RNA-seq of isolated chromaffin cells highlights the role of sex-linked and imprinted genes in adrenal medulla development
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Adrenal chromaffin cells and sympathetic neurons synthesize and release catecholamines, and both cell types are derived from neural crest precursors. However, they have different developmental histories, with sympathetic neurons derived directly from neural crest precursors while adrenal chromaffin cells arise from neural crest-derived cells that express Schwann cell markers. We have sought to identify the genes, including imprinted genes, which regulate the development of the two cell types in mice. We developed a method of separating the two cell types as early as E12.5, using differences in expression of enhanced yellow fluorescent protein driven from the tyrosine hydroxylase gene, and then used RNA sequencing to confirm the characteristic molecular signatures of the two cell types. We identified genes differentially expressed by adrenal chromaffin cells and sympathetic neurons. Deletion of a gene highly expressed by adrenal chromaffin cells, NIK-related kinase, a gene on the X-chromosome, results in reduced expression of adrenaline-synthesizing enzyme, phenyl-N-methyl transferase, by adrenal chromaffin cells and changes in cell cycle dynamics. Finally, many imprinted genes are up-regulated in chromaffin cells and may play key roles in their development.
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RNA-seq data showed selectively higher expression of Nod1 in adrenal chromaffin cells compared to sympathetic nerves.
“RNA-seq data showed selectively higher expression of Nod1 in adrenal chromaffin cells compared to sympathetic nerves (Chan et al., 2019).”
From Intestinal microbiota modulates adrenomedullary response through Nod1 sensing in chromaffin cells (2021) · cites this paper as Chan et al., 2019
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Intestinal microbiota modulates adrenomedullary response through Nod1 sensing in chromaffin cells
Xiang, C., Chen, P., Zhang, Q., Li, Y., Pan, Y., Xie, W., Sun, J., & Liu, Z. (2021) · iScience · doi:10.1016/j.isci.2021.102849 · Cited by 15 · see citing works
- Authors
- Chan, W. H., Komada, M., Fukushima, T., Southard-Smith, E. M., Anderson, C. R., & Wakefield, M. J.
- Affiliations
- The University of Melbourne (AU)
- Tokyo Institute of Technology (JP)
- Corresponding author
- Chan, Wing Hei
- Wakefield, Matthew J.
- Venue
- Scientific Reports
- Published
- 2019-03-08
- Volume
- 9
- Issue
- 1
- Pages
- 3929-3929
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6408553
- OpenAlex
- W2921717935
- Cited by
- 24
- References
- 60
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 7 · 2022: 4 · 2021: 7 · 2020: 2
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by)
- Funders
- Department of Health | National Health and Medical Research Council (1063822)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
- Health Sciences › Medicine › Surgery › Congenital gastrointestinal and neural anomalies
- Keywords
- adrenal chromaffin cells, sympathetic neurons, genomic imprinting, sex-linked genes, phenylethanolamine N-methyltransferase, catecholamine synthesis, tyrosine hydroxylase, neural crest, cell cycle kinetics, X chromosome, gene expression profiling
- MeSH terms
- RNA-Seq, Adrenal Medulla, Animals, Bacterial Proteins, Cell Separation, Female, Luminescent Proteins, Male, Mice, Inbred C57BL, Mice, Transgenic, Pregnancy, Protein Serine-Threonine Kinases, Mice, Knockout, Genomic Imprinting, Gene Expression Regulation, Developmental, Chromaffin Cells, Intracellular Signaling Peptides and Proteins, Genes, X-Linked, Mice, Neural Stem Cells, Gene Ontology
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