A combination of enhancer/silencer modules regulates spatially restricted expression of <i>cadherin‐7</i> in neural epithelium

Prasad, Maneeshi S.; Paulson, Alicia F.

doi:10.1002/dvdy.22675

Cited by 8 publications

(6 citation statements)

References 43 publications

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“…Moreover, cadherin-6 knockdown in NCC alters the subcellular distribution of active Rho, which is known to promote localized actomyosin contraction, a crucial step for apical NCC detachment ( Clay and Halloran, 2014 ). Another study demonstrated that cadherin-7 is upregulated in migrating NCCs in response to ectopic Wnt activation ( Prasad and Paulson, 2011 ). Likewise, Fujita et al (2016) demonstrated that cadherin-7 directly induces FoxD3 expression when stimulated by BMP2/Wnt3a signaling and plays important roles in this process of NCC formation.…”

Section: Roles Of P75 Ntr In Neural Crest Cell Migmentioning

confidence: 99%

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

Wislet

Vandervelden

Rogister

2018

Front. Mol. Neurosci.

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The p75 neurotrophin receptor (p75NTR), also known as low-affinity nerve growth factor, belongs to the tumor necrosis factor family of receptors. p75NTR is widely expressed in the nervous system during the development, as well as, in the neural crest population, since p75NTR has been described as ubiquitously expressed and considered as a neural crest marker. Neural crest cells (NCCs) constitute an transient population accurately migrating and invading, with precision, defined sites of the embryo. During migration, NCCs are guided along distinct migratory pathways by specialized molecules present in the extracellular matrix or on the surfaces of those cells. Two main processes direct NCC migration during the development: (1) an epithelial-to-mesenchymal transition and (2) a process known as contact inhibition of locomotion. In adults, p75NTR remains expressed by NCCs and has been identified in an increasing number of cancer cells. Nonetheless, the regulation of the expression of p75NTR and the underlying mechanisms in stem cell biology or cancer cells have not yet been sufficiently addressed. The main objective of this review is therefore to analyze elements of our actual knowledge regarding p75NTR roles during the development (mainly focusing on neural crest development) and see how we can transpose that information from development to cancer (and vice versa) to better understand the link between p75NTR and cell migration and invasion. In this review, we successively analyzed the molecular mechanisms of p75NTR when it interacts with several coreceptors and/or effectors. We then analyzed which signaling pathways are the most activated or linked to NCC migration during the development. Regarding cancer, we analyzed the described molecular pathways underlying cancer cell migration when p75NTR was correlated to cancer cell migration and invasion. From those diverse sources of information, we finally summarized potential molecular mechanisms underlying p75NTR activation in cell migration and invasion that could lead to new research areas to develop new therapeutic protocols.

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Section: Roles Of P75 Ntr In Neural Crest Cell Migmentioning

confidence: 99%

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

Wislet

Vandervelden

Rogister

2018

Front. Mol. Neurosci.

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“…Moreover, despite the common treatment of enhancers and silencers as 2 distinct groups of regulatory elements, a few elements in a variety of eukaryotic systems (Bessis et al, 1997;Jiang et al, 1993;Kallunki et al, 1998;Kehayova et al, 2011;Koike et al, 1995;Prasad and Paulson, 2011;Schaeffer et al, 1995;Simpson et al, 1986;Stathopoulos and Levine, 2005) (e.g., 2 in Drosophila melanogaster, 4 in mouse) have been found to exhibit both activities; in other words, they are bifunctional elements that can act as either an enhancer or a silencer, depending on the tissue type or cellular conditions. While many TFs can act as either activators or repressors, depending on the context of the ciselement (Ogbourne and Antalis, 1998) or interactions with other regulators (Fry and Farnham, 1999), bifunctionality of a CRM does not require such TFs, since different activators or repressors could bind the same element in different tissues.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Silencers in Drosophila Serve a Dual Role as Transcriptional Enhancers in Alternate Cellular Contexts

et al. 2020

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A major challenge in biology is to understand how complex gene expression patterns are encoded in the genome. While transcriptional enhancers have been studied extensively, few transcriptional silencers have been identified, and they remain poorly understood. Here, we used a novel strategy to screen hundreds of sequences for tissue-specific silencer activity in whole Drosophila embryos. Almost all of the transcriptional silencers that we identified were also active enhancers in other cellular contexts. These elements are bound by more transcription factors than non-silencers. A subset of these silencers forms long-range contacts with promoters. Deletion of a silencer caused derepression of its target gene. Our results challenge the common practice of treating enhancers and silencers as separate classes of regulatory elements and suggest the possibility that thousands or more bifunctional CRMs remain to be discovered in Drosophila and 10 4 -10 5 in humans.

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“…Some other positional candidate genes in the 18q chromosomal region with potential relevance to PTB include the following: CD226 is a member of the immunoglobulin (Ig) superfamily, and the variants in CD226 antigen (CD226) gene (Wieczorek et al, 2009;Qiu et al, 2012;Song et al, 2012); the cadherin 7 gene (CDH7) (Prasad and Paulson, 2011;Redies et al, 2012); the rotatin gene (RTTN) (Kheradmand Kia et al, 2012); and, the precerebellin 2 (CBLN2) (Matsuda and Yuzaki, 2011;Clarke et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Localization of a major susceptibility locus influencing preterm birth

Chittoor¹,

Farook²,

Puppala³

et al. 2013

Molecular Human Reproduction

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Preterm birth (PTB) is a complex trait, but little is known regarding its major genetic determinants. The objective of this study is to localize genes that influence susceptibility to PTB in Mexican Americans (MAs), a minority population in the USA, using predominantly microfilmed birth certificate-based data obtained from the San Antonio Family Birth Weight Study. Only 1302 singleton births from 288 families with information on PTB and significant covariates were considered for genetic analysis. PTB is defined as a childbirth that occurs at <37 completed weeks of gestation, and the prevalence of PTB in this sample was 6.4%. An ∼10 cM genetic map was used to conduct a genome-wide linkage analysis using the program SOLAR. The heritability of PTB was high (h(2) ± SE: 0.75 ± 0.20) and significant (P = 4.5 × 10(-5)), after adjusting for the significant effects of birthweight and birth order. We found significant evidence for linkage of PTB (LOD = 3.6; nominal P = 2.3 × 10(-5); empirical P = 1.0 × 10(-5)) on chromosome 18q between markers D18S1364 and D18S541. Several other chromosomal regions (2q, 9p, 16q and 20q) were also potentially linked with PTB. A strong positional candidate gene in the 18q linked region is SERPINB2 or PAI-2, a member of the plasminogen activator system that is associated with various reproductive processes. In conclusion, to our knowledge, perhaps for the first time in MAs or US populations, we have localized a major susceptibility locus for PTB on chromosome 18q21.33-q23.

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A combination of enhancer/silencer modules regulates spatially restricted expression of cadherin‐7 in neural epithelium

Cited by 8 publications

References 43 publications

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

Transcriptional Silencers in Drosophila Serve a Dual Role as Transcriptional Enhancers in Alternate Cellular Contexts

Localization of a major susceptibility locus influencing preterm birth

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