Neural Crest Cell Evolution

Muñoz, William A.; Trainor, Paul A.

doi:10.1016/bs.ctdb.2014.11.001

Cited by 28 publications

(18 citation statements)

References 104 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The emergence of vertebrates was accompanied by several important cellular and developmental milestones. These included among others the origin of an adaptive immune system, the emergence of neural crest cells and complex neuronal networks, and the appearance of synchronized and complex symmetric segmentation patterns 28 29 30 . Because NAF-1 is linked to several different neurological disorders 1 10 11 13 18 , it is plausible that the origin of NAF-1 through ancestral CISD duplication and differentiation coincided with the origin of specialized neuronal cells in vertebrates, and that NAF-1 conferred important adaptive functions for the maintenance of these neuronal cells.…”

Section: Discussionmentioning

confidence: 99%

Phylogenetic analysis of eukaryotic NEET proteins uncovers a link between a key gene duplication event and the evolution of vertebrates

Inupakutika

Sengupta

Nechushtai

et al. 2017

Sci Rep

View full text Add to dashboard Cite

NEET proteins belong to a unique family of iron-sulfur proteins in which the 2Fe-2S cluster is coordinated by a CDGSH domain that is followed by the “NEET” motif. They are involved in the regulation of iron and reactive oxygen metabolism, and have been associated with the progression of diabetes, cancer, aging and neurodegenerative diseases. Despite their important biological functions, the evolution and diversification of eukaryotic NEET proteins are largely unknown. Here we used the three members of the human NEET protein family (CISD1, mitoNEET; CISD2, NAF-1 or Miner 1; and CISD3, Miner2) as our guides to conduct a phylogenetic analysis of eukaryotic NEET proteins and their evolution. Our findings identified the slime mold Dictyostelium discoideum’s CISD proteins as the closest to the ancient archetype of eukaryotic NEET proteins. We further identified CISD3 homologs in fungi that were previously reported not to contain any NEET proteins, and revealed that plants lack homolog(s) of CISD3. Furthermore, our study suggests that the mammalian NEET proteins, mitoNEET (CISD1) and NAF-1 (CISD2), emerged via gene duplication around the origin of vertebrates. Our findings provide new insights into the classification and expansion of the NEET protein family, as well as offer clues to the diverged functions of the human mitoNEET and NAF-1 proteins.

show abstract

Section: Discussionmentioning

confidence: 99%

Phylogenetic analysis of eukaryotic NEET proteins uncovers a link between a key gene duplication event and the evolution of vertebrates

Inupakutika

Sengupta

Nechushtai

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…After delamination from the neural folds, NC cells migrate ventrally and extensively, giving rise to a wide variety of differentiated cell types, e.g., neurons, glia, bone, cartilage, and connective tissue of the head (Bronner-Fraser, 2004; Crane and Trainor, 2006; Meulemans and Bronner-Fraser, 2004; Munoz and Trainor, 2015; Trainor, 2005b). Labeling and tracking NC have been essential for understanding the NC contribution to different tissue and cell types, which is fundamental for organogenesis.…”

Section: Introductionmentioning

confidence: 99%

Specific and spatial labeling of P0‐Cre versus Wnt1‐Cre in cranial neural crest in early mouse embryos

Chen

Ishan

Yang

et al. 2017

Genesis

View full text Add to dashboard Cite

P0-Cre and Wnt1-Cre mouse lines have been widely used in combination with loxP-flanked mice to label and genetically modify neural crest (NC) cells and their derivatives. Wnt1-Cre has been regarded as the gold standard and there have been concerns about the specificity of P0-Cre because it is not clear about the timing and spatial distribution of the P0-Cre transgene in labeling NC cells at early embryonic stages. We re-visited P0-Cre and Wnt1-Cre models in the labeling of NC cells in early mouse embryos with a focus on cranial NC. We found that R26-lacZ Cre reporter responded to Cre activity more reliably than CAAG-lacZ Cre reporter during early embryogenesis. Cre immunosignals in P0-Cre and reporter (lacZ and RFP) activity in P0-Cre/R26-lacZ and P0-Cre/R26-RFP embryos were detected in the cranial NC and notochord regions in E8.0–9.5 (4–19 somite) embryos. P0-Cre transgene expression was observed in migrating NC cells and was more extensive in the forebrain and hindbrain but not apparent in the midbrain. Differences in the Cre distribution patterns of P0-Cre and Wnt1-Cre were profound in the midbrain and hindbrain regions, i.e., extensive in the midbrain of Wnt1-Cre and in the hindbrain of P0-Cre embryos. The difference between P0-Cre and Wnt1-Cre in labeling cranial NC may provide a better explanation of the differential distributions of their NC derivatives and of the phenotypes caused by Cre-driven genetic modifications.

show abstract

“…This increasing complexity of the ECM has been concomitant with the appearance of novel structures including the neural crest and endothelium-lined vasculature in vertebrates or of mammary glands in mammals. 36,37 In addition, sequence analysis has revealed the presence of an RGD motif in the carboxy-terminal region of the zebrafish sequence and two consensus potential binding sites, RGD and LDV, for integrins, 38,39 which are known ECM protein receptors, in the amino-terminal region of mammalian sequences of SNED1 (Figure 1), suggesting that the protein has further evolved, likely to support the development of mammalian-specific structures, as has occurred for other ECM proteins.…”

Section: Sned1 Is Conserved Among All Vertebrates and Presents Key Fementioning

confidence: 99%

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Barqué

Jan

Fuente

et al. 2018

Preprint

View full text Add to dashboard Cite

AbstractBackgroundThe extracellular matrix (ECM) is a fundamental component of multicellular organisms that orchestrates developmental processes and controls cell and tissue organization. We previously identified the novel ECM protein SNED1 as a promoter of breast cancer metastasis and showed that its level of expression negatively correlated with survival of breast cancer patients. Here we sought to identify the roles of SNED1 during murine development and in physiology.ResultsWe generated two novel Sned1 knockout mouse strains and showed that Sned1 is essential since homozygous ablation of the gene led to ~67% early neonatal lethality. Phenotypic analysis of the surviving knockout mice obtained revealed a role for SNED1 in the development of craniofacial and skeletal structures since Sned1 knockout resulted in growth defects, nasal cavity occlusion, and craniofacial malformations. Sned1 is widely expressed in embryos, notably in neural-crest derivatives. We further show here that mice with a neural-crest-cell-specific deletion of Sned1 survive, but display facial anomalies partly phenocopying the global knockout mice.ConclusionsOur results demonstrate requisite roles for SNED1 during development and neonatal survival. Importantly, the deletion of 2q37.3 in humans, a region that includes the SNED1 locus, has been associated with facial dysmorphism and short stature.

show abstract

Neural Crest Cell Evolution

Cited by 28 publications

References 104 publications

Phylogenetic analysis of eukaryotic NEET proteins uncovers a link between a key gene duplication event and the evolution of vertebrates

Phylogenetic analysis of eukaryotic NEET proteins uncovers a link between a key gene duplication event and the evolution of vertebrates

Specific and spatial labeling of P0‐Cre versus Wnt1‐Cre in cranial neural crest in early mouse embryos

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Contact Info

Product

Resources

About