Chordin-like protein 1 promotes neuronal differentiation by inhibiting bone morphogenetic protein-4 in neural stem cells

Gao, Weilu; Zhang, Sheng‐Quan; Zhang, Hui; Wan, Bo; Yin, Zongsheng

doi:10.3892/mmr.2013.1310

Cited by 25 publications

(24 citation statements)

References 30 publications

(31 reference statements)

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“…Unlike chordin, CHRDL1 also binds TGF-b2 (Nakayama et al 2001). When overexpressed, CHRDL1 induces secondary axis formation in early Xenopus embryos, dorsalizes zebrafish embryos, represses BMP-4 activity during dorsoventral patterning of chick retina, impairs distal digit formation in chick limbs, and promotes neuronal differentiation of adult neural stem cells (Coffinier et al 2001;Nakayama et al 2001;Sakuta et al 2001;Branam et al 2010;Allen et al 2013;Gao et al 2013). Interestingly, CHRDL1 enhances BMP-4 and BMP-7 signaling in several cell lines when expressed alone, but switches into a selective BMP-7 antagonist when in complex with Twsg1.…”

Section: Other Modulators Of Chordinmentioning

confidence: 99%

Agonists and Antagonists of TGF-β Family Ligands

Chang

2016

Cold Spring Harb Perspect Biol

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The discovery of the transforming growth factor β (TGF-β) family ligands and the realization that their bioactivities need to be tightly controlled temporally and spatially led to intensive research that has identified a multitude of extracellular modulators of TGF-β family ligands, uncovered their functions in developmental and pathophysiological processes, defined the mechanisms of their activities, and explored potential modulator-based therapeutic applications in treating human diseases. These studies revealed a diverse repertoire of extracellular and membrane-associated molecules that are capable of modulating TGF-β family signals via control of ligand availability, processing, ligand-receptor interaction, and receptor activation. These molecules include not only soluble ligand-binding proteins that were conventionally considered as agonists and antagonists of TGF-β family of growth factors, but also extracellular matrix (ECM) proteins and proteoglycans that can serve as "sink" and control storage and release of both the TGF-β family ligands and their regulators. This extensive network of soluble and ECM modulators helps to ensure dynamic and cell-specific control of TGF-β family signals. This article reviews our knowledge of extracellular modulation of TGF-β growth factors by diverse proteins and their molecular mechanisms to regulate TGF-β family signaling.

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Section: Other Modulators Of Chordinmentioning

confidence: 99%

Agonists and Antagonists of TGF-β Family Ligands

Chang

2016

Cold Spring Harb Perspect Biol

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“…The condition was genetically linked to the long arm of the X-chromosome over twenty years ago (Xq12-q26; MGC1) [2], [4] but the underlying genetic cause, mutations in CHRDL1 (MIM 300350), has only recently been discovered [3]. CHRDL1 encodes ventroptin (or neuralin-1, neurogenesin-1, chordin-like 1), a secreted bone morphogenetic protein (BMP) antagonist [5]. To date, presumed loss-of-function mutations in CHRDL1 have been described in eight unrelated families affected with MGC1 [3], [6].…”

Section: Introductionmentioning

confidence: 99%

Association of CHRDL1 Mutations and Variants with X-linked Megalocornea, Neuhäuser Syndrome and Central Corneal Thickness

Davidson¹,

Cheong²,

Hysi

et al. 2014

PLoS ONE

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We describe novel CHRDL1 mutations in ten families with X-linked megalocornea (MGC1). Our mutation-positive cohort enabled us to establish ultrasonography as a reliable clinical diagnostic tool to distinguish between MGC1 and primary congenital glaucoma (PCG). Megalocornea is also a feature of Neuhäuser or megalocornea-mental retardation (MMR) syndrome, a rare condition of unknown etiology. In a male patient diagnosed with MMR, we performed targeted and whole exome sequencing (WES) and identified a novel missense mutation in CHRDL1 that accounts for his MGC1 phenotype but not his non-ocular features. This finding suggests that MMR syndrome, in some cases, may be di- or multigenic. MGC1 patients have reduced central corneal thickness (CCT); however no X-linked loci have been associated with CCT, possibly because the majority of genome-wide association studies (GWAS) overlook the X-chromosome. We therefore explored whether variants on the X-chromosome are associated with CCT. We found rs149956316, in intron 6 of CHRDL1, to be the most significantly associated single nucleotide polymorphism (SNP) (p = 6.81×10−6) on the X-chromosome. However, this association was not replicated in a smaller subset of whole genome sequenced samples. This study highlights the importance of including X-chromosome SNP data in GWAS to identify potential loci associated with quantitative traits or disease risk.

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“…This region overlaps the gene CHRDL1 , which is a member of the bone morphogenetic protein ( BMP ) superfamily and antagonizes the function of BMP4 (Webb et al., 2012). It may play an important role in embryonic bone formation and neural stem cell differentiation (Gao, Zhang, Zhang, Wan, & Yin, ). CHRDL1 was demonstrated to aid the proliferation and survival of bone marrow‐derived human mesenchymal stem cells (hMSCs) and to help with the regeneration of human cartilage (Taylor et al., ).…”

Section: Discussionmentioning

confidence: 99%

Detecting selection signatures on the X chromosome of the Chinese Debao pony

Liu

Pan

Zhao

et al. 2018

J Animal Breeding Genetics

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The X chromosome shows a special interaction between demographic factors and genetic variation, and the analysis of X-linked genomic variation can therefore provide insights into the unique effects of demography and selection on the horse genome that cannot be readily detected by autosomal markers. Debao (DB) ponies have experienced intense selective pressure for the development of their small stature (<106 cm at adult height). To identify selective sweeps on the X chromosome of the DB pony, we performed a genome-wide scan of three Chinese horse breeds using an Equine SNP70 BeadChip. Using Yili and Mongolian horses (>134 cm at adult height) as reference groups, both F and XP-EHH revealed that five regions on the X chromosome were under strong selection, resulting in 95 overlapping genes. Seven of these genes, SMS, PHEX, ACSL4, CHRDL1, CACNA1F, DKC1 and CDKL5, are involved in bone development, growth hormone secretion and fat deposition. The region showing the strongest selection pressure was located at the position of 86.6-87.5 Mb. The subsequent genome-wide association analysis of the adult height of three Chinese horse breeds detected the two most significant SNPs in the same region, and these two SNPs overlapped with the gene CHRDL1. As a member of the bone morphogenetic protein (BMP) superfamily, CHRDL1 antagonizes the function of BMP4 and plays an important role in embryonic bone formation and cartilage generation. Our results provide new insights into the X-linked selection in Chinese Debao pony.

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Chordin-like protein 1 promotes neuronal differentiation by inhibiting bone morphogenetic protein-4 in neural stem cells

Cited by 25 publications

References 30 publications

Agonists and Antagonists of TGF-β Family Ligands

Agonists and Antagonists of TGF-β Family Ligands

Association of CHRDL1 Mutations and Variants with X-linked Megalocornea, Neuhäuser Syndrome and Central Corneal Thickness

Detecting selection signatures on the X chromosome of the Chinese Debao pony

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