangl2-deleted cells are typically dispersed throughout the neuroepithelium, and each non-autonomously prevents apical constriction by an average of five Vangl2-replete neighbours. This inhibition of apical constriction involves reduced myosin-II recruitment to neighbour cell borders and shortening of basally-extending microtubule tails, which are known to facilitate apical constriction. Vangl2-deleted cells themselves continue to apically constrict and preferentially recruit myosin-II to their apical cell cortex rather than to apical cap sarcomere-like organisations. Such non-autonomous effects can explain how post-zygotic mutations affecting a minority of cells can cause catastrophic failure of morphogenesis leading to clinically important birth defects.

show abstract

Folate receptor 1 is necessary for neural plate cell apical constriction during Xenopus neural tube formation

Cited by 24 publications

References 76 publications

Folate action in nervous system development and disease

Folate action in nervous system development and disease

Insights into the Etiology of Mammalian Neural Tube Closure Defects from Developmental, Genetic and Evolutionary Studies

Cell non-autonomy amplifies disruption of neurulation by mosaic Vangl2 deletion

Contact Info

Product

Resources

About